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Lipid homeostasis, lipotoxicity and the metabolic syndrome

Unger, Roger H., Clark, Gregory O., Scherer, Philipp E., Orci, Lelio·2010·Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
DOI 10.1016/j.bbalip.2009.10.006
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Abstract

In the 20th century industrialized nations have become afflicted with an unprecedented pandemic of increased adiposity. In the United States, the epicenter of the epidemic, over 2/3 of the population, is overweight and 1 of every 6 Americans carries the diagnosis of metabolic syndrome. Although genes determine susceptibility to environmental factors, the epidemic is clearly due to increased consumption of calorie-dense, highly lipogenic foods, coupled with a marked decrease in physical exertion resulting from modern technologies. If this lifestyle continues, morbid consequences are virtually inevitable. They include type II diabetes and a cluster of disorders known as "the metabolic syndrome" usually appearing in middle age. The morbid consequences of the chronic caloric surplus are buffered before middle age by the partitioning of these calories as fat in the adipocyte compartment which is specifically designed to store triglycerides. Leptin has been proposed as the major hormonal regulator of the partitioning of surplus calories. However, multiple factors can determine the storage capacity of the fat tissue and when it is exceeded ectopic lipid deposition begins. The organs affected in metabolic syndrome include skeletal muscle, liver, heart and pancreas, which are now known to contain abnormal levels of triglycerides. While neutral fat is probably harmless, it is an index of ectopic lipid overload. Fatty acid derivatives can interfere with the function of the cell and ulti…

