有氧运动联合膳食控制对2型糖尿病大鼠血清Visfatin水平的影响及相关因素的研究
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摘要
目的:探讨有氧运动联合膳食控制对2型糖尿病大鼠血清visfatin水平的影响,并分析其他相关指标的变化。
方法:选用6周龄雄性SD大鼠62只,大鼠随机抽取8只大鼠作为正常对照组(Control,C组),喂以标准普通饲料。其余54只SD大鼠在喂饲高糖高脂膳食的基础上,腹腔注射小剂量的链脲佐菌素(streptozotocin,STZ),建立2型糖尿病动物模型。然后将2型糖尿病大鼠随机分成4组:DM对照组(DM Control group,DM,n=9)、DM+运动锻炼组(DM+Exercise training group,DME,n=10)、DM+膳食控制组(DM+Diet control group,DMD,n=10)、DM+运动锻炼+膳食控制组(DM+Exercise training + Diet control,DMED,n=10)。DM组大鼠继续喂饲高脂高糖饲料,不进行运动锻炼;运动锻炼采用每天进行60min的无负重游泳运动,每周6次;膳食控制采用与DM组等量的标准普通饲料。13周后,检测各组大鼠FPG、TG、TC、FINS和Visfatin的含量。
结果:①2型糖尿病大鼠模型建立后第13周,与C组相比,DM组大鼠的FPG显著升高(P<0.01);通过双因素方差分析,有氧运动可以降低糖尿病大鼠FPG水平(P<0.05),而膳食控制对糖尿病大鼠FPG水平没有显著性影响(P>0.05),有氧运动联合膳食控制对降低糖尿病大鼠FPG水平没有显著性交互作用(P>0.05)。②2型糖尿病大鼠模型建立后第13周,DM组大鼠与C组大鼠相比,血清胰岛素浓度显著降低(P<0.01),但HOMA-IR无显著性变化(P>0.05)。通过双因素方差分析,膳食控制可以显著性提高糖尿病大鼠FINS水平(P<0.05),但有氧运动和有氧运动联合膳食控制可使糖尿病大鼠FINS水平进一步升高,但无显著的交互作用(P>0.05);有氧运动或膳食控制对DM大鼠的HOMA-IR均无显著性影响(P>0.05),且两者无显著的交互作用(P>0.05)。
③2型糖尿病大鼠模型建立后第13周,DM组大鼠与C组大鼠相比,血清内酯素浓度显著升高(P<0.01);通过双因素方差分析,13周的中强度的游泳训练对降低糖尿病大鼠血清内脂素含量有显著性的影响;与DM组相比,虽然DMD组血清内脂素含量降低很多,但通过双因素方差分析,膳食控制对降低糖尿病大鼠血清内脂素含量无显著性影响(P>0.05);而有氧运动和膳食控制可以进一步降低糖尿病大鼠的血清visfatin浓度,但无显著的交互作用(P>0.05)。
④2型糖尿病大鼠模型建立后第13周,与C组相比,DM组血清总胆固醇浓度和甘油三酯浓度显著升高(P<0.01);通过双因素方差分析,有氧运动或膳食控制均能显著地降低糖尿病大鼠的TC浓度(P<0.05),而且有氧运动和膳食控制对降低糖尿病大鼠的TC浓度具有明显的交互作用(P<0.05);膳食控制能显著地降低糖尿病大鼠的TG浓度(P<0.01),有氧运动并不能使糖尿病大鼠的TG浓度显著降低,而且,有氧运动联合膳食控制虽然可使糖尿病大鼠的TG浓度进一步降低,但没有显著的交互作用(P>0.05)
结论:①本研究所建立的糖尿病模型是成功的;在糖尿病的治疗中,单纯地依靠膳食控制并不能有效地降低糖尿病大鼠的FPG,而有氧运动对控制糖尿病大鼠的FPG具有非常显著的作用,在膳食控制的基础上进行有氧运动对降低糖尿病大鼠的血糖水平更加有效。与此同时,2型糖尿病大鼠血清visfatin水平显著升高。可能是2型糖尿病发生发展过程中对胰岛素分泌下降,血糖水平升高的一种代偿机制。
②13周的有氧运动能够增加胰岛β细胞分泌胰岛素的能力;单纯的膳食控制能有效地增加糖尿病大鼠的FINS的含量;在膳食控制的基础上进行有氧运动对降低糖尿病大鼠的血糖水平更加有效,对2型糖尿病的治疗具有非常重要的作用,但无显著的交互作用。
③有氧运动可使糖尿病大鼠血清visfatin的水平显著降低;13周的膳食控制对降低2型糖尿病大鼠血清visfatin水平影响不大;有氧运动联合膳食控制虽然能使2型糖尿病大鼠血清visfatin含量进一步降低,但没有显著的交互作用;且血糖水平与血液中visfatin水平之间有着密切的关系,可能是调节visfatin合成和分泌的主要因素。
④有氧运动、膳食控制以及有氧运动联合膳食控制对改善2型糖尿病大鼠的脂代谢具有积极的作用。与此同时,血清visfatin水平对血脂代谢的调节也具有一定的作用,但是它们之间的确切关系还有待于进一步研究。
To explore the effect of aerobic exercise joint dietary control on the visfatin plasma levels in type 2 diabetic rats and analyze the changes in other relevant indicators. Method:
Chose 62 single of 6-week-old SD rats which were male, Eight rats were randomly selected as normal control group of rats (Control, C group), and fed with normal standard diet. The remaining 54 SD rats which were feed high-fat and high-sugar diet were injected of low-dose streptozotocin though abdominal cavity to establish animal models of type 2 diabetes. and then the rats of type 2 diabetes were randomly divided into 4 groups : DM control group (n=9), DM+ aerobic exercise training group (n=10), DM+ Diet control group (n=10), DM+ aerobic exercise training + Diet control group (n=10). The DM group’s rats which were continued to feed high-fat and high-sugar diet were not exercise; Exercise were used 60 minutes’unloaded swimming for 13 weeks, 6 times per week; The dietary control use the general contour of the standard diet of the DM group. 13 weeks later, FPG, TG, TC, FINS, Visfatin of every group’s rats were examined. Results:
①After 13 weeks of the establishment of type 2 diabetes model, compared with C group, the FPG contents increased significantly in DM group(P<0.01); Through the double factor variance analysis, aerobic exercise can lower FPG levels in diabetic rats (P<0.05), And the effect of dietary control on FPG levels in diabetic rats did not significantly(P>0.05), exercise joint dietary control did not display an obvious interaction on lowering FPG levels in diabetic tats(P>0.05).
②After 13 weeks of the establishment of type 2 diabetes model, compared with C group, the serum insulin concentration decreased significantly in DM group(P<0.01), but the HOMA-IR was no significant changes. Through the double factor variance analysis, diet control can increase the FINS level in diabetic rats significantly(P<0.05), aerobic exercise and aerobic exercise joint dietary control in diabetic rats could further increase the level of FINS, but no significant interaction(P>0.05); there was neither significantly effect of aerobic exercise nor dietary control to improve the DM group of HOMA-IR(P>0.05), and there was no significant interaction(P>0.05).
