慢性重型肝炎患者物质能量代谢特点及营养干预措施研究
|
摘要
本文通过对慢性肝炎、慢性重型肝炎和肝硬化患者物质能量代谢的测定,研究慢重肝患者的物质能量代谢特点;通过睡前进食的方法观察改善慢重肝患者糖代谢紊乱的可能性;应用RT-PCR及免疫组化方法研究慢重肝肝组织中部分与糖代谢相关因子的表达,探讨慢性重型肝炎患者葡萄糖代谢紊乱的发生机制。
研究表明,慢重肝患者三大营养素氧化供能比例失调,能量摄入低于能量消耗,机体呈低代谢和失平衡状态,慢重肝患者的死亡发生率与能量失衡的严重程度呈正相关,即时给与低浓度的葡萄糖溶液可以改变患者的呼吸商;通过对部分慢重肝患者给予睡前进食干预措施的观察,呼吸商得到改善,碳水化合物的氧化率提高,脂肪、蛋白质分解降低,由于能量代谢的改善利于了肝细胞的修复,在一定程度上降低慢重肝患者的病死率;实验结果显示慢重肝肝组织中葡萄糖激酶mRNA和GLUT-2、GLUT-1表达减少,可见缺氧诱导因子的表达。肝脏葡萄糖激酶mRNA表达水平与葡萄糖氧化代谢障碍的严重程度呈正相关。
本研究结论是,对于慢性重型肝炎患者,睡前进食一定量的碳水化合物,能够改善呼吸商和能量代谢,促进肝细胞的修复;糖代谢障碍的机制与肝脏GCK- mRNA、GLUT-2、GLUT-1表达减少及肝细胞缺氧状态密切相关。
Objective:
To analyze the characteristic of carbohydrate, protein, fat and energy metabolism in patients with chronic severe hepatitis; to research on the effects of a late evening snack on the Substrate and energy metabolism; to understand the mechanisms of carbohydrate metabolism disturbance in patients with chronic severe hepatitis by studying the expression of GCKmRNA and GLUT-2, HIF-1, GLUT-1 in hepatic tissues of patients with sever chronic hepatitis, to provide a theoretical basis for the individual of clinical nutritional support.
Methods:
Indirect calorimetry was employed to detect resting energy expenditure (REE), RQ, oxidation rates of protein (PRO), fat (FAT) and carbohydrate (CHO) in 100 cases of sever chronic hepatitis, 100 cases of liver cirrosis and 82 cases recovered from chronic viral hepatitis patients. Energy intake was determined by 1-3 days before REE measurement diet recall.
30 patients with the early and middle stage of severe chronic hepatitis B were recruited and they were randomly divided into two groups, we administered an oral supplement with carbohydrate food(200kcal) to patients in study groups at before bedtime, the meal intakes were investigated and were calculated by meal expert software system at the same times; indirect calorimetry employed to detect the REE, RQ, oxidation rates of protein, fat and carbohydrate in these patients; the level of serum liver function, fasting blood glucose and PTA et were detected by Olympus640 auto analyse system, MELD scores of patients in study groups were calculated.
The expression of GCK mRNA in hepatic tissues of 10 cases with sever chronic hepatitis and 10 cases with liver cirrhosis (Child-pugh A) were directed by RT-PCR technique; The expression of GLUT-2, GLUT-1 and HIF-1 in hepatic tissues of 10 cases with sever chronic hepatitis, 10 cases with liver cirrhosis, 10 cases with chronic hepatitis and 5 normal control subjects were directed by immunohistochemistry.
Detection:
Indirect calorimetry was employed to detect REE, RQ, oxidation rates of protein, fat and carbohydrate; the meal intakes were investigated and were calculated by meal expert software system at the same times; the level of serum liver function, fasting blood glucose and PTA et were detected by Olympus640 auto analyse system; the expression of GCK mRNA in hepatic tissues were directed by RT-PCR technique; the expression of GLUT-2 , HIF-1, GLUT-1 in hepatic tissues were directed by immunohistochemistry.
Results:
1. The REE of patients with sever chronic hepatitis, liver cirrhosis and chronic hepatitis were 1402.05±480.07, 1274.27±316.36 and 1396.77±384.80kcal/day, lower than the value of predicted derived from H-B equation. The RQ and the oxidation rates of carbohydrate were significantly lower in sever chronic hepatitis than that in patients with liver cirrhosis and chronic hepatitis, the oxidation rates of fat was higher(p=0.000).
2. The RQ of non-survivor groups with sever chronic hepatitis was lower than the value of survivor groups, 0.81±0.07 vs 0.86±0.04, p=0.000. The oxidation rates of carbohydrate were significantly lower in non-survivor groups than that in survivor groups, the oxidation rates of fat and protein was higher(p= 0.000, 0.002, 0.009).
3. The energy intakes of patients with sever chronic hepatitis, liver cirrhosis and chronic hepatitis were 1252.86±501.80 kcal/day, 1623.78±477.69 kcal/day and 1705.36±463.99 kcal/day,that was significantly lower in sever chronic hepatitis than that in patients with liver cirrhosis and chronic hepatitis(p=0.000); energy, fat and protein intakes were lower than consumption, and was a negative balance; The energy intakes were significantly higher in survivor groups with sever chronic hepatitis than in non-survivor groups.
4. After a late evening snack, the carbohydrate intake in study group increased, REE has no significant change, RQ were significantly higher in study group than that in control group at the 14th day(0.87±0.07 vs 0.82±0.07,p<0.05); the oxidation rates in study and control group of protein,fat and carbohydrate were respectively 20.6±9.0 vs 28.9±11.4,30.1±20.5 vs 35.9±32.7 and 49.2±24.6 vs 37.8±30.8, the oxidation rates of protein and fat decreased and carbohydrate increased(p<0.05); ALB, PTA and FBS were significantly higher in study group than that in control group at the 14th day [(34.4±13.1 vs 30.6±9.8)g/l,(68.8±33.2 vs 38.0±29.0)%,(5.3±0.1 vs 4.3±0.2) mmol/l,p<0.05]。
5. The expression level of GCK mRNA in hepatic tissues with sever chronic hepatitis was lower than with liver cirrhosis (1.13±0.11 vs 1.44±0.14,p<0.05). The level of GCK mRNA of hepatic tissues with sever chronic hepatitis had positive correlation with the oxidation rates of carbohydrate(r=0.845,P<0.01), and had no correlation with the fasting blood glucose. The expression of GLUT-2 and GLUT-1 reduced and HIF-1 was found in hepatic tissues with sever chronic hepatitis.
Conclusion:
1. Patients with severe chronic hepatitis are in low energy expenditure state, energy intakes and consumption was imbalance, energy was mainly supplied with fat and protein in early morning. The oxidation rates of protein and fat reduced and carbohydrate increased. Low metabolism is a self-protection of body in patients with severe chronic hepatitis.
2. RQ is better than REE to reflect the body's metabolic status of the three major nutrients and the severity of the disease.
3. Oral supplementation with carbohydrate food in the patients with sever chronic hepatitis before bedtime could improve RQ, increase in glucose oxidation, decrease fat and protein catabolism.
4. The level of GCK mRNA had closely relationship with the oxidation and usage of carbohydrate, the expression of HIF-1 prompt hypoxia in liver cell; the expression reduced of GCK mRNA and GLUT-2 and GLUT-1 in hepatic tissues were one of carbohydrate metabolism disturbance mechanisms in patients with chronic severe hepatitis.
研究表明,慢重肝患者三大营养素氧化供能比例失调,能量摄入低于能量消耗,机体呈低代谢和失平衡状态,慢重肝患者的死亡发生率与能量失衡的严重程度呈正相关,即时给与低浓度的葡萄糖溶液可以改变患者的呼吸商;通过对部分慢重肝患者给予睡前进食干预措施的观察,呼吸商得到改善,碳水化合物的氧化率提高,脂肪、蛋白质分解降低,由于能量代谢的改善利于了肝细胞的修复,在一定程度上降低慢重肝患者的病死率;实验结果显示慢重肝肝组织中葡萄糖激酶mRNA和GLUT-2、GLUT-1表达减少,可见缺氧诱导因子的表达。肝脏葡萄糖激酶mRNA表达水平与葡萄糖氧化代谢障碍的严重程度呈正相关。
本研究结论是,对于慢性重型肝炎患者,睡前进食一定量的碳水化合物,能够改善呼吸商和能量代谢,促进肝细胞的修复;糖代谢障碍的机制与肝脏GCK- mRNA、GLUT-2、GLUT-1表达减少及肝细胞缺氧状态密切相关。
Objective:
To analyze the characteristic of carbohydrate, protein, fat and energy metabolism in patients with chronic severe hepatitis; to research on the effects of a late evening snack on the Substrate and energy metabolism; to understand the mechanisms of carbohydrate metabolism disturbance in patients with chronic severe hepatitis by studying the expression of GCKmRNA and GLUT-2, HIF-1, GLUT-1 in hepatic tissues of patients with sever chronic hepatitis, to provide a theoretical basis for the individual of clinical nutritional support.
Methods:
Indirect calorimetry was employed to detect resting energy expenditure (REE), RQ, oxidation rates of protein (PRO), fat (FAT) and carbohydrate (CHO) in 100 cases of sever chronic hepatitis, 100 cases of liver cirrosis and 82 cases recovered from chronic viral hepatitis patients. Energy intake was determined by 1-3 days before REE measurement diet recall.
30 patients with the early and middle stage of severe chronic hepatitis B were recruited and they were randomly divided into two groups, we administered an oral supplement with carbohydrate food(200kcal) to patients in study groups at before bedtime, the meal intakes were investigated and were calculated by meal expert software system at the same times; indirect calorimetry employed to detect the REE, RQ, oxidation rates of protein, fat and carbohydrate in these patients; the level of serum liver function, fasting blood glucose and PTA et were detected by Olympus640 auto analyse system, MELD scores of patients in study groups were calculated.
