Lipopolysaccharide binding protein, obesity status and incidence of metabolic syndrome: a prospective study among middle-aged and older Chinese

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• 作者：Xin Liu (1)
  Ling Lu (1)
  Pang Yao (1)
  Yiwei Ma (1)
  Feijie Wang (1)
  Qianlu Jin (1)
  Xingwang Ye (1)
  Huaixing Li (1)
  Frank B. Hu (2) (3)
  Liang Sun (1)
  Xu Lin (1)
  
• 关键词：Lipopolysaccharide binding protein ; Metabolic syndrome ; Obesity ; Prospective cohort study
• 刊名：Diabetologia
• 出版年：2014
• 出版时间：September 2014
• 年：2014
• 卷：57
• 期：9
• 页码：1834-1841
• 全文大小：213 KB
• 参考文献：1. Zhao L (2013) The gut microbiota and obesity: from correlation to causality. Nat Rev Microbiol 11:639-47 CrossRef
  2. Vijay-Kumar M, Aitken JD, Carvalho FA et al (2010) Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5. Science 328:228-31 CrossRef
  3. Qin J, Li Y, Cai Z et al (2012) A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature 490:55-0 CrossRef
  4. Kemp DM (2013) Does chronic low-grade endotoxemia define susceptibility of obese humans to insulin resistance via dietary effects on gut microbiota? Adipocyte 2:188-90 CrossRef
  5. Mehta NN, McGillicuddy FC, Anderson PD et al (2010) Experimental endotoxemia induces adipose inflammation and insulin resistance in humans. Diabetes 59:172-81 CrossRef
  6. Novitsky TJ (1998) Limitations of the Limulus amebocyte lysate test in demonstrating circulating lipopolysaccharides. Ann N Y Acad Sci 851:416-21 CrossRef
  7. Schumann RR (2011) Old and new findings on lipopolysaccharide-binding protein: a soluble pattern-recognition molecule. Biochem Soc Trans 39:989-93 CrossRef
  8. Ruiz AG, Casafont F, Crespo J et al (2007) Lipopolysaccharide-binding protein plasma levels and liver TNF-alpha gene expression in obese patients: evidence for the potential role of endotoxin in the pathogenesis of non-alcoholic steatohepatitis. Obes Surg 17:1374-380 CrossRef
  9. Sun L, Yu Z, Ye X et al (2010) A marker of endotoxemia is associated with obesity and related metabolic disorders in apparently healthy Chinese. Diabetes Care 33:1925-932 CrossRef
  10. Teixeira TF, Souza NC, Chiarello PG et al (2012) Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors. Clin Nutr 31:735-40 CrossRef
  11. Manco M, Putignani L, Bottazzo GF (2010) Gut microbiota, lipopolysaccharides, and innate immunity in the pathogenesis of obesity and cardiovascular risk. Endocr Rev 31:817-44 CrossRef
  12. Gonzalez-Quintela A, Alonso M, Campos J, Vizcaino L, Loidi L, Gude F (2013) Determinants of serum concentrations of lipopolysaccharide-binding protein (LBP) in the adult population: the role of obesity. PLoS One 8:e54600 CrossRef
  13. Moreno-Navarrete JM, Escote X, Ortega F et al (2013) A role for adipocyte-derived lipopolysaccharide-binding protein in inflammation- and obesity-associated adipose tissue dysfunction. Diabetologia 56:2524-537 CrossRef
  14. Zong G, Zhu J, Sun L et al (2013) Associations of erythrocyte fatty acids in the de novo lipogenesis pathway with risk of metabolic syndrome in a cohort study of middle-aged and older Chinese. Am J Clin Nutr 98:319-26 CrossRef
  15. Sun L, Zong G, Pan A et al (2013) Elevated plasma ferritin is associated with increased incidence of type 2 diabetes in middle-aged and elderly Chinese adults. J Nutr 143:1459-465 CrossRef
  16. Yu Z, Ye X, Wang J et al (2009) Associations of physical activity with inflammatory factors, adipocytokines, and metabolic syndrome in middle-aged and older chinese people. Circulation 119:2969-977 CrossRef
  17. Zhou BF (2002) Predictive values of body mass index and waist circumference for risk factors of certain related diseases in Chinese adults—study on optimal cut-off points of body mass index and waist circumference in Chinese adults. Biomed Environ Sci 15:83-6
  18. Grundy SM, Cleeman JI, Daniels SR et al (2005) Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement. Circulation 112:2735-752 CrossRef
  19. Zou G (2004) A modified Poisson regression approach to prospective studies with binary data. Am J Epidemiol 159:702-06 CrossRef
  20. Cani PD, Amar J, Iglesias MA et al (2007) Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56:1761-772 CrossRef
  21. Bartolome N, Aspichueta P, Martinez MJ et al (2012) Biphasic adaptative responses in VLDL metabolism and lipoprotein homeostasis during Gram-negative endotoxemia. Innate Immun 18:89-9 CrossRef
  22. Feingold KR, Staprans I, Memon RA et al (1992) Endotoxin rapidly induces changes in lipid metabolism that produce hypertriglyceridemia: low doses stimulate hepatic triglyceride production while high doses inhibit clearance. J Lipid Res 33:1765-776
  23. Sugita H, Kaneki M, Tokunaga E et al (2002) Inducible nitric oxide synthase plays a role in LPS-induced hyperglycemia and insulin resistance. Am J Physiol Endocrinol Metab 282:E386–E394
  24. Gornik I, Vujaklija A, Lukic E, Madzarac G, Gasparovic V (2010) Hyperglycemia in sepsis is a risk factor for development of type II diabetes. J Crit Care 25:263-69 CrossRef
  25. Visschers RG, Olde Damink SW, Schreurs M, Winkens B, Soeters PB, van Gemert WG (2009) Development of hypertriglyceridemia in patients with enterocutaneous fistulas. Clin Nutr 28:313-17 CrossRef
  26. Hudgins LC, Parker TS, Levine DM et al (2003) A single intravenous dose of endotoxin rapidly alters serum lipoproteins and lipid transfer proteins in normal volunteers. J Lipid Res 44:1489-498 CrossRef
  27. Zong G, Ye X, Sun L et al (2012) Associations of erythrocyte palmitoleic acid with adipokines, inflammatory markers, and the metabolic syndrome in middle-aged and older Chinese. Am J Clin Nutr 96:970-76 CrossRef
  28. Fantuzzi G (2005) Adipose tissue, adipokines, and inflammation. J Allergy Clin Immunol 115:911-19, quiz 920 CrossRef
  29. Shah R, Hinkle CC, Haris L, Mehta NN, Putt ME, Reilly MP (2012) Adipose genes down-regulated during experimental endotoxemia are also suppressed in obesity. J Clin Endocrinol Metab 97:E2152–E2159 CrossRef
  30. Pini M, Castellanos KJ, Rhodes DH, Fantuzzi G (2013) Obesity and IL-6 interact in modulating the response to endotoxemia in mice. Cytokine 61:71-7 CrossRef
  