③After 13 weeks of the establishment of type 2 diabetes model, compared with C group, the visfatin plasma concentrations significantly increased(P<0.01); Through the double factor variance analysis, there was significant impact of 13 weeks of strength training for swimming to lower plasma visfatin concentrations in diabetic rats; compared with the DM group, Although the visfatin plasma concentration lowered too much in DMD group, through the double factor variance analysis, there was no significant impact of dietary control to lower the visfatin plasma concentration(P>0.05); aerobic exercise and diet control can further reduce the visfatin plasma concentration in diabetic rats,and there was no significant interaction(P>0.05).
④After 13 weeks of the establishment of type 2 diabetes modle, compared with C group, the serum total cholesterol concentration and the serum triglyceride concentration increased significantly(P<0.01); Through the double factor variance analysis, both of aerobic exercise and dietary control could significantly lower the total cholesterol concentration in type 2 diabetic rats(P<0.05), and there was significant interaction of both aerobic exercise and dietary control to lower the total cholesterol concentration in type 2 diabetic rats(P<0.05). Dietary control could lower the triglyceride concentration in type 2 diabetic rats(P<0.01)significantly, but aerobic exercise could not , although aerobic exercise joint dietary control could further lower the triglyceride concentration in type 2 diabetic rats, there was no significant interaction (P>0.05).
Conclusion:
①Establishing of the Model of type 2 diabetes in this research was successful. Dietary control only could not effectively lower the FPG concentration; And aerobic exercise training has a very significant role to control the FPG of diabetic rats, on the base of the diet control, aerobic exercise training was more effective to reduce the fasting plasma glucose levels which in diabetic rats. At the same time, the visfatin plasma levels which in type 2 diabetic rats was significantly increased.
②13 weeks of aerobic exercise training could improve the capacity of which Pancreaticβ-cell secreted insulin in type 2 diabetes rats; Although aerobic exercise joint dietary control could increase the insulin concentration in type 2 diabetes rats, and it had a very important role in the treatment of type 2 diabetes, there was no significant interaction.
③Aerobic exercise could significantly lower the level of visfatin plasma in type 2 diabetic rats ; There was little effect on lowering the visfatin plasma concentration of 13 weeks of dietary control in type 2 diabetic rats; Aerobic exercise joint dietary control could further lower the visfatin plasma content in type 2 diabetes rats, but there was no significant interaction; And there was a close relationship between blood glucose levels and visfatin levels. It might be a main factor on regulating the visfatin’s synthesis and secretion.
④It was an active role in improving lipid metabolism for aerobic exercise training、dietary control and aerobic exercise joint dietary control. At the same time, it was also a role in regulating the lipid metabolism for visfatin plasma levels, However, the precise relationship between them had to be further studied.
方法:选用6周龄雄性SD大鼠62只,大鼠随机抽取8只大鼠作为正常对照组(Control,C组),喂以标准普通饲料。其余54只SD大鼠在喂饲高糖高脂膳食的基础上,腹腔注射小剂量的链脲佐菌素(streptozotocin,STZ),建立2型糖尿病动物模型。然后将2型糖尿病大鼠随机分成4组:DM对照组(DM Control group,DM,n=9)、DM+运动锻炼组(DM+Exercise training group,DME,n=10)、DM+膳食控制组(DM+Diet control group,DMD,n=10)、DM+运动锻炼+膳食控制组(DM+Exercise training + Diet control,DMED,n=10)。DM组大鼠继续喂饲高脂高糖饲料,不进行运动锻炼;运动锻炼采用每天进行60min的无负重游泳运动,每周6次;膳食控制采用与DM组等量的标准普通饲料。13周后,检测各组大鼠FPG、TG、TC、FINS和Visfatin的含量。
结果:①2型糖尿病大鼠模型建立后第13周,与C组相比,DM组大鼠的FPG显著升高(P<0.01);通过双因素方差分析,有氧运动可以降低糖尿病大鼠FPG水平(P<0.05),而膳食控制对糖尿病大鼠FPG水平没有显著性影响(P>0.05),有氧运动联合膳食控制对降低糖尿病大鼠FPG水平没有显著性交互作用(P>0.05)。②2型糖尿病大鼠模型建立后第13周,DM组大鼠与C组大鼠相比,血清胰岛素浓度显著降低(P<0.01),但HOMA-IR无显著性变化(P>0.05)。通过双因素方差分析,膳食控制可以显著性提高糖尿病大鼠FINS水平(P<0.05),但有氧运动和有氧运动联合膳食控制可使糖尿病大鼠FINS水平进一步升高,但无显著的交互作用(P>0.05);有氧运动或膳食控制对DM大鼠的HOMA-IR均无显著性影响(P>0.05),且两者无显著的交互作用(P>0.05)。
③2型糖尿病大鼠模型建立后第13周,DM组大鼠与C组大鼠相比,血清内酯素浓度显著升高(P<0.01);通过双因素方差分析,13周的中强度的游泳训练对降低糖尿病大鼠血清内脂素含量有显著性的影响;与DM组相比,虽然DMD组血清内脂素含量降低很多,但通过双因素方差分析,膳食控制对降低糖尿病大鼠血清内脂素含量无显著性影响(P>0.05);而有氧运动和膳食控制可以进一步降低糖尿病大鼠的血清visfatin浓度,但无显著的交互作用(P>0.05)。
④2型糖尿病大鼠模型建立后第13周,与C组相比,DM组血清总胆固醇浓度和甘油三酯浓度显著升高(P<0.01);通过双因素方差分析,有氧运动或膳食控制均能显著地降低糖尿病大鼠的TC浓度(P<0.05),而且有氧运动和膳食控制对降低糖尿病大鼠的TC浓度具有明显的交互作用(P<0.05);膳食控制能显著地降低糖尿病大鼠的TG浓度(P<0.01),有氧运动并不能使糖尿病大鼠的TG浓度显著降低,而且,有氧运动联合膳食控制虽然可使糖尿病大鼠的TG浓度进一步降低,但没有显著的交互作用(P>0.05)
结论:①本研究所建立的糖尿病模型是成功的;在糖尿病的治疗中,单纯地依靠膳食控制并不能有效地降低糖尿病大鼠的FPG,而有氧运动对控制糖尿病大鼠的FPG具有非常显著的作用,在膳食控制的基础上进行有氧运动对降低糖尿病大鼠的血糖水平更加有效。与此同时,2型糖尿病大鼠血清visfatin水平显著升高。可能是2型糖尿病发生发展过程中对胰岛素分泌下降,血糖水平升高的一种代偿机制。
②13周的有氧运动能够增加胰岛β细胞分泌胰岛素的能力;单纯的膳食控制能有效地增加糖尿病大鼠的FINS的含量;在膳食控制的基础上进行有氧运动对降低糖尿病大鼠的血糖水平更加有效,对2型糖尿病的治疗具有非常重要的作用,但无显著的交互作用。
③有氧运动可使糖尿病大鼠血清visfatin的水平显著降低;13周的膳食控制对降低2型糖尿病大鼠血清visfatin水平影响不大;有氧运动联合膳食控制虽然能使2型糖尿病大鼠血清visfatin含量进一步降低,但没有显著的交互作用;且血糖水平与血液中visfatin水平之间有着密切的关系,可能是调节visfatin合成和分泌的主要因素。
④有氧运动、膳食控制以及有氧运动联合膳食控制对改善2型糖尿病大鼠的脂代谢具有积极的作用。与此同时,血清visfatin水平对血脂代谢的调节也具有一定的作用,但是它们之间的确切关系还有待于进一步研究。
To explore the effect of aerobic exercise joint dietary control on the visfatin plasma levels in type 2 diabetic rats and analyze the changes in other relevant indicators. Method:
Chose 62 single of 6-week-old SD rats which were male, Eight rats were randomly selected as normal control group of rats (Control, C group), and fed with normal standard diet. The remaining 54 SD rats which were feed high-fat and high-sugar diet were injected of low-dose streptozotocin though abdominal cavity to establish animal models of type 2 diabetes. and then the rats of type 2 diabetes were randomly divided into 4 groups : DM control group (n=9), DM+ aerobic exercise training group (n=10), DM+ Diet control group (n=10), DM+ aerobic exercise training + Diet control group (n=10). The DM group’s rats which were continued to feed high-fat and high-sugar diet were not exercise; Exercise were used 60 minutes’unloaded swimming for 13 weeks, 6 times per week; The dietary control use the general contour of the standard diet of the DM group. 13 weeks later, FPG, TG, TC, FINS, Visfatin of every group’s rats were examined. Results:
①After 13 weeks of the establishment of type 2 diabetes model, compared with C group, the FPG contents increased significantly in DM group(P<0.01); Through the double factor variance analysis, aerobic exercise can lower FPG levels in diabetic rats (P<0.05), And the effect of dietary control on FPG levels in diabetic rats did not significantly(P>0.05), exercise joint dietary control did not display an obvious interaction on lowering FPG levels in diabetic tats(P>0.05).