The expression of GCK mRNA in hepatic tissues of 10 cases with sever chronic hepatitis and 10 cases with liver cirrhosis (Child-pugh A) were directed by RT-PCR technique; The expression of GLUT-2, GLUT-1 and HIF-1 in hepatic tissues of 10 cases with sever chronic hepatitis, 10 cases with liver cirrhosis, 10 cases with chronic hepatitis and 5 normal control subjects were directed by immunohistochemistry.
Detection:
Indirect calorimetry was employed to detect REE, RQ, oxidation rates of protein, fat and carbohydrate; the meal intakes were investigated and were calculated by meal expert software system at the same times; the level of serum liver function, fasting blood glucose and PTA et were detected by Olympus640 auto analyse system; the expression of GCK mRNA in hepatic tissues were directed by RT-PCR technique; the expression of GLUT-2 , HIF-1, GLUT-1 in hepatic tissues were directed by immunohistochemistry.
Results:
1. The REE of patients with sever chronic hepatitis, liver cirrhosis and chronic hepatitis were 1402.05±480.07, 1274.27±316.36 and 1396.77±384.80kcal/day, lower than the value of predicted derived from H-B equation. The RQ and the oxidation rates of carbohydrate were significantly lower in sever chronic hepatitis than that in patients with liver cirrhosis and chronic hepatitis, the oxidation rates of fat was higher(p=0.000).
2. The RQ of non-survivor groups with sever chronic hepatitis was lower than the value of survivor groups, 0.81±0.07 vs 0.86±0.04, p=0.000. The oxidation rates of carbohydrate were significantly lower in non-survivor groups than that in survivor groups, the oxidation rates of fat and protein was higher(p= 0.000, 0.002, 0.009).
3. The energy intakes of patients with sever chronic hepatitis, liver cirrhosis and chronic hepatitis were 1252.86±501.80 kcal/day, 1623.78±477.69 kcal/day and 1705.36±463.99 kcal/day,that was significantly lower in sever chronic hepatitis than that in patients with liver cirrhosis and chronic hepatitis(p=0.000); energy, fat and protein intakes were lower than consumption, and was a negative balance; The energy intakes were significantly higher in survivor groups with sever chronic hepatitis than in non-survivor groups.
4. After a late evening snack, the carbohydrate intake in study group increased, REE has no significant change, RQ were significantly higher in study group than that in control group at the 14th day(0.87±0.07 vs 0.82±0.07,p<0.05); the oxidation rates in study and control group of protein,fat and carbohydrate were respectively 20.6±9.0 vs 28.9±11.4,30.1±20.5 vs 35.9±32.7 and 49.2±24.6 vs 37.8±30.8, the oxidation rates of protein and fat decreased and carbohydrate increased(p<0.05); ALB, PTA and FBS were significantly higher in study group than that in control group at the 14th day [(34.4±13.1 vs 30.6±9.8)g/l,(68.8±33.2 vs 38.0±29.0)%,(5.3±0.1 vs 4.3±0.2) mmol/l,p<0.05]。
5. The expression level of GCK mRNA in hepatic tissues with sever chronic hepatitis was lower than with liver cirrhosis (1.13±0.11 vs 1.44±0.14,p<0.05). The level of GCK mRNA of hepatic tissues with sever chronic hepatitis had positive correlation with the oxidation rates of carbohydrate(r=0.845,P<0.01), and had no correlation with the fasting blood glucose. The expression of GLUT-2 and GLUT-1 reduced and HIF-1 was found in hepatic tissues with sever chronic hepatitis.
Conclusion:
1. Patients with severe chronic hepatitis are in low energy expenditure state, energy intakes and consumption was imbalance, energy was mainly supplied with fat and protein in early morning. The oxidation rates of protein and fat reduced and carbohydrate increased. Low metabolism is a self-protection of body in patients with severe chronic hepatitis.
2. RQ is better than REE to reflect the body's metabolic status of the three major nutrients and the severity of the disease.
3. Oral supplementation with carbohydrate food in the patients with sever chronic hepatitis before bedtime could improve RQ, increase in glucose oxidation, decrease fat and protein catabolism.
4. The level of GCK mRNA had closely relationship with the oxidation and usage of carbohydrate, the expression of HIF-1 prompt hypoxia in liver cell; the expression reduced of GCK mRNA and GLUT-2 and GLUT-1 in hepatic tissues were one of carbohydrate metabolism disturbance mechanisms in patients with chronic severe hepatitis.
引文
[1]姚光弼临床肝脏病学.上海:上海科学技术出版社,2004,740-743.
[2]杨绍基.传染病学.人民卫生出版社,2008,41-42.
[3]许天蕴,赵秀娥.2型糖尿病及代谢综合征与非酒精性脂肪肝相关因素分析[J].临床内科杂志,2007,24(10):34-36.
[4]洪尚游,万漠彬,赵汉美.重型病毒性肝炎并发低血糖临床分析[J].肝脏杂志,2005,10(2):98-99.
[5]彭劼，张琪，郭亚兵．血糖水平对慢性重型乙型肝炎预后的影响[J].广东医学, 2008,07:21-22.
[6]林建英.慢性重型肝炎血糖变化与预后关系的临床分析[J].中外医疗,2009,05:52.
[7]潘教治,汪建琴.慢性重型肝炎血糖变化与预后关系的临床分析[J].重庆医学,2007,06:73-74.
[8] Takada Y,Ishigure S,Fukunaga K.Large-animal models of fulminant hepatic failure [J].Artif Organs,2003,6(1):9-13.
[9]陈萍.血糖水平对重型肝炎患者预后影响的分析[J].中华肝脏病杂志, 2006,14(8):572-573.
[10]钟乔华.248例病毒性肝炎病人空腹血糖水平检测分析[J].中国医师杂志,1999,1(10):43.
[11]涂燕云.重型病毒性肝炎代谢功能紊乱状况与营养治疗现状[J].右江医学,2004,32 (6):590-592.
[12] Obici S,Lopes-Bertolini G,Curi R,et al.Liver glycogen metabolism during short-term insulin-induced hypoglycemia in fed rats [J].Cell Biochem Funct,2008,26(7):755-759.
[13]许超宇,顾琳,朱宇佳,等.糖代谢紊乱与重型肝炎预后的关系[J].实用医学杂志,2008,22:81-82.
[14] Gundling F,Schumm-Draeger PM,Schepp W.Hepatogenous Diabetes- Diagnostics and Treatment.Z Gastroenterol,2009,47(5):436-445.
[15] Chen JW,Nielsen MF,Caumo A,et al.Changes in bioactive IGF-I and IGF-binding protein-1 during an oral glucose tolerance test in patients with liver cirrhosis[J]. Eur J Endocrinol.2006,155(2):285-292.
[16] Sibley SD,Palmer JP,Hirsch IB,et al.Visceral obesity,hepatic lipase activity,and dyslipidemia in type 1 diabetes[J] .Clin Endocrinol Metab,2003,88(7):3379-3384.
[17] Hetty A,Wilson S,Kuo P,et al.Liver transplantation improves cirrhosis associated impaired oral glucose tolerance [J].Transplantation,2000,69(11): 2451-2454.
[18]韩红梅,朴云峰,全红梅.肝源性糖尿病125例临床分析[J].临床肝胆病杂志,2007,23(3):214-215.
[19]池肇春.实用临床肝病学[M].北京:中国医药科技出版社,1999∶740-743.
[20] Landau BR.Methods for measuring glycogen cycling.American Journal of Physiology,Endocrinology and Metabolism,2001,281:413-419.
[21] Lei WY,Wang TE,Chen TL,et al.Insulinoma causing hypoglycemia in a patient with type 2 diabetes [J].Formos Med Assoc,2007,106(5):392-396.
[22]唐华,王旭霞,赵曙光,等.瘦素与肝源性糖尿病患者胰岛素抵抗的相关性研究[J].西南国防医药,2009,2,32-34.
[23] Roden M,Petersen KF,Shulman GI.Nuclear magnetic resonance studies of hepatic glucose metabolism in humans.Recent Progress in Hormone Research 2001,56:219-237.
[24] Tamura A,Ishihara H,Suzuki S,et a1.Hypoglycemia associated with hyperinsulinemia in a subject with type 2 diabetes and liver cirrhosis.Nippon Naika Gakkai Zasshi,2006,95 (7):1371-1374.
[25] Home PD,Pacini G.Hepatic dysfunction and insulin insensitivity in type 2 diabetes mellitus:a critical target for insulin-sensitizing agents.Diabetes Obes Metab,2008,10(9):699-718.
[26] Miyamoto I,Miyakoshi H,Nagaiy,et a1.Characterization of the insulin resistance in liver cirrhosis with non-insulin dependantdiabetes mellitus.Endocrinol JPN,1992,39:421-429.
[27] Zhang X,Shen W,Shen DM.A clinical analysis of liver disease patients with abnormal glucose metabolism.Zhonghua Gan Zang Bing Za Zhi,2006 ,14(4):289-292.
[28] Conchillo M,Prieto J,Quiroga J.Insulin-like growth factor I (IGF-I) and liver cirrhosis.Rev Esp Enferm Dig,2007,99(3):156-164.
[29] Shmueli E,Miell JP,Stewart M,et al.High insulin-like growth factor binding protein 1 levels in cirrhosis:link with insulin resistance [J].Hepatology,1996, 24(1):127-133.
[30] Shintani Y,Fujie H,Miyoshi H,et al.Hepatitis C virus infection and diabetes: direct involvement of the virus in the development of insulin resistance [J].Gastroenterology,2004,126 (3):840.
[31] Lin SY,Wang YY,Sheu WH.Increased serum soluble tumor necrosis factor receptor levels are associated with insulin resistance in liver cirrhosis [J].Metabolism,2004,53:922.
[32] Overexpressing cellular glutathione peroxidase PNAS 2004,101:8852-8857.
[33] Fritsche L,Weigert C,H?ring HU,et al.How insulin receptor substrate proteins regulate the metabolic capacity of the liver--implications for health and disease[J].Curr Med Chem,2008,15(13):1316-1329.
[34] Lawrence MC,McKern NM,Ward CW.Insulin receptor structure and its implications for the IGF-1 receptor[J].Curr Opin Struct Biol,2007,17(6):699-705.