• 作者单位：Xin Liu (1)
  Ling Lu (1)
  Pang Yao (1)
  Yiwei Ma (1)
  Feijie Wang (1)
  Qianlu Jin (1)
  Xingwang Ye (1)
  Huaixing Li (1)
  Frank B. Hu (2) (3)
  Liang Sun (1)
  Xu Lin (1)
  
  1. Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and University of Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, 200031, People’s Republic of China
  2. Department of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA
  3. Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
  
• ISSN：1432-0428

文摘

Aims/hypothesis Although microbiota-derived endotoxaemia has previously been shown to induce metabolic disorders, data from population-based longitudinal studies are scarce. This study therefore investigated the associations between lipopolysaccharide binding protein (LBP) levels and 6?year incident metabolic syndrome (MetS), as well as the potentially modifying effects of obesity status in middle-aged and older Chinese men and women. Methods A total of 2,529 men and women aged 50-0?years from Beijing and Shanghai, China, were followed for 6?years. Those free of MetS at baseline (1,312) were included in the analyses for the risk of developing MetS. Baseline plasma LBP was measured using an ELISA kit. Results During the 6?year follow-up, 449 (34.2%) participants developed MetS. Baseline LBP was significantly associated with BMI, waist circumference, blood lipid profile and C-reactive protein (CRP) both at baseline and during follow-up (all p--.05). The RR for incident MetS comparing extreme quartiles of LBP was 1.28 (95% CI 1.04, 1.58), after multivariate adjustment including BMI and CRP. In stratified analysis, LBP was positively associated with incident MetS only in normal-weight participants (RR, comparing extreme tertiles, 1.59; 95% CI 1.18, 2.15; p trend--.002), but not in their overweight/obese counterparts (RR, comparing extreme tertiles, 0.99; 95% CI 0.80, 1.22; p trend--.880). A significant interaction was observed between LBP and obesity status (p interaction--.013). Conclusions/interpretation Our study suggested that elevated plasma LBP was associated with an increased risk of developing MetS among middle-aged and older Chinese, especially in normal-weight individuals.