②After 13 weeks of the establishment of type 2 diabetes model, compared with C group, the serum insulin concentration decreased significantly in DM group(P<0.01), but the HOMA-IR was no significant changes. Through the double factor variance analysis, diet control can increase the FINS level in diabetic rats significantly(P<0.05), aerobic exercise and aerobic exercise joint dietary control in diabetic rats could further increase the level of FINS, but no significant interaction(P>0.05); there was neither significantly effect of aerobic exercise nor dietary control to improve the DM group of HOMA-IR(P>0.05), and there was no significant interaction(P>0.05).
③After 13 weeks of the establishment of type 2 diabetes model, compared with C group, the visfatin plasma concentrations significantly increased(P<0.01); Through the double factor variance analysis, there was significant impact of 13 weeks of strength training for swimming to lower plasma visfatin concentrations in diabetic rats; compared with the DM group, Although the visfatin plasma concentration lowered too much in DMD group, through the double factor variance analysis, there was no significant impact of dietary control to lower the visfatin plasma concentration(P>0.05); aerobic exercise and diet control can further reduce the visfatin plasma concentration in diabetic rats,and there was no significant interaction(P>0.05).
④After 13 weeks of the establishment of type 2 diabetes modle, compared with C group, the serum total cholesterol concentration and the serum triglyceride concentration increased significantly(P<0.01); Through the double factor variance analysis, both of aerobic exercise and dietary control could significantly lower the total cholesterol concentration in type 2 diabetic rats(P<0.05), and there was significant interaction of both aerobic exercise and dietary control to lower the total cholesterol concentration in type 2 diabetic rats(P<0.05). Dietary control could lower the triglyceride concentration in type 2 diabetic rats(P<0.01)significantly, but aerobic exercise could not , although aerobic exercise joint dietary control could further lower the triglyceride concentration in type 2 diabetic rats, there was no significant interaction (P>0.05).
Conclusion:
①Establishing of the Model of type 2 diabetes in this research was successful. Dietary control only could not effectively lower the FPG concentration; And aerobic exercise training has a very significant role to control the FPG of diabetic rats, on the base of the diet control, aerobic exercise training was more effective to reduce the fasting plasma glucose levels which in diabetic rats. At the same time, the visfatin plasma levels which in type 2 diabetic rats was significantly increased.
②13 weeks of aerobic exercise training could improve the capacity of which Pancreaticβ-cell secreted insulin in type 2 diabetes rats; Although aerobic exercise joint dietary control could increase the insulin concentration in type 2 diabetes rats, and it had a very important role in the treatment of type 2 diabetes, there was no significant interaction.
③Aerobic exercise could significantly lower the level of visfatin plasma in type 2 diabetic rats ; There was little effect on lowering the visfatin plasma concentration of 13 weeks of dietary control in type 2 diabetic rats; Aerobic exercise joint dietary control could further lower the visfatin plasma content in type 2 diabetes rats, but there was no significant interaction; And there was a close relationship between blood glucose levels and visfatin levels. It might be a main factor on regulating the visfatin’s synthesis and secretion.
④It was an active role in improving lipid metabolism for aerobic exercise training、dietary control and aerobic exercise joint dietary control. At the same time, it was also a role in regulating the lipid metabolism for visfatin plasma levels, However, the precise relationship between them had to be further studied.
引文
[1]Fukuhara A, Matsuda M, Nishizawa M, et al. Visfatin: a protein secreted by visceral fat that mimics the effects of insulin. Science, 2005, 307:426-430
[2]Berndt J, Kloting N, Kralisch S, et al. Plasma visfatin concentrations and fat depot specific mRNA expression in humans[J]. Diabetes, 2005, 54(10):2911-2916.
[3]Antuna-Puente, Feve B, Fellahi S, et al. Adipokines:The missing link between insulin resistance and obesity. Diabetes Metab. 2008, 34(1):2-11.
[4]Curat C A, WegnerV, SengenesV, et al. Macrophages in human visceral adipose tissue: increased accumulation in obesity and a source of resistin and visfatin.Diabetologia, 2006; 49(4): 744-747
[5]Kitani T, Okuno S, Fujisawa H.Growth phase-dependent changes in the subcellular localization of pre-B-cell colony-enhancing factor[J]. FEBS Letters, 2003, 544(123): 74-78
[6]Christopher H, Harvey FL. Visfatin: a new adipokine[J]Science, 2005, 307(5708): 366-367
[7]Tanaka M, Nozaki M, Fukuhara A, et al. Visfatin is released from 3T3-L1 adipocytes via a non-classical pathway. Biochem Biophys Res Commun. 2007, 359(2): 194-201. Epub 2007 May 25.