[35]刘淑娥,肖丹.肝源性糖尿病临床分析[J].中日友好医院学报,2003,17 (3):153.
[36] Shi DR,Dong CL,Lu L,et al.Relationship between glucose metabolic disorders and expression of insulin receptor in posthepatitic cirrhosis hepatocyte and HBV DNA in pancreatic cells[J].Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi,2003,17(4):372-374.
[37] Draznin B.Molecular mechanisms of insulin resistance:serine phosphorylationof insulin receptor substrate-1 and increased expression of p85alpha:the two sides of a coin.Diabetes,2006,55(8):2392-2397.
[38] Van Harmelen V,Rydén M,Sj?lin E,et al.A role of lipin in human obesity and insulin resistance : relation to adipocyte glucose transport and GLUT4 expression[J].Lipid Res,2007,48(1):201-206.
[39] Fernández-Veledo S,Hernandez R,Teruel T,et al.Ceramide mediates TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes[J].Arch Physiol Biochem,2006,112(1):13-22.
[40] Dong X,Park S,Lin X,et al.Irs1 and Irs2 signaling is essential for hepatic glucose homeostasis and systemic growth[J] .Clin Invest,2006,116(1):101-114.
[41] Carvalho E,Kotani K,Peroni O,et al.Adipose-specific overexpression of GLUT4 reverses insulin resistance and diabetes in mice lacking GLUT4 selectively in muscle[J].Am J Physiol Endocrinol Metab,2005,289(4):E551-561.
[42] Kubota N,Kubota T,Itoh S,et al.Dynamic functional relay between insulin receptor substrate 1 and 2 in hepatic insulin signaling during fasting and feeding[J].Cell Metab,2008,8(1):49-64.
[43]蒋斌,宋世兵,袁炯,等.肝移植术后糖尿病的初步研究[J].肝胆外科杂志,2004,12 (3):190.
[44]朱飞燕.肝硬变患者糖耐量减低和肝原性糖尿病的发病机理[J].临床消化病杂志,1999,11 (3):142.
[45]张霞,沈薇.肝病伴糖代谢异常患者的临床分析[J].中华肝脏病杂志,2006,4(14):289.
[46] Bhimma R,Coovadia HM.Hepatitis B virus-associated nephropathy[J].Am J Nephrol.2004,24(2):198-211.
[47]闫惠平,郎振为,黄德庄,等.地高辛素标记探针原位杂交法检测肝和肝外组织中乙型肝炎病毒DNA[J].中华内科杂志,1994,33(3):168-171.
[48]苟小林,张咪玲,朱爱华,等.肝硬化所致肝源性糖尿病糖代谢和胰岛素分泌特点的临床研究.延安大学学报,2009,1:28-32.
[49]解奕瑞,朱彪.2008年浙江省感染病、肝病学术年会论文汇编,2008.
[50]吴邦富,林丽莉,胡品津.肝硬化患者口服葡萄糖耐量试验的变化.实用肝脏病杂志,2004,7 (1):25.
[51]胡亚莉,陈惠贤.肝病患者糖代谢30例分析报告.九江医学,2004,19 (2):95.
[52]庄辉.积极控制乙型肝炎病毒感染[J].中华医学信息导报,2006,2l(6):12.
[53] Shimoda T,Shikata T,Karasawa T.Light microscopic localization of hepatitis B virus antigens in the human pancreas.Possibility of multiplication of hepatitis B virus in the human pancreas[J].Gastroenterology,1981,81(6):998-1005.
[54]陆立,时德仁,周燕,等.胰腺乙型肝炎病毒感染及其糖尿病的关系[J].临床军医杂志,2001,29 (2):71.
[55]时德仁,东传凌,陆立等.肝硬化时糖代谢紊乱与肝细胞胰岛素受体及胰腺细胞HBV DNA表达的关系[J].中华实验和临床病毒学杂志,2003,17(4):372-374.
[56] Persico M,Masarone M,La Mura V,et al.Clinical expression of insulin resistance in hepatitis C and B virus-related chronic hepatitis:differences and similarities[J].World J Gastroenterol,2009,15(4):462-466.
[57] Moucari R,Asselah T,Cazals-Hatem D,et al.Insulin resistance in chronic hepatitis C:association with genotypes 1 and 4,serum HCV RNA level,and liver fibrosis[J].Gastroenterology,2008,134(2):416-423.
[58]郑宏庭,邓华聪.葡萄糖激酶与糖尿病的研究进展[J].中国临床康复,2004,8(27):5960-5961.
[59]张亚莉,王剑青,陶建蜀,等.葡萄糖激酶基因微卫星DNA多态性与2型糖尿病的相关性研究[J].贵州医药,2006(9):771-773.
[60]马晓伟,钱荣立,王艳荣等.实验性非胰岛素依赖型糖尿病大鼠肝脏葡萄糖激酶活性的改变[J].中华内科杂志,1998,37:91-94.
[61] Kr?henbühl L,Lang C,Lüdes S,et a1.Reduced hepatic glycogen stores in patients with liver cirrhosis.Liver Int,2003,23(2):101-109.
[62] Almanza-Pérez JC,Blancas-Flores G,García-Macedo R,et al.Leptin and its association with obesity and type 2 diabetes.Gac Med Mex,2008,144(6):535-542.
[63] Farooqi IS,O'Rahilly S.Leptin:a pivotal regulator of human energy homeostasis[J].Am J Clin Nutr,2009,89(3):980-984.
[64] Figlewicz DP,Benoit SC.Insulin,leptin,and food reward:update 2008.Am J Physiol Regul Integr Comp Physiol,2009,296(1):9-19.
[65] Frühbeck G.Intracellular signalling pathways activated by leptin[J].Biochem J,2006,393:7-20.
[66] Yokaichiya DK,Galembeck E,Torres BB,et al.Insulin and leptin relations in obesity:a multimedia approach.Adv Physiol Educ,2008,32(3):231-236.
[67] Kosztáczky B,Fóris G,Paragh G Jr,et al.Leptin stimulates endogenous cholesterol synthesis in human monocytes:New role of an old player in atherosclerotic plaque formation . Leptin-induced increase in cholesterol synthesis. Int J Biochem Cell Biol,2007,39(9):1637-1645.
[68] Kohno D,Nakata M,Maekawa F,et al.Leptin suppresses ghrelin-induced activation of neuropeptide Y neurons in the arcuate nucleus via phosphatidylinositol 3- kinase- and phosphodiesterase 3- mediated pathway.Endocrinology,2007,148(5):2251-2263.
[69] Yu Y,Hu SK,Yan H.The study of insulin resistance and leptin resistance on the model of simplicity obesity rats by curcumin[ J ].Zhonghua Yu Fang Yi Xue Za Zhi,2008,42(11):818-822.
[70] Benomar Y,Naour N,Aubourgl A,et al.Insulin and leptin induce Glut4 plasma membrane translocation and glucose up take in a human neuronal cell line by a PB kinase dependent[ J ].Endocrinology,2006,147 (5):2550-2556.
[71] Forhead AJ,Lamb CA,Franko KL,et al.Role of leptin in the regulation of growth and carbohydrate metabolism in the ovine fetus during late gestation[ J ].J Physiol,2008,586(9):2393-2403.
[72] Borba-Murad GR,Mario EG, Bassoli BK,Comparative acute effects of leptinand insulin on gluconeogenesis and ketogenesis in perfused rat liver.Cell Biochem Funct,2005,23(6):405-413.
[73] Susan A,Loranne A.Leptin enhances glycogen storage in hepatecytes by inhibition of phesphorylase and exerts an additive effect with insulin.Diabetes,1999 48(1):15-20.
[74] Cao XP,Ming WY,Cheng H,et a1.Efects of leptin on gluco-oxidation and glucokinase gene expression in cultured liver cells[J].Chin J Endecfinol Metab,l999,15(3):131-133.
[75] Robinson-Rechavi M,Carpentier AS,Dufraisse M,et a1.How many nuclear hormone receptors are there in the human genome? [J] Trends Genet,2001,17(10):554-556.
[76] Edwards PA,Kennedy MA,Mak PA.LXRs;oxysterol-activated nuclear receptors that regulate genes controlling lipid homeostasis.Vascul Pharmacol, 2002,38:249-256.
[77] Talukdar S,Hilgartner FB.The mechanism mediating the activation of acetyl-coenzyme A carboxylase-{alpha}gene transcription by the liver X receptor agonist TO-901317[J].J Lipid Res,2006,47(11):2451-2461.
[78] Wente W,Brenner MB,Zitzer H,et a1.Activation of liver X receptors and retinoid X receptors induces growth arrest and apoptosis in insulin-secreting cells[J].Endocrinology,2007,148(4):1843-1849.
[79] Zelcer N,Tontonoz P.Liver X receptors as integrators of metabolic and inflammatory signaling[J].J Clin Invest,2006,116(3):607-614.
[80] Houck KA , Borchert KM , Hepler CD , et al . T0901317 is a dual LXR/FXR agonist.Mol Genet Metab,2004,83:184-187.
[81] Glass CK,Rosenfeld MG.The coregulator exchange in transcriptional functions of nuclear receptors [J].Genes Dev,2000,14(2):121-141.
[82] Barish GD, Evans RM.PPARs and LXRs:atherosclerosis goes nuclear.Trends Endocrinol Metab,2004,15:158-165.
[83] Cummins CL,VoHe DH,Zhang Y,et a1.Liver X receptors regulate adrenalcholesterol balance[J].J Clin Invest,2006,116(7):1902-1912.
[84] Rastinejad F.Retinoid X receptor and its partners in the nuclear receptor family[J].Curr Opin Struct Biol,2001,11(1):33-38.
[85] Yang C,McDonald JG,Patel A,et a1.Sterol intermediates from cholesterol biosynthetic pathway as liver X receptor Ligands[J].J Biol Chem,2006,281(38):7816-7826.