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  1. Ford, 2002, Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey, JAMA, 287, 356, 10.1001/jama.287.3.356 · DOI · Paper page
  2. Reaven, 1988, Banting lecture 1988. Role of insulin resistance in human disease, Diabetes, 37, 1595, 10.2337/diabetes.37.12.1595 · DOI
  3. Ford, 2005, Prevalence of the metabolic syndrome defined by the International Diabetes Federation among adults in the U.S, Diabetes Care, 28, 2745, 10.2337/diacare.28.11.2745 · DOI
  4. H.F.a.B. Wells, Jean C., Dietary assessment of major trends in U.S. food consumption, 1970–2005, in: USDA (Ed.), Economic Information Bulletin No. (E1B-33), 2008, p. 27.
  5. Lanningham-Foster, 2003, Labor saved, calories lost: the energetic impact of domestic labor-saving devices, Obes. Res., 11, 1178, 10.1038/oby.2003.162 · DOI · Paper page
  6. Pelleymounter, 1995, Effects of the obese gene product on body weight regulation in ob/ob mice, Science, 269, 540, 10.1126/science.7624776 · DOI · Paper page
  7. Shimabukuro, 1997, Direct antidiabetic effect of leptin through triglyceride depletion of tissues, Proc. Natl. Acad. Sci. U. S. A., 94, 4637, 10.1073/pnas.94.9.4637 · DOI
  8. Zhou, 1997, Induction by leptin of uncoupling protein-2 and enzymes of fatty acid oxidation, Proc. Natl. Acad. Sci. U. S. A., 94, 6386, 10.1073/pnas.94.12.6386 · DOI
  9. Szczepaniak, 2005, Magnetic resonance spectroscopy to measure hepatic triglyceride content: prevalence of hepatic steatosis in the general population, Am. J. Physiol., 288, E462
  10. Scherer, 1995, A novel serum protein similar to C1q, produced exclusively in adipocytes, J. Biol. Chem., 270, 26746, 10.1074/jbc.270.45.26746 · DOI
  11. Elmquist, 2001, Hypothalamic pathways underlying the endocrine, autonomic, and behavioral effects of leptin, Physiol. Behav., 74, 703, 10.1016/S0031-9384(01)00613-8 · DOI
  12. Unger, 2001, Diseases of liporegulation: new perspective on obesity and related disorders, FASEB J., 15, 312, 10.1096/fj.00-0590 · DOI
  13. McGavock, 2006, Adiposity of the heart, revisited, Ann. Intern. Med., 144, 517, 10.7326/0003-4819-144-7-200604040-00011 · DOI
  14. Chiu, 2001, A novel mouse model of lipotoxic cardiomyopathy, J. Clin. Invest., 107, 813, 10.1172/JCI10947 · DOI
  15. Pillutla, 2005, Perfusion of hearts with triglyceride-rich particles reproduces the metabolic abnormalities in lipotoxic cardiomyopathy, Am. J. Physiol. Endocrinol. Metab., 288, E1229, 10.1152/ajpendo.00273.2004 · DOI
  16. Lee, 2007, Metabolic mechanisms of failure of intraportally transplanted pancreatic beta-cells in rats: role of lipotoxicity and prevention by leptin, Diabetes, 56, 2295, 10.2337/db07-0460 · DOI
  17. Cruz, 2001, Glucose and insulin stimulate heparin-releasable lipoprotein lipase activity in mouse islets and INS-1 cells. A potential link between insulin resistance and beta-cell dysfunction, J. Biol. Chem., 276, 12162, 10.1074/jbc.M010707200 · DOI
  18. Chen, 1996, Disappearance of body fat in normal rats induced by adenovirus-mediated leptin gene therapy, Proc. Natl. Acad. Sci. U. S. A., 93, 14795, 10.1073/pnas.93.25.14795 · DOI
  19. Lee, 2006, Recombinant methionyl human leptin therapy in replacement doses improves insulin resistance and metabolic profile in patients with lipoatrophy and metabolic syndrome induced by the highly active antiretroviral therapy, J. Clin. Endocrinol. Metab., 91, 2605, 10.1210/jc.2005-1545 · DOI · Paper page
  20. Lee, 2006, Alpha-lipoic acid prevents lipotoxic cardiomyopathy in acyl CoA-synthase transgenic mice, Biochem. Biophys. Res. Commun., 344, 446, 10.1016/j.bbrc.2006.03.062 · DOI
  21. Smith, 2007, Metformin and exercise reduce muscle FAT/CD36 and lipid accumulation and blunt the progression of high-fat diet-induced hyperglycemia, Am. J. Physiol. Endocrinol. Metab., 293, E172, 10.1152/ajpendo.00677.2006 · DOI
  22. Yu, 2004, Leptinomimetic effects of the AMP kinase activator AICAR in leptin-resistant rats: prevention of diabetes and ectopic lipid deposition, Diabetologia, 47, 2012, 10.1007/s00125-004-1570-9 · DOI
  23. Higa, 1999, Troglitazone prevents mitochondrial alterations, beta cell destruction, and diabetes in obese prediabetic rats, Proc. Natl. Acad. Sci. U. S. A., 96, 11513, 10.1073/pnas.96.20.11513 · DOI
  24. Sreenan, 1996, Prevention of hyperglycemia in the Zucker diabetic fatty rat by treatment with metformin or troglitazone, Am. J. Physiol., 271, E742
  25. Zhou, 2000, Lipotoxic heart disease in obese rats: implications for human obesity, Proc. Natl. Acad. Sci. U. S. A., 97, 1784, 10.1073/pnas.97.4.1784 · DOI · Paper page
  26. Nawrocki, 2006, Mice lacking adiponectin show decreased hepatic insulin sensitivity and reduced responsiveness to peroxisome proliferator-activated receptor gamma agonists, J. Biol. Chem., 281, 2654, 10.1074/jbc.M505311200 · DOI
  27. Kiraly, 2007, Attenuation of type 2 diabetes mellitus in the male Zucker diabetic fatty rat: the effects of stress and non-volitional exercise, Metabolism, 56, 732, 10.1016/j.metabol.2006.12.022 · DOI
  28. Pold, 2005, Long-term AICAR administration and exercise prevents diabetes in ZDF rats, Diabetes, 54, 928, 10.2337/diabetes.54.4.928 · DOI
  29. Ruderman, 1981, The “metabolically-obese,” normal-weight individual, Am. J. Clin. Nutr., 34, 1617, 10.1093/ajcn/34.8.1617 · DOI · Paper page
  30. Winder, 1996, Inactivation of acetyl-CoA carboxylase and activation of AMP-activated protein kinase in muscle during exercise, Am. J. Physiol., 270, E299
  31. Ohneda, 1995, Caloric restriction in obese pre-diabetic rats prevents beta-cell depletion, loss of beta-cell GLUT 2 and glucose incompetence, Diabetologia, 38, 173, 10.1007/BF00400091 · DOI
  32. Agarwal, 2003, Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways, Trends Endocrinol. Metab., 14, 214, 10.1016/S1043-2760(03)00078-X · DOI
  33. Addy, 2003, Hypoadiponectinemia is associated with insulin resistance, hypertriglyceridemia, and fat redistribution in human immunodeficiency virus-infected patients treated with highly active antiretroviral therapy, J. Clin. Endocrinol. Metab., 88, 627, 10.1210/jc.2002-020795 · DOI
  34. Abate, 2005, ENPP1/PC-1 K121Q polymorphism and genetic susceptibility to type 2 diabetes, Diabetes, 54, 1207, 10.2337/diabetes.54.4.1207 · DOI
  35. Wang, 2008, Adipogenic capacity and the susceptibility to type 2 diabetes and metabolic syndrome, Proc. Natl. Acad. Sci. U. S. A., 105, 6139, 10.1073/pnas.0801981105 · DOI
  36. Cullberg, 1985, Lipid metabolic studies in women with a polycystic ovary syndrome during treatment with a low-dose desogestrel-ethinylestradiol combination, Acta Obstet. Gynecol. Scand., 64, 203, 10.3109/00016348509155113 · DOI
  37. Garris, 2004, Ovarian hypercytolipidemia induced by obese (ob/ob) and diabetes (db/db) mutations: basis of female reproductive tract involution II, Tissue Cell, 36, 157, 10.1016/j.tice.2004.01.001 · DOI
  38. Murosaki, 1997, Apoptosis of intestinal intraepithelial lymphocytes induced by exogenous and endogenous glucocorticoids, Microbiol. Immunol., 41, 139, 10.1111/j.1348-0421.1997.tb01179.x · DOI

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Metadata

Authors
Unger, R. H., Clark, G. O., Scherer, P. E., & Orci, L.
Venue
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
Publisher
Elsevier BV
Published
2010-03
Volume
1801
Issue
3
Pages
209-214
ISSN
1388-1981
DOI
10.1016/j.bbalip.2009.10.006
Cited by
511
References
10
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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