[8]Samal B, Sun Y, Stearns G, et al. Cloning and characterization of the cDNA encodinga novel human pre-B-cell colony-enhancing factor[J]. Mol Cell Biol, 1994, 14(2): 1431-1437
[9]Satoh H, Nguyen MT, Miles PD, et al. Adenovirus-mediated chronic“hyperresistinemia”leads to in vivo insulin resistance in normal rats [J]. J Clin Invest, 2004, 114: 224-231
[10]Ort T, Arjona AA, MacDougall JR, et al. Recombinant human FIZZ3/resistin stimulates lipolysis in cultured human adipocytes, mouse adipose explants and in normal mice.Endocrinology, 2005, 146:2200-2209
[11]Steppan CM, Wang J, Whiteman EL, et al. Activation of SOCS-3 by resistin. Mol Cell Biol, 2005, 25: 1569-1575
[12]Rangwala SM, Rich AS, Rhoades B, et al. Abnormal glucose homeostasis due to chronic hyperresistinemia. Diabetes, 2004, 53: 1937-1941
[13]蓝丹,经承学,等.前B细胞集落促进因子诱导正常人及重型先天性中性粒细胞减少症患者髓系细胞分化功能研究.广西医科大学博士学位论文. 2008
[14]Banerjee RR, Rangwala SM, Shapiro JS, et al. Regulation of fasted blood glucose by resistin. Science, 2004, 303:1195-1198
[15]Yonezawa T, Haga S, Kobayashi Y, et al. Visfatin is present in bovine mammary epithelial cells, lactating mammary gland and milk, and its expression is regulated by cAMP pathway. FEBS Lett. 2006, 580(28-29): 6635-43. Epub 2006 Nov 15.
[16]Ognjanovic S, Bao S, Yamamoto SY, et al. Genomic organization of the gene coding for human pre-B-cell colony enhancing factor and expression in human fetal membranes[J]. J Mol Endocrinol, 2001, 26(2): 107-117
[17]Patrone L, DamoreaM A, LeeM B, et al. Genes expressed during the IFNγ-induced maturation of p re-B cells [J]. Mol Immunol, 2001, 38(8): 597-606
[18]Kralisch S, Klein J, Lossner U, et al. Interleukin-6 is a negative regulator of visfatin gene expression in 3T3-L1 adipocytes [J]. Am J Physiol Endocrinol Metab, 2005, 289(4): E586-E590
[19]Arner P. Visfatin-A true or false trail to type 2 diabetes mellitus [J]. J Clin Endocrinol Metab, 2006, 91(1): 28-30.
[20]Ognjanovic S, Bryant-Greenwood GD. Pre-B cell colony-enhancing factor, a novel cytokine of human fetal membranes [J]. Am J Obstet Gynecol, 2002, 187(4): 1051-1058.
[21]HaiderD G, Schaller G, Kap iotis S, et al. The release of the adipocytokine visfatin is regulated by glucose and insulin [J]. Diabetologia, 2006, 49(8): 1909-1914.
[22]Choi K C, Ryu O H, Lee KW, et al. Effect of PPAR-alpha and-gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats[J]. Biochem Biophys ResCommun, 2005, 336(3): 747-531.
[23]Kohzo Takebayashi, Mariko Suetsugu, Sadao Wakabayashi, et al. Association between plasma visfatin and vascular endothelial function in patients with type 2 diabetes mellitus, Metabolism. 2007; 56(4): 451-8.
[24]Haider DG, Pleiner J, Francesconi M, etal. Exercise training lowers plasma visfatin concentrations in patients with type 1 diabetes. J Clin Endocrinol Metab. 2006, 91(11): 4702-4. Epub 2006 Aug 8.
[25]Frydelund-Larsen L, Akerstrom T, Nielsen S, et al. Visfatin mRNA expression in human subcutaneous adipose tissue is regulated by exercise [J]. Am J Physiol Endocrinol Metab. 2007, 292: E24-E31.
[26]Gaber T, Dziurla R, Tschirschmann M, et al. The effect of hypoxia on the expression of pbef in CD4+ lymphocytes [J]. Ann RheumDis, 2006, 65(6): 455.
[27]Bae S K, Kim S R, Kim J G, et al. Hypoxic induction of human visfatin gene is directly mediated by hypoxia-inducible factor-1[J].FEBS Lett, 2006, 580(17): 4105-4113.
[28]Beltowski J. Apelin and visfatin: Unique "beneficial" adipokines upregulated in obesity?[J]. Med Sci Monit, 2006; 12(9): LE17-18.
[29]Jacqueline M, Stephens, Antonio J, et al. An update on visfatin/Pre-B cell colonyenhancing factor, an ubiquitously expressed, illusive cytokine that is regulated in obesity. Curr opin Lipidol, 2006, 17: 128-131
[30]Ando H, Yanagihara H, Hayashi Y et al. Rhythmic mRNA Expression of Clock Genes and Adipocytokines in Mouse Visceral Adipose Tissue.Endocrinology, 2005; 146(12): 5631-5636
[31]Kitani T, Okuno S, Fujisawa H. Growth phase-dependent changes in the subcellular localization of pre-B-cell colony-enhancing factor [J]. FEBS Lett, 2003, 544(123): 74-78
[32]Jia S H, Li Y, Parodo J, et al. Pre-B cell colony-enhancing factor inhibits neutrophil apoptosis in experimental inflammation and clinical sepsis [J]. J Clin Invest, 2004, 113(9): 1318-1327
[33]Moon B, Kwan JJ, Duddy N, et al. Resistin inhibits glucose uptake in L6 cells independently of changes in insulin signaling and GLUT4 translocation. Am J Physiol Endocrinol Metab, 2003, 285: E106-E115
[34]Ye SQ, Zhang LQ, Adyshev D, et al. Pre-B-cell colony-enhancing factor is critically involved in thrombin induced lung endothelial cell barrier dysregulation [J]. Microvasc Res, 2005, 70(3): 142-151
[35]Revollo J R, Grimm A A, Imai S. The NAD biosynthesis pathwaymediated by nicotinamide phosphoribosyl transferase Regulates Sir2 Activity in mammalian cells[J]. J Biol Chem, 2004, 279(49): 50754-50763
[36]Vander Veer E, Nong Z, O’Neil C, et al. Pre-B-cell colony-enhancing factor regulates NAD+dependent protein deacetylase activity and promotes vascular smooth muscle cell maturation[J]. Circ Res, 2005, 97(1): 25-34
[37]Reaven GM. Role of insulin resistance in human disease. Diabetes, 1988; 37(I2):1595-1609
[38]赵志刚,张会峰.代谢综合症的研究进展[J].中国临床保健杂志, 2007, 10:91
[39]Eckel R, Grundy SM, Zimmet PZ, et al. Metabolic syndrome [J]. Lancet, 2005, 365(9468): 1415-1428.
[40]Dandona P, AljadaA, ChaudhuriA, et al. Metabolic syndrome: a comprehensive perspective based on interactions between obesity, diabetes, and inflammation [J]. Circulation, 2005, 111(11): 1448-1454.
[41]Evans RM, Barish GD, Wang YX. PPARs and complex journey to obesity [J]. NatMed, 2004, 10(4): 355-361.
[42]Grundy SM, Brewer HB Jr, Cleeman JI, et al. Definition of metabolic syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition [J]. Circulation, 2004, 109(3): 433-438.
[43]Reaven GM. The metabolic syndrome or the insulin resistance syndrome? Difference names, different comcepts, and different goals [J]. Endocrinol Metab Clin N Am, 2004, 33(5): 283-286.