[86] Stulnig TM,Stefensen KR,Gao H,et a1.Novel roles of liver X receptors exposed by gene expression profiling in liver and adipose tissue[J].Mol Pharmacol,2002,62(6):1299-1305.
[87] Stulnig TM,Oppermann U,Stefensen KR,et a1.Liver X receptors downregulate 11 beta-hydroxysteroid dehydrogenase type 1 expression and activity[J].Diabetes,2002,51(8):2426-2433.
[88] Baranowski M.Biological role of liver X receptors[J].J Physiol Pharmacol,2008 ,59:31-55.
[89] Lafitte BA,Chao LC,Li J,et a1.Activation of liver X receptor improves glucose tolerance through coordinate regulation of glucose metabolism in liver and adipose tissue[J].Proc Natl Acad Sci USA,2003,100(9):5419-5424.
[90] Dalen KT,Ulven SM,Bamberg K,et a1.Expression of the insulin- responsive glucose transporter GLUT4 in adipocytes is dependent on liver X receptor alpha[J].J Biol Chem,2003,278(48):48283-48291.
[91] Grefhorst A,van Dijk TH,Hammer A,et a1.Differentia effects of pharmacological liver X receptor activation on hepatic and peripheral insulin sensitivity in lean and ob/ob mice[J].Am J Physiol Endocrinol Metab,2005,289(5):E829-E838.
[92] Cho N,Momose Y.Peroxisome proliferator-activated receptor gamma agonists as insulin sensitizers:from the discovery to recent progress.Curr Top Med Chem,2008,8(17):1483-507..
[93] Fernyhough ME,Okine E,Hausman G,et a1.PPARgamma and GLUT-4 expression as developmental regulators/markers for preadipocyte differentiationinto an adipocyte.Domest Anim Endocrinol,2007,33(4):367-78.
[94] Commerford SR , Vargas L , Dorfman SE , et a1 . Dissection of the insulin-sensitizing effect of liver X receptor ligands.Mol Endocrinol,2007,21(12):3002-3012.
[95] Kase ET,Wensaas AJ,Aas V,et a1.Skeletal muscle lipid accumulation in type 2 diabetes may involve the liver X receptor pathway[J].Diabetes,2005,54(4):1108-1115.
[96] Nomiyama T,Bruemmer D.Liver X receptors as therapeutic targets in metabolism and atherosclerosis.Curr Atheroscler Rep,2008,10(1):88-95.
[97] Hansen MK,Connolly TM.Nuclear receptors as drug targets in obesity,dyslipidemia and atherosclerosis.Curr Opin Investig Drugs,2008,9(3):247-255.
[98] Fiévet C,Staels B.Liver X receptor modulators:effects on lipid metabolism and potential use in the treatment of atherosclerosis.Biochem Pharmacol,2009,77(8):1316-1327.
[99] Bensinger SJ,Tontonoz P.Integration of metabolism and inflammation by lipid-activated nuclear receptors.Nature,2008,454(7203):470-477.
[100] Alaynick WA.Nuclear receptors,mitochondria and lipid metabolism.Mito -chondrion,2008,8(4):329-337.
[101] Jungermann K,Kietzmann T.Zonation of parenchymal and nonparenchymal metabolism in liver[J].Annu Rev Nutr,1996,16:179-203.
[102] Wiegman CH, Bandsma RH, Ouwens M ,et a1. Hepatic VLDL production in ob/ob mice is not stimulated by massive de novo lipogenesis but is less sensitive to the suppressive effects of insulin[J].Diabetes,2003,52(5):1081-1089.
[103]时德仁,东传凌,陆立,等.肝硬化时肝细胞胰岛素受体和酪氨酸蛋白激酶表达的定量研究.中华肝脏病杂志,2001,9:279-281.
[104] Shi DR,Dong CL,Lu L,et al.Relationship between glucose metabolic disorders and expression of insulin receptor in posthepatitic cirrhosishepatocyte and HBV DNA in pancreatic cells.Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi.2003,17(4):372-374.
[105] Fritsche L,Weigert C,H?ring HU,et al.How insulin receptor substrate proteins regulate the metabolic capacity of the liver--implications for health and disease.Curr Med Chem,2008,15(13):1316-1329.
[106] Han DW. Intestinal endotoxemia as a pathogenetic mechanism in liver failure World J Gastroenterol,2002,8:961.
[107] Iwata H , Soga Y , Meguro M , et al . High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1[J].J Endotoxin Res,2007,13(4):227-34.
[108] de Souza LF,Barreto F,da Silva EG,et al.Regulation of LPS stimulated ROS production in peritoneal macrophages from alloxan-induced diabetic rats:involvement of high glucose and PPARgamma.Life Sci,2007,81(2):153-159.
[109] Andrzejczak D,Górska D,Czarnecka E.Influence of amlodipine and atenolol on lipopolysaccharide (LPS)-induced serum concentrations of TNF-alpha,IL-1,IL-6 in spontaneously hypertensive rats (SHR) .Pharmacol Rep,2006 ,58(5):711-719.
[110] Diya Zhang,Lili Chen,Shenglai Li,et al.Lipopolysaccharide (LPS) of Porphyromonas gingivalis induces IL-1beta,TNF-alpha and IL-6 production by THP-1 cells in a way different from that of Escherichia coli LPS.Innate Immun,2008,14(2):99-107.
[111] Metzger S,Nusair S,Planer D,et a1.Inhibition of hepatic gluconeogenesis and enhanced glucose uptake contribute to the development of hypoglycemia in mice bearing interleukin-lbeta-secreting tumor.Endocrinology,2004,145:5150.
[112] Semenza GL.Hypoxia-inducible factor 1 and cancer pathogenesis.IUBMB Life,2008,60(9):591-597.
[113] Semenza GL.HIF-1 and human disease:one highly involved factor[J].Genes Dev,2000,(14):1983-1991.
[114] Scheepers A,Joost HG,Schürmann A.The glucose transporter families SGLT and GLUT: molecular basis of normal and aberrant function.JPEN J Parenter Enteral Nutr,2004,28(5):364-371.
[115] Cano A, Ticus I ,Chabrol B.Glucose transporter type 1 (GLUT-1) deficiency.Rev Neurol (Paris),2008,164(11):896-901.
[116] Yu S,Zhao T,Guo M,et al.Hypoxic preconditioning up-regulates glucose transport activity and glucose transporter (GLUT1 and GLUT3) gene expression after acute anoxic exposure in the cultured rat hippocampal neurons and astrocytes.Brain Res,2008,1211:22-9.
[117]中华传染病与寄生虫病学分会、肝病学会.病毒性肝炎防治方案.中华肝脏病杂志,2000,8(6):324-329.
[118]中华医学会感染病学分会肝衰竭与人工肝学组中华医学会肝病学分会重型肝病与人工肝学组.肝衰竭诊疗指南.中华肝脏病杂志,2006,14(9):19-22.
[119]冯岩梅,孟庆华.静息能量消耗测定在慢性肝病中的应用[J].中国临床营养,2007,15(2):107-110.
[120] Karhunern L,Franssial-Kallunki A ,Rissanen A,et al.Determinants of resting energy expenditure in obese non-diabetic Caucasian women.Int J Obes Relat Metab Disord,1997,21:197-202.
[121]蒋朱明,吴蔚然.肠内营养.北京:人民卫生出版社,2002,28-32.
[122]吴肇汉.实用临床营养治疗学.上海科学技术出版社,2001,374-395.
[123]李刚荣,汪仕良,余斌,等.人体能量消耗间接测定系统的研究.中国生物医学工程学报,1997,16(4):338-345.
[124]庄辉.我国乙型肝炎防治现状及目标[A] .第一届全国疑难重型肝病大会、第四届全国人工肝及血液净化学术年会论文集[C],2008.
[125]陈大明.乙肝防治的情报学研究[D] .中国优秀硕士学位论文全文数据库,2007,(03) .
[126]彭文伟.传染病学.北京:人民卫生出版社,2001,33-36.
[127]王宇明.重型肝炎的内科治疗.中华肝脏病杂志,2001,9(4)244.
[128]张定凤.重型肝炎的发病机理.中华肝脏病杂志,2000,8(5):307.
[129] Béghin L,Michaud L,Turck D,et al.Technical aspects and relevance of energy expenditure and physical activity assessment in clinical research for cystic fibrosis patients.Arch Pediatr,2005,12(7):1139-44.
[130] Arvidsson D,Slinde F,Nordenson A,et al.Validity of the ActiReg system in assessing energy requirement in chronic obstructive pulmonary disease patients[J].Clin Nutr,2006,25(1):68-74.
[131] Avesani CM,Carrero JJ.Estimating total versus resting energy expenditure:methodological considerations[J].Clin Nutr,2009,28(1):103-104.
[132] Bertoli S,Posata A,Battezzati A,et a1.Poor agreement between a portable armband and indirect calorimetry in the assessment of resting energy expenditure[J].Clin Nutr,2008,27(2):307-310.
[133] Owen OE,Holup JL,D’Alessio DA,et a1.A reappraisal of the caloric requirements of men[J].Am J Clin Nutr,1987,46(6):875-885.
[134] Flancbauml,Choban PS,Sambucco S,et al.Comparison of indirect calorimetry,the Fick method,and prediction equations in estimating the energy requirements of critically ill patients[J].Am J Clin Nutr,1999,69:461-466.
[135]于红卫,冯岩梅,孟庆华.能量代谢测定系统(代谢车)临床应用的研究进展[J].中国全科医学,2006,21:78-81.
[136] Tershakovec AM,Kuppler KM,Zemel B,et al.Age,sex,ethnicity,body composition,and resting energy expenditure of obese African American and white children and adolescents[J].Am J Clin Nutr,2002,75:867-871.
[137]任建安,李宁,黎介寿,等.能量代谢监测与营养物质需要量[J].中国实用外科杂志,2001,21(10):631-637.
[138] Kalaitzakis E,Bosaeus I,Ohman L,.Altered postprandial glucose,insulin,leptin,and ghrelin in liver cirrhosis:correlations with energy intake andresting energy expenditure[J].Am J Clin Nutr,2007,85(3):808-815.