[44]邓尚平主编.临床糖尿病学.成都:四川科学技术出版社, 2000. 8: 1-5, 71-72, 187~189, 198-199
[45]张蕙芬,迟家敏.王瑞萍主编.实用糖尿病学.北京:人民卫生出版社, 2002: 22~31
[46]纪立农.代谢综合征与2型糖尿病.国外医学内分泌学分册, 2002; 22(5): 281~282
[47]项坤三.代谢综合征的流行病学和病因学.国外医学内分泌学分册, 2002; 22(5): 280~281
[48]Stern MP. Diabetes and cardiovascular disease. The"commonsoil"hypothesis. Diabetes, 1995; 44(4): 396~374
[49]Haider DG, Schindler K, Schaller G, et al. Increased plasma visfatin concentrations in morbidly obese subjects are reduced after gastric banding. J Clin Endocrinol Metab, 2006, 91(4): 1578-1581
[50]Chen MP, Chung FM, Chang DM, et al. Elevated plasma level of vis-fatin/pre-Bcell colony-enhancing factor in patients with type 2 diabetes melli-tus. J Clin Endocrinol Metab, 2006, 91(1): 295-299
[51]Kloting N, Kloting I. Visfatin: gene expression in isolated adipocytes and sequence analysis in obesWOKW rats compared with lean control rats. Bio-chem Biophys Res Commun, 2005; 332(4): 1070-1072
[52]Derek J. Hausenloy, Shiang-Yong Lim, et al. Cardioprotective actions of the novel adipocytok ine visfatin; Journal of Molecular and CellularCardiology, 42(2007)S217-S218
[53]López-Bermejo A, Chico-JuliàB, Fernàndez-Balsells M, et al. Serum visfatin increases with progressive beta-cell deterioration[J]. Diabetes. 2006 Oct; 55(10): 2871-5
[54]Jos’e Manuel fern’andez-real, et al. Circulating Visfatin Is Associated With Parameters of Iron Metabolism in Subjects With Altered Glucose Toleran–ce, Diabetes Care, 2007; 30(3): 616-620
[55]Hammarstedt A, Pihlajamaki J, Sopasakis V R, et al. Visfatin is an adipo-kine but it is not regulated by thiazolidinediones [J]. J Clin EndocrinolMetab, 2006, 91(3): 1181-1184
[56]Alghasham AA, Barakat YA. Serum visfatin and its relation to insulin resistance and inflammation in type 2 diabetic patients with and without macroangiopathy. Saudi Med J. 2008, 29(2): 185-192.
[57]Dogru T, Sonmez A, Tasci I, et al. Plasma Visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance [J]. Diabetes Res Clin Pract. 2007, 76(1): 24-9. Epub 2006 Sep 7.
[58]Krzyzanowska K, Krugluger W, Mittermayer F, et al. Increased visfatin concentrations in women with gestational diabetesmellitus. Clin Sc(iLond), 2006, 110(5): 605-609
[59]Bottcher Y, Teup serD, Enigk B, et al. Genetic variation in the visfatin gene(PBEF1)and its relation to glucose metabolism and fat depot specific mRNAexpression in humans. J Clin Endocrinol Metab, 2006, 91: 2725-2731
[60]Chan TF, Chen YL, Lee CH, et al. Decreased Plasma Visfatin Concentrations in Women With Gestational Diabetes Mellitus [J]. J Soc Gynecol Investig, 2006, 3(1): 364-367.
[61]Krzyzanowska K, Krugluger W, Mittermayer F, et al. Increased visfatin concentrations in women with gestational diabetes mellitus [J]. Clin Sci(Lond), 2006, 110(5): 605-609.
[62]温彩铃.血浆内脂素水平与2型糖尿病及糖耐量减低患者的相关性研究[J].苏州大学硕士学位论文. 2007.
[63]Zhu J, Schott M, Liu R, et al. Intensive glycemic control lowers plasma visfatin levels in patients with type 2 diabetes. Horm Metab Res. 2008, 40(11): 801-5. Epub 2008 Aug 6.
[64]Su-Ryun Kim, Soo-Kyung Bae, et al. Visfatin promotes angiogenesis by activation of extracellular signal-regulated kinase 1/2, Biochemical and Biophysical Research Communications, 357(2007): 150–156.
[65]Pagano C, Soardo G, Pilon C, et al. Increased serum visfatin in nonalcoholic fatty liver disease is related to liver disease severity and not to insulin resistance[J]. J Clin EndocrinolMetab, 2006, 91(3): 1081-1086.
[66]Jarrar MH, Baranova A, Collantes R, et al. Adipokines and cytokines in non-alcoholic fatty liver disease[J]. Aliment Pharmacol Ther. 2008, 28(2): 266-267
[67]Soardo G, Pagsno C, Donnini D, et al. Circulating And Adipose Tissue Expression Of Visfatin In Nonacohlic Fatty Liver Disease[J]. Journal of Hepatology, 2006, 44: S263-S264
[68]Dong-il Seo, Eun-Jung Yoo, Kang-Il Limet, et al. Plasma visfatin response to combined exercise training in healthy women. FASEB[J]. 2007, 4(21)A931
[69]Choi. Effect of exercise training on plasma visfatin and eotaxin levels. Eur J Endocrinol. 2007 Oct; 157(4): 437-42
[70]林文弢,李颖,翁锡全.间歇性低氧和运动对高脂饮食诱导胰岛素抵抗大鼠血清内脂素的影响[J].中国运动医学杂志, 2008, 27(2): 160-164
[71]Dominik G, Haider, Johannes Pleiner, et al. Exercise Training Lowers Plasma Visfatin Concentrations in Patients with Type 1 Diabetes[J]. The Journal of Clinical Endocrinology & Metabolism. 2006, 91(11): 4702-4704
[72]De Luis DA, Gonzalez Sagrado M, Conde R, et al. Effect of a hypocaloric diet on serum visfatin in obese non-diabetic patients. Nutrition. 2008 Jun; 24(6): 517-21. Epub 2008 Mar 17.
[1]Trayhum P, Beattie JH. Physiological role of adipose tissue: white adipose tissue as all endocrine and secretory organ. Proc Nutr Soc, 2001, 60: 329-339.
[2]Fukuhara A, Matsuda M, Nishzawa M, et al. Visfatin: a protein secreted by visceral fat that mimics the effects of insulin. Science, 2005, 307: 426-430.
[3]Samal B, Sun Y, Stearns G, et al. Cloning and characterization of the cDNA encoding a novel human pre-B-cell colony-enhancing factor.Mol Cell Biol, 1994, 14: 1431-1437.
[4]Jia SH, Li Y, Parodo J, et al. Pre-B cell colony-Enhancing factor inhibits neutrophil apoptosis in experimental inflammation and clinical sepsis. J Clin Invest, 2004, 113: 1318-1327.
[5]Ognjanovic S, Bryant-Greenwood GD. Pre-B cell colony-enhancing factor, a novel cytokine of human fetal membranes. Am J Obstet Gynecol, 2002, 187: 1051-1058.
[6]戴筱英.餐后不同时间运动对糖尿病患者的降糖作用.现代康复, 2001, 5(7):104
[7]倪红霞.高糖高脂饮食诱导的大鼠Ⅱ型糖尿病模型.北华大学学报(自然科学版).2005, 7(5): 440-442
[8]Alghasham AA, Barakat YA. Serum visfatin and its relation to insulin resistance and inflammation in type 2 diabetic patients with and without macroangiopathy. Saudi Med J. 2008, 29(2): 185-92.
[9]Chen MP, Chung FM, Chang DM, et al. Elevated plasma level of visfatin/pre-B cell colony-enhancing factor in patients with type 2 diabetes mellitus [J]. J Clin Endocrinol Metab, 2006, 91(1): 295-299.
[10]王步标,华明,邓树勋等.人体生理学[M].高等教育出版社, 2003: 250-254
[11]Kraliseh S, Klein J, Lossner U, et al. Interleukin-6 is a negative regulator of visfatin gene expression in 3T3-L1 adipocytes. Am J Physiol Endocrinol Metab, 2005; 289(4): E586-E590.
[12]Sethi JK, Vidal-Puig A. Visfatin: the missing link between intra-abdominal obesity and diabetes[J]. Trends Mol Med, 2005, 11: 344-347.
[13] Choi SB, Jang JS, Hong SM, et al. Exercise and dexamethasone oppositely modulate beta-cell function and survival via independent pathways in 90% pancreatectomized rats [J]. Endocrinol. 2006, 190(2): 471-452.
[14]Brema I, Hatunic M, Finucane F, et al. Plasma visfatin is reduced after aerobic exercise in early onset type 2 diabetes mellitus. Diabetes Obes Metab. 2008, 10(7): 600-2. Epub 2008 May 12.
[15]Paquot N, Tappy L. Adipocytokines: link between obesity, type 2 diabetes and atherosclerosis. Rev Med Liege. 2005, 60(5-6):369-73.
[16]Dominik G, Haider, Johannes Pleiner, et al. Exercise Training Lowers Plasma Visfatin Concentrations in Patients with Type 1 Diabetes[J]. The Journal of Clinical Endocrinology & Metabolism. 2006, 91(11): 4702-4704
[17]Kralisch S, Klein J, Lossner U, et al. Hormonal regulation of the novel adipocytokine visfatin in 3T3-L1 adipocvtes. J Endocrinol Metab, 2005, 185: R1-R8.
[18]Turpaev K, Bouton C, DietA, et al. Analysis of differentially expressed genes in nitric oxide-exposed human monocytic cells. Free Radic BiolMed, 2005, 38(10): 1392-1400
[19]张月华,龚志刚,敖禾花等.有氧运动与营养干预Ⅱ型糖尿病大鼠糖脂代谢影响的实验研究.辽宁体育科技, 2007, 29(5): 20-24
[20]De Luis DA, Gonzalez Sagrado M, Conde R, et al. Effect of a hypocaloric diet on serum visfatin in obese non-diabetic patients. Nutrition. 2008, 24(6): 517-21. Epub 2008 Mar 17.
[2]Berndt J, Kloting N, Kralisch S, et al. Plasma visfatin concentrations and fat depot specific mRNA expression in humans[J]. Diabetes, 2005, 54(10):2911-2916.
[3]Antuna-Puente, Feve B, Fellahi S, et al. Adipokines:The missing link between insulin resistance and obesity. Diabetes Metab. 2008, 34(1):2-11.
[4]Curat C A, WegnerV, SengenesV, et al. Macrophages in human visceral adipose tissue: increased accumulation in obesity and a source of resistin and visfatin.Diabetologia, 2006; 49(4): 744-747
[5]Kitani T, Okuno S, Fujisawa H.Growth phase-dependent changes in the subcellular localization of pre-B-cell colony-enhancing factor[J]. FEBS Letters, 2003, 544(123): 74-78
[6]Christopher H, Harvey FL. Visfatin: a new adipokine[J]Science, 2005, 307(5708): 366-367
[7]Tanaka M, Nozaki M, Fukuhara A, et al. Visfatin is released from 3T3-L1 adipocytes via a non-classical pathway. Biochem Biophys Res Commun. 2007, 359(2): 194-201. Epub 2007 May 25.
[8]Samal B, Sun Y, Stearns G, et al. Cloning and characterization of the cDNA encodinga novel human pre-B-cell colony-enhancing factor[J]. Mol Cell Biol, 1994, 14(2): 1431-1437
[9]Satoh H, Nguyen MT, Miles PD, et al. Adenovirus-mediated chronic“hyperresistinemia”leads to in vivo insulin resistance in normal rats [J]. J Clin Invest, 2004, 114: 224-231
[10]Ort T, Arjona AA, MacDougall JR, et al. Recombinant human FIZZ3/resistin stimulates lipolysis in cultured human adipocytes, mouse adipose explants and in normal mice.Endocrinology, 2005, 146:2200-2209
[11]Steppan CM, Wang J, Whiteman EL, et al. Activation of SOCS-3 by resistin. Mol Cell Biol, 2005, 25: 1569-1575
[12]Rangwala SM, Rich AS, Rhoades B, et al. Abnormal glucose homeostasis due to chronic hyperresistinemia. Diabetes, 2004, 53: 1937-1941
[13]蓝丹,经承学,等.前B细胞集落促进因子诱导正常人及重型先天性中性粒细胞减少症患者髓系细胞分化功能研究.广西医科大学博士学位论文. 2008
[14]Banerjee RR, Rangwala SM, Shapiro JS, et al. Regulation of fasted blood glucose by resistin. Science, 2004, 303:1195-1198
[15]Yonezawa T, Haga S, Kobayashi Y, et al. Visfatin is present in bovine mammary epithelial cells, lactating mammary gland and milk, and its expression is regulated by cAMP pathway. FEBS Lett. 2006, 580(28-29): 6635-43. Epub 2006 Nov 15.
[16]Ognjanovic S, Bao S, Yamamoto SY, et al. Genomic organization of the gene coding for human pre-B-cell colony enhancing factor and expression in human fetal membranes[J]. J Mol Endocrinol, 2001, 26(2): 107-117
[17]Patrone L, DamoreaM A, LeeM B, et al. Genes expressed during the IFNγ-induced maturation of p re-B cells [J]. Mol Immunol, 2001, 38(8): 597-606
[18]Kralisch S, Klein J, Lossner U, et al. Interleukin-6 is a negative regulator of visfatin gene expression in 3T3-L1 adipocytes [J]. Am J Physiol Endocrinol Metab, 2005, 289(4): E586-E590
[19]Arner P. Visfatin-A true or false trail to type 2 diabetes mellitus [J]. J Clin Endocrinol Metab, 2006, 91(1): 28-30.
[20]Ognjanovic S, Bryant-Greenwood GD. Pre-B cell colony-enhancing factor, a novel cytokine of human fetal membranes [J]. Am J Obstet Gynecol, 2002, 187(4): 1051-1058.
[21]HaiderD G, Schaller G, Kap iotis S, et al. The release of the adipocytokine visfatin is regulated by glucose and insulin [J]. Diabetologia, 2006, 49(8): 1909-1914.
[22]Choi K C, Ryu O H, Lee KW, et al. Effect of PPAR-alpha and-gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats[J]. Biochem Biophys ResCommun, 2005, 336(3): 747-531.
[23]Kohzo Takebayashi, Mariko Suetsugu, Sadao Wakabayashi, et al. Association between plasma visfatin and vascular endothelial function in patients with type 2 diabetes mellitus, Metabolism. 2007; 56(4): 451-8.