[139] Yoshiyuki Miwa , Hisataka Moriwaki . Nocturnal energy and BCAA supplementation in patients with liver cirrhosis.Hepatology Research,2004,30: 63-66.
[140] Guglielmi FW,Panella C,Buda A,et al.Nutritional state and energy balance in cirrhotic patients with or without hypermetabolism.Multicentre prospective study by the‘Nutritional Problems in Gastroenterology’Section of the Italian Society of Gastroenterology (SIGE).Dig Liver Dis,2005,37:681-688.
[141]周爱儒.生物化学.北京:人民卫生出版社,2002,49-367.
[142]金惠铭.病理生理学.北京:人民卫生出版社,2001,227-228.
[143] Yamanaka-Okumura H,Nakamura T,Takeuchi H,et al.Effect of late evening snack with rice ball on energy metabolism in liver cirrhosis.Eur J Clin Nutr,2006,60(9):1067-1072.
[144] Lubos Sobotk.临床营养基础(蔡威译).复旦大学出版社,2002,23.
[145]葛可佑.中国营养科学全书.人民卫生出版社,2004.
[146] Plauth M,CabréE,Riggio O,et al.ESPEN Guidelines on Enteral Nutrition:Liver disease.Clin Nutr,2007,26(2):272.
[147]陈规划,蔡常洁.重型肝炎肝移植的治疗进展[J].中国普外基础与临床杂志,2007,14(2):132-133.
[148] Wu YM.Liver transplantation for hepatic failure [J].Transplant Proceedings,2004,36 (8):22-26.
[149]李兰娟.肝衰竭和人工肝研究进展.浙江医学,2008,30(5):425-427.
[150] Owen OE,Reichle FA,Mozzoli MA,et al.Hepatic,gut,and renal substrate flux rates in patients with hepatic cirrhosis.Clin Invest,1981,68(1):240-252.
[151]孟庆华,于红卫,冯岩梅,等.慢性重型病毒性肝炎患者的能量代谢特点及相关性研究[J].中华医学杂志,2007,87(42):2982-2985.
[152]丁惠国,汪俊韬,王宝恩.肝硬化患者营养不良、能量代谢异常与营养支持[J].中国临床营养杂志,2002,10(4):281-283.
[153] Doi J,Shiraishi K,Haida M,et al.Abnormality of energy metabolism in theskeletal muscle of patients with liver cirrhosis and changes under administration of glucose and branched-chain amino acids[J].Tokai J Exp Clin Med,2004 ,29(4):191-198.
[154] Tsuchiya M,Sakaida I,Okamoto M,et al.The effect of a late evening snack in patients with liver cirrhosis.Hepatol Res,2005,31(2):95-103.
[155] Korenaga K,Korenaga M,Uchida K,et al.Effects of a late evening snack combined with alpha-glucosidase inhibitor on liver cirrhosis[J].Hepatol Res,2008,38(11):1087-1097.
[156] Kamath PS,Wiesner RH,Malinchoc M,et al.A model to predict survival inpatients with end-stage liver disease [J].Hepatology,2001,33:464-470.
[157] Ishigami M,Honda T,Okumura A,et al.Use of the Model for End-Stage Liver Disease (MELD) score to predict 1-year survival of Japanese patients with cirrhosis and to determine who will benefit from living donor liver transplantation[J].J Gastroenterol,2008,43(5):363-368..
[158]岳建荣,李藕,张丽萍.慢性重型肝炎患者低血糖监测及护理干预[J].临床和实验医学杂志,2006,5(6):788-789.
[159]于红卫,孟庆华,张汾燕等.慢性重型乙型肝炎患者低血糖机制的探讨[J].临床肝胆病杂志,2008,24(3):175-178.
[160]于红卫,孟庆华,张汾燕,等.慢性重型乙型肝炎患者低血糖与能量代谢、胰岛素样生长因子-1的相关性[J].中国临床营养,2008,16 (1):8-11.
[161]于淑清,孟庆华,倪明美,等.慢性重型病毒性肝炎患者的营养状况分析及营养干预[J].中国临床营养杂志,2006,14(6):360-336.
[162] Yutaka Nakaya,Kiwamu Okita,Kazuyuki Suzuki,et al.BCAA-enriched snack improves nutritional state of cirrhosis[J].Nutrition,2007,23:113-120.
[163]范春蕾,武燕京,丁惠国,等.慢性重型病毒性肝炎的能量代谢及糖、蛋白质、脂肪氧化[J].中国临床营养杂志,2006,14 (2):110-114.
[164]郝建宇,杨昭徐.葡萄糖激酶在肝硬化糖代谢异常中的实验研究[J].北京医学,2005,27(6):351-353.
[165] Agius L . Glucokinase and molecular aspects of liver glycogenmetabolism[J].Biochem J,2008,414(1):1-18.
[166] Cifuentes D,Martínez-Pons C,García-Rocha M,et al.Hepatic glycogen synthesis in the absence of glucokinase: the case of embryonic liver[J].J Biol Chem,2008 ,283(9):5642-5649.
[167] Kramer J,Moeller EL,Hachey A,et al.Differential expression of GLUT2 in pancreatic islets and kidneys of New and Old World nonhuman primates[J].Am J Physiol Regul Integr Comp Physiol,2009,296(3):786-793.
[168] Kietzmann T,Dimova EY,Flügel D,et al.Oxygen:modulator of physiological and pathophysiological processes in the liver[J] . Z Gastroenterol,2006,44(1):67-76.
[169] Porzio O,Marlier LN,FedericiM,et al.GLUT2 and glucokinase expression is coordinately regulated by sulfonylurea[J].Mol Cell Endocrinol,1999,153-155.
[170] Frese T,Bazwinsky I,Mühlbauer E,et al.Circadian and age-dependent expression patterns of GLUT2 and glucokinase in the pancreatic beta-cell of diabetic and nondiabetic rats[J].Horm Metab Res,2007,39(8):567-574.
[171] Kimura K,Iwano M,Higgins DF,et al.Stable expression of HIF-1alpha in tubular epithelial cells promotes interstitial fibrosis[J].Am J Physiol Renal Physiol,2008,295(4):1023-1029.
[172]马正伟.缺氧对大鼠肝细胞糖代谢的影响及机制研究-缺氧诱导因子-1的作用.第三军医大学博士学位论文集(1998038).第三军医大学(重庆),2001.
[173]戚华兵,汪仕良,王凤君.严重烧伤大鼠葡萄糖转运体1蛋白表达的实验研究[J].第三军医大学学报,2001,25(18):1613-1616.
[174] Petty JC,Lana SE,Thamm DH,et al.Glucose transporter 1 expression in canine osteosarcoma[J].Vet Comp Oncol,2008,6(2):133-140.
[175] Rajaganeshan R,Prasad R,Guillou PJ,et al.The role of hypoxia in recurrence following resection of Dukes' B colorectal cancer[J].Int J Colorectal Dis,2008,23(11):1049-1055.
[176] Vaupel P,Mayer A.Hypoxia in cancer:significance and impact on clinical outcome[J].Cancer Metastasis Rev,2007,26(2):225-239.
[177]梁辉,窦科峰.肝癌组织中HIF-1α及Glut-1基因蛋白表达及意义[J].中国癌症杂志,2008,18(3):181-184.
[2]杨绍基.传染病学.人民卫生出版社,2008,41-42.
[3]许天蕴,赵秀娥.2型糖尿病及代谢综合征与非酒精性脂肪肝相关因素分析[J].临床内科杂志,2007,24(10):34-36.
[4]洪尚游,万漠彬,赵汉美.重型病毒性肝炎并发低血糖临床分析[J].肝脏杂志,2005,10(2):98-99.
[5]彭劼，张琪，郭亚兵．血糖水平对慢性重型乙型肝炎预后的影响[J].广东医学, 2008,07:21-22.
[6]林建英.慢性重型肝炎血糖变化与预后关系的临床分析[J].中外医疗,2009,05:52.
[7]潘教治,汪建琴.慢性重型肝炎血糖变化与预后关系的临床分析[J].重庆医学,2007,06:73-74.
[8] Takada Y,Ishigure S,Fukunaga K.Large-animal models of fulminant hepatic failure [J].Artif Organs,2003,6(1):9-13.
[9]陈萍.血糖水平对重型肝炎患者预后影响的分析[J].中华肝脏病杂志, 2006,14(8):572-573.
[10]钟乔华.248例病毒性肝炎病人空腹血糖水平检测分析[J].中国医师杂志,1999,1(10):43.
[11]涂燕云.重型病毒性肝炎代谢功能紊乱状况与营养治疗现状[J].右江医学,2004,32 (6):590-592.
[12] Obici S,Lopes-Bertolini G,Curi R,et al.Liver glycogen metabolism during short-term insulin-induced hypoglycemia in fed rats [J].Cell Biochem Funct,2008,26(7):755-759.
[13]许超宇,顾琳,朱宇佳,等.糖代谢紊乱与重型肝炎预后的关系[J].实用医学杂志,2008,22:81-82.
[14] Gundling F,Schumm-Draeger PM,Schepp W.Hepatogenous Diabetes- Diagnostics and Treatment.Z Gastroenterol,2009,47(5):436-445.
[15] Chen JW,Nielsen MF,Caumo A,et al.Changes in bioactive IGF-I and IGF-binding protein-1 during an oral glucose tolerance test in patients with liver cirrhosis[J]. Eur J Endocrinol.2006,155(2):285-292.
[16] Sibley SD,Palmer JP,Hirsch IB,et al.Visceral obesity,hepatic lipase activity,and dyslipidemia in type 1 diabetes[J] .Clin Endocrinol Metab,2003,88(7):3379-3384.
[17] Hetty A,Wilson S,Kuo P,et al.Liver transplantation improves cirrhosis associated impaired oral glucose tolerance [J].Transplantation,2000,69(11): 2451-2454.
[18]韩红梅,朴云峰,全红梅.肝源性糖尿病125例临床分析[J].临床肝胆病杂志,2007,23(3):214-215.
[19]池肇春.实用临床肝病学[M].北京:中国医药科技出版社,1999∶740-743.