[24]Haider DG, Pleiner J, Francesconi M, etal. Exercise training lowers plasma visfatin concentrations in patients with type 1 diabetes. J Clin Endocrinol Metab. 2006, 91(11): 4702-4. Epub 2006 Aug 8.
[25]Frydelund-Larsen L, Akerstrom T, Nielsen S, et al. Visfatin mRNA expression in human subcutaneous adipose tissue is regulated by exercise [J]. Am J Physiol Endocrinol Metab. 2007, 292: E24-E31.
[26]Gaber T, Dziurla R, Tschirschmann M, et al. The effect of hypoxia on the expression of pbef in CD4+ lymphocytes [J]. Ann RheumDis, 2006, 65(6): 455.
[27]Bae S K, Kim S R, Kim J G, et al. Hypoxic induction of human visfatin gene is directly mediated by hypoxia-inducible factor-1[J].FEBS Lett, 2006, 580(17): 4105-4113.
[28]Beltowski J. Apelin and visfatin: Unique "beneficial" adipokines upregulated in obesity?[J]. Med Sci Monit, 2006; 12(9): LE17-18.
[29]Jacqueline M, Stephens, Antonio J, et al. An update on visfatin/Pre-B cell colonyenhancing factor, an ubiquitously expressed, illusive cytokine that is regulated in obesity. Curr opin Lipidol, 2006, 17: 128-131
[30]Ando H, Yanagihara H, Hayashi Y et al. Rhythmic mRNA Expression of Clock Genes and Adipocytokines in Mouse Visceral Adipose Tissue.Endocrinology, 2005; 146(12): 5631-5636
[31]Kitani T, Okuno S, Fujisawa H. Growth phase-dependent changes in the subcellular localization of pre-B-cell colony-enhancing factor [J]. FEBS Lett, 2003, 544(123): 74-78
[32]Jia S H, Li Y, Parodo J, et al. Pre-B cell colony-enhancing factor inhibits neutrophil apoptosis in experimental inflammation and clinical sepsis [J]. J Clin Invest, 2004, 113(9): 1318-1327
[33]Moon B, Kwan JJ, Duddy N, et al. Resistin inhibits glucose uptake in L6 cells independently of changes in insulin signaling and GLUT4 translocation. Am J Physiol Endocrinol Metab, 2003, 285: E106-E115
[34]Ye SQ, Zhang LQ, Adyshev D, et al. Pre-B-cell colony-enhancing factor is critically involved in thrombin induced lung endothelial cell barrier dysregulation [J]. Microvasc Res, 2005, 70(3): 142-151
[35]Revollo J R, Grimm A A, Imai S. The NAD biosynthesis pathwaymediated by nicotinamide phosphoribosyl transferase Regulates Sir2 Activity in mammalian cells[J]. J Biol Chem, 2004, 279(49): 50754-50763
[36]Vander Veer E, Nong Z, O’Neil C, et al. Pre-B-cell colony-enhancing factor regulates NAD+dependent protein deacetylase activity and promotes vascular smooth muscle cell maturation[J]. Circ Res, 2005, 97(1): 25-34
[37]Reaven GM. Role of insulin resistance in human disease. Diabetes, 1988; 37(I2):1595-1609
[38]赵志刚,张会峰.代谢综合症的研究进展[J].中国临床保健杂志, 2007, 10:91
[39]Eckel R, Grundy SM, Zimmet PZ, et al. Metabolic syndrome [J]. Lancet, 2005, 365(9468): 1415-1428.
[40]Dandona P, AljadaA, ChaudhuriA, et al. Metabolic syndrome: a comprehensive perspective based on interactions between obesity, diabetes, and inflammation [J]. Circulation, 2005, 111(11): 1448-1454.
[41]Evans RM, Barish GD, Wang YX. PPARs and complex journey to obesity [J]. NatMed, 2004, 10(4): 355-361.
[42]Grundy SM, Brewer HB Jr, Cleeman JI, et al. Definition of metabolic syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition [J]. Circulation, 2004, 109(3): 433-438.
[43]Reaven GM. The metabolic syndrome or the insulin resistance syndrome? Difference names, different comcepts, and different goals [J]. Endocrinol Metab Clin N Am, 2004, 33(5): 283-286.
[44]邓尚平主编.临床糖尿病学.成都:四川科学技术出版社, 2000. 8: 1-5, 71-72, 187~189, 198-199
[45]张蕙芬,迟家敏.王瑞萍主编.实用糖尿病学.北京:人民卫生出版社, 2002: 22~31
[46]纪立农.代谢综合征与2型糖尿病.国外医学内分泌学分册, 2002; 22(5): 281~282
[47]项坤三.代谢综合征的流行病学和病因学.国外医学内分泌学分册, 2002; 22(5): 280~281
[48]Stern MP. Diabetes and cardiovascular disease. The"commonsoil"hypothesis. Diabetes, 1995; 44(4): 396~374
[49]Haider DG, Schindler K, Schaller G, et al. Increased plasma visfatin concentrations in morbidly obese subjects are reduced after gastric banding. J Clin Endocrinol Metab, 2006, 91(4): 1578-1581
[50]Chen MP, Chung FM, Chang DM, et al. Elevated plasma level of vis-fatin/pre-Bcell colony-enhancing factor in patients with type 2 diabetes melli-tus. J Clin Endocrinol Metab, 2006, 91(1): 295-299
[51]Kloting N, Kloting I. Visfatin: gene expression in isolated adipocytes and sequence analysis in obesWOKW rats compared with lean control rats. Bio-chem Biophys Res Commun, 2005; 332(4): 1070-1072
[52]Derek J. Hausenloy, Shiang-Yong Lim, et al. Cardioprotective actions of the novel adipocytok ine visfatin; Journal of Molecular and CellularCardiology, 42(2007)S217-S218
[53]López-Bermejo A, Chico-JuliàB, Fernàndez-Balsells M, et al. Serum visfatin increases with progressive beta-cell deterioration[J]. Diabetes. 2006 Oct; 55(10): 2871-5
[54]Jos’e Manuel fern’andez-real, et al. Circulating Visfatin Is Associated With Parameters of Iron Metabolism in Subjects With Altered Glucose Toleran–ce, Diabetes Care, 2007; 30(3): 616-620
[55]Hammarstedt A, Pihlajamaki J, Sopasakis V R, et al. Visfatin is an adipo-kine but it is not regulated by thiazolidinediones [J]. J Clin EndocrinolMetab, 2006, 91(3): 1181-1184
[56]Alghasham AA, Barakat YA. Serum visfatin and its relation to insulin resistance and inflammation in type 2 diabetic patients with and without macroangiopathy. Saudi Med J. 2008, 29(2): 185-192.
[57]Dogru T, Sonmez A, Tasci I, et al. Plasma Visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance [J]. Diabetes Res Clin Pract. 2007, 76(1): 24-9. Epub 2006 Sep 7.