[20] Landau BR.Methods for measuring glycogen cycling.American Journal of Physiology,Endocrinology and Metabolism,2001,281:413-419.
[21] Lei WY,Wang TE,Chen TL,et al.Insulinoma causing hypoglycemia in a patient with type 2 diabetes [J].Formos Med Assoc,2007,106(5):392-396.
[22]唐华,王旭霞,赵曙光,等.瘦素与肝源性糖尿病患者胰岛素抵抗的相关性研究[J].西南国防医药,2009,2,32-34.
[23] Roden M,Petersen KF,Shulman GI.Nuclear magnetic resonance studies of hepatic glucose metabolism in humans.Recent Progress in Hormone Research 2001,56:219-237.
[24] Tamura A,Ishihara H,Suzuki S,et a1.Hypoglycemia associated with hyperinsulinemia in a subject with type 2 diabetes and liver cirrhosis.Nippon Naika Gakkai Zasshi,2006,95 (7):1371-1374.
[25] Home PD,Pacini G.Hepatic dysfunction and insulin insensitivity in type 2 diabetes mellitus:a critical target for insulin-sensitizing agents.Diabetes Obes Metab,2008,10(9):699-718.
[26] Miyamoto I,Miyakoshi H,Nagaiy,et a1.Characterization of the insulin resistance in liver cirrhosis with non-insulin dependantdiabetes mellitus.Endocrinol JPN,1992,39:421-429.
[27] Zhang X,Shen W,Shen DM.A clinical analysis of liver disease patients with abnormal glucose metabolism.Zhonghua Gan Zang Bing Za Zhi,2006 ,14(4):289-292.
[28] Conchillo M,Prieto J,Quiroga J.Insulin-like growth factor I (IGF-I) and liver cirrhosis.Rev Esp Enferm Dig,2007,99(3):156-164.
[29] Shmueli E,Miell JP,Stewart M,et al.High insulin-like growth factor binding protein 1 levels in cirrhosis:link with insulin resistance [J].Hepatology,1996, 24(1):127-133.
[30] Shintani Y,Fujie H,Miyoshi H,et al.Hepatitis C virus infection and diabetes: direct involvement of the virus in the development of insulin resistance [J].Gastroenterology,2004,126 (3):840.
[31] Lin SY,Wang YY,Sheu WH.Increased serum soluble tumor necrosis factor receptor levels are associated with insulin resistance in liver cirrhosis [J].Metabolism,2004,53:922.
[32] Overexpressing cellular glutathione peroxidase PNAS 2004,101:8852-8857.
[33] Fritsche L,Weigert C,H?ring HU,et al.How insulin receptor substrate proteins regulate the metabolic capacity of the liver--implications for health and disease[J].Curr Med Chem,2008,15(13):1316-1329.
[34] Lawrence MC,McKern NM,Ward CW.Insulin receptor structure and its implications for the IGF-1 receptor[J].Curr Opin Struct Biol,2007,17(6):699-705.
[35]刘淑娥,肖丹.肝源性糖尿病临床分析[J].中日友好医院学报,2003,17 (3):153.
[36] Shi DR,Dong CL,Lu L,et al.Relationship between glucose metabolic disorders and expression of insulin receptor in posthepatitic cirrhosis hepatocyte and HBV DNA in pancreatic cells[J].Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi,2003,17(4):372-374.
[37] Draznin B.Molecular mechanisms of insulin resistance:serine phosphorylationof insulin receptor substrate-1 and increased expression of p85alpha:the two sides of a coin.Diabetes,2006,55(8):2392-2397.
[38] Van Harmelen V,Rydén M,Sj?lin E,et al.A role of lipin in human obesity and insulin resistance : relation to adipocyte glucose transport and GLUT4 expression[J].Lipid Res,2007,48(1):201-206.
[39] Fernández-Veledo S,Hernandez R,Teruel T,et al.Ceramide mediates TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes[J].Arch Physiol Biochem,2006,112(1):13-22.
[40] Dong X,Park S,Lin X,et al.Irs1 and Irs2 signaling is essential for hepatic glucose homeostasis and systemic growth[J] .Clin Invest,2006,116(1):101-114.
[41] Carvalho E,Kotani K,Peroni O,et al.Adipose-specific overexpression of GLUT4 reverses insulin resistance and diabetes in mice lacking GLUT4 selectively in muscle[J].Am J Physiol Endocrinol Metab,2005,289(4):E551-561.
[42] Kubota N,Kubota T,Itoh S,et al.Dynamic functional relay between insulin receptor substrate 1 and 2 in hepatic insulin signaling during fasting and feeding[J].Cell Metab,2008,8(1):49-64.
[43]蒋斌,宋世兵,袁炯,等.肝移植术后糖尿病的初步研究[J].肝胆外科杂志,2004,12 (3):190.
[44]朱飞燕.肝硬变患者糖耐量减低和肝原性糖尿病的发病机理[J].临床消化病杂志,1999,11 (3):142.
[45]张霞,沈薇.肝病伴糖代谢异常患者的临床分析[J].中华肝脏病杂志,2006,4(14):289.
[46] Bhimma R,Coovadia HM.Hepatitis B virus-associated nephropathy[J].Am J Nephrol.2004,24(2):198-211.
[47]闫惠平,郎振为,黄德庄,等.地高辛素标记探针原位杂交法检测肝和肝外组织中乙型肝炎病毒DNA[J].中华内科杂志,1994,33(3):168-171.
[48]苟小林,张咪玲,朱爱华,等.肝硬化所致肝源性糖尿病糖代谢和胰岛素分泌特点的临床研究.延安大学学报,2009,1:28-32.
[49]解奕瑞,朱彪.2008年浙江省感染病、肝病学术年会论文汇编,2008.
[50]吴邦富,林丽莉,胡品津.肝硬化患者口服葡萄糖耐量试验的变化.实用肝脏病杂志,2004,7 (1):25.
[51]胡亚莉,陈惠贤.肝病患者糖代谢30例分析报告.九江医学,2004,19 (2):95.
[52]庄辉.积极控制乙型肝炎病毒感染[J].中华医学信息导报,2006,2l(6):12.
[53] Shimoda T,Shikata T,Karasawa T.Light microscopic localization of hepatitis B virus antigens in the human pancreas.Possibility of multiplication of hepatitis B virus in the human pancreas[J].Gastroenterology,1981,81(6):998-1005.
[54]陆立,时德仁,周燕,等.胰腺乙型肝炎病毒感染及其糖尿病的关系[J].临床军医杂志,2001,29 (2):71.
[55]时德仁,东传凌,陆立等.肝硬化时糖代谢紊乱与肝细胞胰岛素受体及胰腺细胞HBV DNA表达的关系[J].中华实验和临床病毒学杂志,2003,17(4):372-374.
[56] Persico M,Masarone M,La Mura V,et al.Clinical expression of insulin resistance in hepatitis C and B virus-related chronic hepatitis:differences and similarities[J].World J Gastroenterol,2009,15(4):462-466.
[57] Moucari R,Asselah T,Cazals-Hatem D,et al.Insulin resistance in chronic hepatitis C:association with genotypes 1 and 4,serum HCV RNA level,and liver fibrosis[J].Gastroenterology,2008,134(2):416-423.
[58]郑宏庭,邓华聪.葡萄糖激酶与糖尿病的研究进展[J].中国临床康复,2004,8(27):5960-5961.
[59]张亚莉,王剑青,陶建蜀,等.葡萄糖激酶基因微卫星DNA多态性与2型糖尿病的相关性研究[J].贵州医药,2006(9):771-773.
[60]马晓伟,钱荣立,王艳荣等.实验性非胰岛素依赖型糖尿病大鼠肝脏葡萄糖激酶活性的改变[J].中华内科杂志,1998,37:91-94.
[61] Kr?henbühl L,Lang C,Lüdes S,et a1.Reduced hepatic glycogen stores in patients with liver cirrhosis.Liver Int,2003,23(2):101-109.
[62] Almanza-Pérez JC,Blancas-Flores G,García-Macedo R,et al.Leptin and its association with obesity and type 2 diabetes.Gac Med Mex,2008,144(6):535-542.
[63] Farooqi IS,O'Rahilly S.Leptin:a pivotal regulator of human energy homeostasis[J].Am J Clin Nutr,2009,89(3):980-984.
[64] Figlewicz DP,Benoit SC.Insulin,leptin,and food reward:update 2008.Am J Physiol Regul Integr Comp Physiol,2009,296(1):9-19.
[65] Frühbeck G.Intracellular signalling pathways activated by leptin[J].Biochem J,2006,393:7-20.
[66] Yokaichiya DK,Galembeck E,Torres BB,et al.Insulin and leptin relations in obesity:a multimedia approach.Adv Physiol Educ,2008,32(3):231-236.
[67] Kosztáczky B,Fóris G,Paragh G Jr,et al.Leptin stimulates endogenous cholesterol synthesis in human monocytes:New role of an old player in atherosclerotic plaque formation . Leptin-induced increase in cholesterol synthesis. Int J Biochem Cell Biol,2007,39(9):1637-1645.
[68] Kohno D,Nakata M,Maekawa F,et al.Leptin suppresses ghrelin-induced activation of neuropeptide Y neurons in the arcuate nucleus via phosphatidylinositol 3- kinase- and phosphodiesterase 3- mediated pathway.Endocrinology,2007,148(5):2251-2263.
[69] Yu Y,Hu SK,Yan H.The study of insulin resistance and leptin resistance on the model of simplicity obesity rats by curcumin[ J ].Zhonghua Yu Fang Yi Xue Za Zhi,2008,42(11):818-822.
[70] Benomar Y,Naour N,Aubourgl A,et al.Insulin and leptin induce Glut4 plasma membrane translocation and glucose up take in a human neuronal cell line by a PB kinase dependent[ J ].Endocrinology,2006,147 (5):2550-2556.
[71] Forhead AJ,Lamb CA,Franko KL,et al.Role of leptin in the regulation of growth and carbohydrate metabolism in the ovine fetus during late gestation[ J ].J Physiol,2008,586(9):2393-2403.