[58]Krzyzanowska K, Krugluger W, Mittermayer F, et al. Increased visfatin concentrations in women with gestational diabetesmellitus. Clin Sc(iLond), 2006, 110(5): 605-609
[59]Bottcher Y, Teup serD, Enigk B, et al. Genetic variation in the visfatin gene(PBEF1)and its relation to glucose metabolism and fat depot specific mRNAexpression in humans. J Clin Endocrinol Metab, 2006, 91: 2725-2731
[60]Chan TF, Chen YL, Lee CH, et al. Decreased Plasma Visfatin Concentrations in Women With Gestational Diabetes Mellitus [J]. J Soc Gynecol Investig, 2006, 3(1): 364-367.
[61]Krzyzanowska K, Krugluger W, Mittermayer F, et al. Increased visfatin concentrations in women with gestational diabetes mellitus [J]. Clin Sci(Lond), 2006, 110(5): 605-609.
[62]温彩铃.血浆内脂素水平与2型糖尿病及糖耐量减低患者的相关性研究[J].苏州大学硕士学位论文. 2007.
[63]Zhu J, Schott M, Liu R, et al. Intensive glycemic control lowers plasma visfatin levels in patients with type 2 diabetes. Horm Metab Res. 2008, 40(11): 801-5. Epub 2008 Aug 6.
[64]Su-Ryun Kim, Soo-Kyung Bae, et al. Visfatin promotes angiogenesis by activation of extracellular signal-regulated kinase 1/2, Biochemical and Biophysical Research Communications, 357(2007): 150–156.
[65]Pagano C, Soardo G, Pilon C, et al. Increased serum visfatin in nonalcoholic fatty liver disease is related to liver disease severity and not to insulin resistance[J]. J Clin EndocrinolMetab, 2006, 91(3): 1081-1086.
[66]Jarrar MH, Baranova A, Collantes R, et al. Adipokines and cytokines in non-alcoholic fatty liver disease[J]. Aliment Pharmacol Ther. 2008, 28(2): 266-267
[67]Soardo G, Pagsno C, Donnini D, et al. Circulating And Adipose Tissue Expression Of Visfatin In Nonacohlic Fatty Liver Disease[J]. Journal of Hepatology, 2006, 44: S263-S264
[68]Dong-il Seo, Eun-Jung Yoo, Kang-Il Limet, et al. Plasma visfatin response to combined exercise training in healthy women. FASEB[J]. 2007, 4(21)A931
[69]Choi. Effect of exercise training on plasma visfatin and eotaxin levels. Eur J Endocrinol. 2007 Oct; 157(4): 437-42
[70]林文弢,李颖,翁锡全.间歇性低氧和运动对高脂饮食诱导胰岛素抵抗大鼠血清内脂素的影响[J].中国运动医学杂志, 2008, 27(2): 160-164
[71]Dominik G, Haider, Johannes Pleiner, et al. Exercise Training Lowers Plasma Visfatin Concentrations in Patients with Type 1 Diabetes[J]. The Journal of Clinical Endocrinology & Metabolism. 2006, 91(11): 4702-4704
[72]De Luis DA, Gonzalez Sagrado M, Conde R, et al. Effect of a hypocaloric diet on serum visfatin in obese non-diabetic patients. Nutrition. 2008 Jun; 24(6): 517-21. Epub 2008 Mar 17.
[1]Trayhum P, Beattie JH. Physiological role of adipose tissue: white adipose tissue as all endocrine and secretory organ. Proc Nutr Soc, 2001, 60: 329-339.
[2]Fukuhara A, Matsuda M, Nishzawa M, et al. Visfatin: a protein secreted by visceral fat that mimics the effects of insulin. Science, 2005, 307: 426-430.
[3]Samal B, Sun Y, Stearns G, et al. Cloning and characterization of the cDNA encoding a novel human pre-B-cell colony-enhancing factor.Mol Cell Biol, 1994, 14: 1431-1437.
[4]Jia SH, Li Y, Parodo J, et al. Pre-B cell colony-Enhancing factor inhibits neutrophil apoptosis in experimental inflammation and clinical sepsis. J Clin Invest, 2004, 113: 1318-1327.
[5]Ognjanovic S, Bryant-Greenwood GD. Pre-B cell colony-enhancing factor, a novel cytokine of human fetal membranes. Am J Obstet Gynecol, 2002, 187: 1051-1058.
[6]戴筱英.餐后不同时间运动对糖尿病患者的降糖作用.现代康复, 2001, 5(7):104
[7]倪红霞.高糖高脂饮食诱导的大鼠Ⅱ型糖尿病模型.北华大学学报(自然科学版).2005, 7(5): 440-442
[8]Alghasham AA, Barakat YA. Serum visfatin and its relation to insulin resistance and inflammation in type 2 diabetic patients with and without macroangiopathy. Saudi Med J. 2008, 29(2): 185-92.
[9]Chen MP, Chung FM, Chang DM, et al. Elevated plasma level of visfatin/pre-B cell colony-enhancing factor in patients with type 2 diabetes mellitus [J]. J Clin Endocrinol Metab, 2006, 91(1): 295-299.
[10]王步标,华明,邓树勋等.人体生理学[M].高等教育出版社, 2003: 250-254
[11]Kraliseh S, Klein J, Lossner U, et al. Interleukin-6 is a negative regulator of visfatin gene expression in 3T3-L1 adipocytes. Am J Physiol Endocrinol Metab, 2005; 289(4): E586-E590.
[12]Sethi JK, Vidal-Puig A. Visfatin: the missing link between intra-abdominal obesity and diabetes[J]. Trends Mol Med, 2005, 11: 344-347.
[13] Choi SB, Jang JS, Hong SM, et al. Exercise and dexamethasone oppositely modulate beta-cell function and survival via independent pathways in 90% pancreatectomized rats [J]. Endocrinol. 2006, 190(2): 471-452.
[14]Brema I, Hatunic M, Finucane F, et al. Plasma visfatin is reduced after aerobic exercise in early onset type 2 diabetes mellitus. Diabetes Obes Metab. 2008, 10(7): 600-2. Epub 2008 May 12.
[15]Paquot N, Tappy L. Adipocytokines: link between obesity, type 2 diabetes and atherosclerosis. Rev Med Liege. 2005, 60(5-6):369-73.
[16]Dominik G, Haider, Johannes Pleiner, et al. Exercise Training Lowers Plasma Visfatin Concentrations in Patients with Type 1 Diabetes[J]. The Journal of Clinical Endocrinology & Metabolism. 2006, 91(11): 4702-4704
[17]Kralisch S, Klein J, Lossner U, et al. Hormonal regulation of the novel adipocytokine visfatin in 3T3-L1 adipocvtes. J Endocrinol Metab, 2005, 185: R1-R8.
[18]Turpaev K, Bouton C, DietA, et al. Analysis of differentially expressed genes in nitric oxide-exposed human monocytic cells. Free Radic BiolMed, 2005, 38(10): 1392-1400
[19]张月华,龚志刚,敖禾花等.有氧运动与营养干预Ⅱ型糖尿病大鼠糖脂代谢影响的实验研究.辽宁体育科技, 2007, 29(5): 20-24
[20]De Luis DA, Gonzalez Sagrado M, Conde R, et al. Effect of a hypocaloric diet on serum visfatin in obese non-diabetic patients. Nutrition. 2008, 24(6): 517-21. Epub 2008 Mar 17.