[72] Borba-Murad GR,Mario EG, Bassoli BK,Comparative acute effects of leptinand insulin on gluconeogenesis and ketogenesis in perfused rat liver.Cell Biochem Funct,2005,23(6):405-413.
[73] Susan A,Loranne A.Leptin enhances glycogen storage in hepatecytes by inhibition of phesphorylase and exerts an additive effect with insulin.Diabetes,1999 48(1):15-20.
[74] Cao XP,Ming WY,Cheng H,et a1.Efects of leptin on gluco-oxidation and glucokinase gene expression in cultured liver cells[J].Chin J Endecfinol Metab,l999,15(3):131-133.
[75] Robinson-Rechavi M,Carpentier AS,Dufraisse M,et a1.How many nuclear hormone receptors are there in the human genome? [J] Trends Genet,2001,17(10):554-556.
[76] Edwards PA,Kennedy MA,Mak PA.LXRs;oxysterol-activated nuclear receptors that regulate genes controlling lipid homeostasis.Vascul Pharmacol, 2002,38:249-256.
[77] Talukdar S,Hilgartner FB.The mechanism mediating the activation of acetyl-coenzyme A carboxylase-{alpha}gene transcription by the liver X receptor agonist TO-901317[J].J Lipid Res,2006,47(11):2451-2461.
[78] Wente W,Brenner MB,Zitzer H,et a1.Activation of liver X receptors and retinoid X receptors induces growth arrest and apoptosis in insulin-secreting cells[J].Endocrinology,2007,148(4):1843-1849.
[79] Zelcer N,Tontonoz P.Liver X receptors as integrators of metabolic and inflammatory signaling[J].J Clin Invest,2006,116(3):607-614.
[80] Houck KA , Borchert KM , Hepler CD , et al . T0901317 is a dual LXR/FXR agonist.Mol Genet Metab,2004,83:184-187.
[81] Glass CK,Rosenfeld MG.The coregulator exchange in transcriptional functions of nuclear receptors [J].Genes Dev,2000,14(2):121-141.
[82] Barish GD, Evans RM.PPARs and LXRs:atherosclerosis goes nuclear.Trends Endocrinol Metab,2004,15:158-165.
[83] Cummins CL,VoHe DH,Zhang Y,et a1.Liver X receptors regulate adrenalcholesterol balance[J].J Clin Invest,2006,116(7):1902-1912.
[84] Rastinejad F.Retinoid X receptor and its partners in the nuclear receptor family[J].Curr Opin Struct Biol,2001,11(1):33-38.
[85] Yang C,McDonald JG,Patel A,et a1.Sterol intermediates from cholesterol biosynthetic pathway as liver X receptor Ligands[J].J Biol Chem,2006,281(38):7816-7826.
[86] Stulnig TM,Stefensen KR,Gao H,et a1.Novel roles of liver X receptors exposed by gene expression profiling in liver and adipose tissue[J].Mol Pharmacol,2002,62(6):1299-1305.
[87] Stulnig TM,Oppermann U,Stefensen KR,et a1.Liver X receptors downregulate 11 beta-hydroxysteroid dehydrogenase type 1 expression and activity[J].Diabetes,2002,51(8):2426-2433.
[88] Baranowski M.Biological role of liver X receptors[J].J Physiol Pharmacol,2008 ,59:31-55.
[89] Lafitte BA,Chao LC,Li J,et a1.Activation of liver X receptor improves glucose tolerance through coordinate regulation of glucose metabolism in liver and adipose tissue[J].Proc Natl Acad Sci USA,2003,100(9):5419-5424.
[90] Dalen KT,Ulven SM,Bamberg K,et a1.Expression of the insulin- responsive glucose transporter GLUT4 in adipocytes is dependent on liver X receptor alpha[J].J Biol Chem,2003,278(48):48283-48291.
[91] Grefhorst A,van Dijk TH,Hammer A,et a1.Differentia effects of pharmacological liver X receptor activation on hepatic and peripheral insulin sensitivity in lean and ob/ob mice[J].Am J Physiol Endocrinol Metab,2005,289(5):E829-E838.
[92] Cho N,Momose Y.Peroxisome proliferator-activated receptor gamma agonists as insulin sensitizers:from the discovery to recent progress.Curr Top Med Chem,2008,8(17):1483-507..
[93] Fernyhough ME,Okine E,Hausman G,et a1.PPARgamma and GLUT-4 expression as developmental regulators/markers for preadipocyte differentiationinto an adipocyte.Domest Anim Endocrinol,2007,33(4):367-78.
[94] Commerford SR , Vargas L , Dorfman SE , et a1 . Dissection of the insulin-sensitizing effect of liver X receptor ligands.Mol Endocrinol,2007,21(12):3002-3012.
[95] Kase ET,Wensaas AJ,Aas V,et a1.Skeletal muscle lipid accumulation in type 2 diabetes may involve the liver X receptor pathway[J].Diabetes,2005,54(4):1108-1115.
[96] Nomiyama T,Bruemmer D.Liver X receptors as therapeutic targets in metabolism and atherosclerosis.Curr Atheroscler Rep,2008,10(1):88-95.
[97] Hansen MK,Connolly TM.Nuclear receptors as drug targets in obesity,dyslipidemia and atherosclerosis.Curr Opin Investig Drugs,2008,9(3):247-255.
[98] Fiévet C,Staels B.Liver X receptor modulators:effects on lipid metabolism and potential use in the treatment of atherosclerosis.Biochem Pharmacol,2009,77(8):1316-1327.
[99] Bensinger SJ,Tontonoz P.Integration of metabolism and inflammation by lipid-activated nuclear receptors.Nature,2008,454(7203):470-477.
[100] Alaynick WA.Nuclear receptors,mitochondria and lipid metabolism.Mito -chondrion,2008,8(4):329-337.
[101] Jungermann K,Kietzmann T.Zonation of parenchymal and nonparenchymal metabolism in liver[J].Annu Rev Nutr,1996,16:179-203.
[102] Wiegman CH, Bandsma RH, Ouwens M ,et a1. Hepatic VLDL production in ob/ob mice is not stimulated by massive de novo lipogenesis but is less sensitive to the suppressive effects of insulin[J].Diabetes,2003,52(5):1081-1089.
[103]时德仁,东传凌,陆立,等.肝硬化时肝细胞胰岛素受体和酪氨酸蛋白激酶表达的定量研究.中华肝脏病杂志,2001,9:279-281.
[104] Shi DR,Dong CL,Lu L,et al.Relationship between glucose metabolic disorders and expression of insulin receptor in posthepatitic cirrhosishepatocyte and HBV DNA in pancreatic cells.Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi.2003,17(4):372-374.
[105] Fritsche L,Weigert C,H?ring HU,et al.How insulin receptor substrate proteins regulate the metabolic capacity of the liver--implications for health and disease.Curr Med Chem,2008,15(13):1316-1329.
[106] Han DW. Intestinal endotoxemia as a pathogenetic mechanism in liver failure World J Gastroenterol,2002,8:961.
[107] Iwata H , Soga Y , Meguro M , et al . High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1[J].J Endotoxin Res,2007,13(4):227-34.
[108] de Souza LF,Barreto F,da Silva EG,et al.Regulation of LPS stimulated ROS production in peritoneal macrophages from alloxan-induced diabetic rats:involvement of high glucose and PPARgamma.Life Sci,2007,81(2):153-159.
[109] Andrzejczak D,Górska D,Czarnecka E.Influence of amlodipine and atenolol on lipopolysaccharide (LPS)-induced serum concentrations of TNF-alpha,IL-1,IL-6 in spontaneously hypertensive rats (SHR) .Pharmacol Rep,2006 ,58(5):711-719.
[110] Diya Zhang,Lili Chen,Shenglai Li,et al.Lipopolysaccharide (LPS) of Porphyromonas gingivalis induces IL-1beta,TNF-alpha and IL-6 production by THP-1 cells in a way different from that of Escherichia coli LPS.Innate Immun,2008,14(2):99-107.
[111] Metzger S,Nusair S,Planer D,et a1.Inhibition of hepatic gluconeogenesis and enhanced glucose uptake contribute to the development of hypoglycemia in mice bearing interleukin-lbeta-secreting tumor.Endocrinology,2004,145:5150.
[112] Semenza GL.Hypoxia-inducible factor 1 and cancer pathogenesis.IUBMB Life,2008,60(9):591-597.
[113] Semenza GL.HIF-1 and human disease:one highly involved factor[J].Genes Dev,2000,(14):1983-1991.
[114] Scheepers A,Joost HG,Schürmann A.The glucose transporter families SGLT and GLUT: molecular basis of normal and aberrant function.JPEN J Parenter Enteral Nutr,2004,28(5):364-371.
[115] Cano A, Ticus I ,Chabrol B.Glucose transporter type 1 (GLUT-1) deficiency.Rev Neurol (Paris),2008,164(11):896-901.
[116] Yu S,Zhao T,Guo M,et al.Hypoxic preconditioning up-regulates glucose transport activity and glucose transporter (GLUT1 and GLUT3) gene expression after acute anoxic exposure in the cultured rat hippocampal neurons and astrocytes.Brain Res,2008,1211:22-9.
[117]中华传染病与寄生虫病学分会、肝病学会.病毒性肝炎防治方案.中华肝脏病杂志,2000,8(6):324-329.
[118]中华医学会感染病学分会肝衰竭与人工肝学组中华医学会肝病学分会重型肝病与人工肝学组.肝衰竭诊疗指南.中华肝脏病杂志,2006,14(9):19-22.
[119]冯岩梅,孟庆华.静息能量消耗测定在慢性肝病中的应用[J].中国临床营养,2007,15(2):107-110.
[120] Karhunern L,Franssial-Kallunki A ,Rissanen A,et al.Determinants of resting energy expenditure in obese non-diabetic Caucasian women.Int J Obes Relat Metab Disord,1997,21:197-202.
[121]蒋朱明,吴蔚然.肠内营养.北京:人民卫生出版社,2002,28-32.
[122]吴肇汉.实用临床营养治疗学.上海科学技术出版社,2001,374-395.
[123]李刚荣,汪仕良,余斌,等.人体能量消耗间接测定系统的研究.中国生物医学工程学报,1997,16(4):338-345.
[124]庄辉.我国乙型肝炎防治现状及目标[A] .第一届全国疑难重型肝病大会、第四届全国人工肝及血液净化学术年会论文集[C],2008.
[125]陈大明.乙肝防治的情报学研究[D] .中国优秀硕士学位论文全文数据库,2007,(03) .
[126]彭文伟.传染病学.北京:人民卫生出版社,2001,33-36.
[127]王宇明.重型肝炎的内科治疗.中华肝脏病杂志,2001,9(4)244.
[128]张定凤.重型肝炎的发病机理.中华肝脏病杂志,2000,8(5):307.
[129] Béghin L,Michaud L,Turck D,et al.Technical aspects and relevance of energy expenditure and physical activity assessment in clinical research for cystic fibrosis patients.Arch Pediatr,2005,12(7):1139-44.
[130] Arvidsson D,Slinde F,Nordenson A,et al.Validity of the ActiReg system in assessing energy requirement in chronic obstructive pulmonary disease patients[J].Clin Nutr,2006,25(1):68-74.
[131] Avesani CM,Carrero JJ.Estimating total versus resting energy expenditure:methodological considerations[J].Clin Nutr,2009,28(1):103-104.
[132] Bertoli S,Posata A,Battezzati A,et a1.Poor agreement between a portable armband and indirect calorimetry in the assessment of resting energy expenditure[J].Clin Nutr,2008,27(2):307-310.
[133] Owen OE,Holup JL,D’Alessio DA,et a1.A reappraisal of the caloric requirements of men[J].Am J Clin Nutr,1987,46(6):875-885.
[134] Flancbauml,Choban PS,Sambucco S,et al.Comparison of indirect calorimetry,the Fick method,and prediction equations in estimating the energy requirements of critically ill patients[J].Am J Clin Nutr,1999,69:461-466.
[135]于红卫,冯岩梅,孟庆华.能量代谢测定系统(代谢车)临床应用的研究进展[J].中国全科医学,2006,21:78-81.
[136] Tershakovec AM,Kuppler KM,Zemel B,et al.Age,sex,ethnicity,body composition,and resting energy expenditure of obese African American and white children and adolescents[J].Am J Clin Nutr,2002,75:867-871.
[137]任建安,李宁,黎介寿,等.能量代谢监测与营养物质需要量[J].中国实用外科杂志,2001,21(10):631-637.
[138] Kalaitzakis E,Bosaeus I,Ohman L,.Altered postprandial glucose,insulin,leptin,and ghrelin in liver cirrhosis:correlations with energy intake andresting energy expenditure[J].Am J Clin Nutr,2007,85(3):808-815.
[139] Yoshiyuki Miwa , Hisataka Moriwaki . Nocturnal energy and BCAA supplementation in patients with liver cirrhosis.Hepatology Research,2004,30: 63-66.
[140] Guglielmi FW,Panella C,Buda A,et al.Nutritional state and energy balance in cirrhotic patients with or without hypermetabolism.Multicentre prospective study by the‘Nutritional Problems in Gastroenterology’Section of the Italian Society of Gastroenterology (SIGE).Dig Liver Dis,2005,37:681-688.
[141]周爱儒.生物化学.北京:人民卫生出版社,2002,49-367.
[142]金惠铭.病理生理学.北京:人民卫生出版社,2001,227-228.
[143] Yamanaka-Okumura H,Nakamura T,Takeuchi H,et al.Effect of late evening snack with rice ball on energy metabolism in liver cirrhosis.Eur J Clin Nutr,2006,60(9):1067-1072.
[144] Lubos Sobotk.临床营养基础(蔡威译).复旦大学出版社,2002,23.
[145]葛可佑.中国营养科学全书.人民卫生出版社,2004.
[146] Plauth M,CabréE,Riggio O,et al.ESPEN Guidelines on Enteral Nutrition:Liver disease.Clin Nutr,2007,26(2):272.
[147]陈规划,蔡常洁.重型肝炎肝移植的治疗进展[J].中国普外基础与临床杂志,2007,14(2):132-133.
[148] Wu YM.Liver transplantation for hepatic failure [J].Transplant Proceedings,2004,36 (8):22-26.
[149]李兰娟.肝衰竭和人工肝研究进展.浙江医学,2008,30(5):425-427.
[150] Owen OE,Reichle FA,Mozzoli MA,et al.Hepatic,gut,and renal substrate flux rates in patients with hepatic cirrhosis.Clin Invest,1981,68(1):240-252.
[151]孟庆华,于红卫,冯岩梅,等.慢性重型病毒性肝炎患者的能量代谢特点及相关性研究[J].中华医学杂志,2007,87(42):2982-2985.
[152]丁惠国,汪俊韬,王宝恩.肝硬化患者营养不良、能量代谢异常与营养支持[J].中国临床营养杂志,2002,10(4):281-283.
[153] Doi J,Shiraishi K,Haida M,et al.Abnormality of energy metabolism in theskeletal muscle of patients with liver cirrhosis and changes under administration of glucose and branched-chain amino acids[J].Tokai J Exp Clin Med,2004 ,29(4):191-198.
[154] Tsuchiya M,Sakaida I,Okamoto M,et al.The effect of a late evening snack in patients with liver cirrhosis.Hepatol Res,2005,31(2):95-103.
[155] Korenaga K,Korenaga M,Uchida K,et al.Effects of a late evening snack combined with alpha-glucosidase inhibitor on liver cirrhosis[J].Hepatol Res,2008,38(11):1087-1097.
[156] Kamath PS,Wiesner RH,Malinchoc M,et al.A model to predict survival inpatients with end-stage liver disease [J].Hepatology,2001,33:464-470.
[157] Ishigami M,Honda T,Okumura A,et al.Use of the Model for End-Stage Liver Disease (MELD) score to predict 1-year survival of Japanese patients with cirrhosis and to determine who will benefit from living donor liver transplantation[J].J Gastroenterol,2008,43(5):363-368..
[158]岳建荣,李藕,张丽萍.慢性重型肝炎患者低血糖监测及护理干预[J].临床和实验医学杂志,2006,5(6):788-789.
[159]于红卫,孟庆华,张汾燕等.慢性重型乙型肝炎患者低血糖机制的探讨[J].临床肝胆病杂志,2008,24(3):175-178.
[160]于红卫,孟庆华,张汾燕,等.慢性重型乙型肝炎患者低血糖与能量代谢、胰岛素样生长因子-1的相关性[J].中国临床营养,2008,16 (1):8-11.
[161]于淑清,孟庆华,倪明美,等.慢性重型病毒性肝炎患者的营养状况分析及营养干预[J].中国临床营养杂志,2006,14(6):360-336.
[162] Yutaka Nakaya,Kiwamu Okita,Kazuyuki Suzuki,et al.BCAA-enriched snack improves nutritional state of cirrhosis[J].Nutrition,2007,23:113-120.
[163]范春蕾,武燕京,丁惠国,等.慢性重型病毒性肝炎的能量代谢及糖、蛋白质、脂肪氧化[J].中国临床营养杂志,2006,14 (2):110-114.
[164]郝建宇,杨昭徐.葡萄糖激酶在肝硬化糖代谢异常中的实验研究[J].北京医学,2005,27(6):351-353.
[165] Agius L . Glucokinase and molecular aspects of liver glycogenmetabolism[J].Biochem J,2008,414(1):1-18.
[166] Cifuentes D,Martínez-Pons C,García-Rocha M,et al.Hepatic glycogen synthesis in the absence of glucokinase: the case of embryonic liver[J].J Biol Chem,2008 ,283(9):5642-5649.
[167] Kramer J,Moeller EL,Hachey A,et al.Differential expression of GLUT2 in pancreatic islets and kidneys of New and Old World nonhuman primates[J].Am J Physiol Regul Integr Comp Physiol,2009,296(3):786-793.
[168] Kietzmann T,Dimova EY,Flügel D,et al.Oxygen:modulator of physiological and pathophysiological processes in the liver[J] . Z Gastroenterol,2006,44(1):67-76.
[169] Porzio O,Marlier LN,FedericiM,et al.GLUT2 and glucokinase expression is coordinately regulated by sulfonylurea[J].Mol Cell Endocrinol,1999,153-155.
[170] Frese T,Bazwinsky I,Mühlbauer E,et al.Circadian and age-dependent expression patterns of GLUT2 and glucokinase in the pancreatic beta-cell of diabetic and nondiabetic rats[J].Horm Metab Res,2007,39(8):567-574.
[171] Kimura K,Iwano M,Higgins DF,et al.Stable expression of HIF-1alpha in tubular epithelial cells promotes interstitial fibrosis[J].Am J Physiol Renal Physiol,2008,295(4):1023-1029.
[172]马正伟.缺氧对大鼠肝细胞糖代谢的影响及机制研究-缺氧诱导因子-1的作用.第三军医大学博士学位论文集(1998038).第三军医大学(重庆),2001.
[173]戚华兵,汪仕良,王凤君.严重烧伤大鼠葡萄糖转运体1蛋白表达的实验研究[J].第三军医大学学报,2001,25(18):1613-1616.
[174] Petty JC,Lana SE,Thamm DH,et al.Glucose transporter 1 expression in canine osteosarcoma[J].Vet Comp Oncol,2008,6(2):133-140.
[175] Rajaganeshan R,Prasad R,Guillou PJ,et al.The role of hypoxia in recurrence following resection of Dukes' B colorectal cancer[J].Int J Colorectal Dis,2008,23(11):1049-1055.
[176] Vaupel P,Mayer A.Hypoxia in cancer:significance and impact on clinical outcome[J].Cancer Metastasis Rev,2007,26(2):225-239.
[177]梁辉,窦科峰.肝癌组织中HIF-1α及Glut-1基因蛋白表达及意义[J].中国癌症杂志,2008,18(3):181-184.