Pichardo-Bahena R, Paz-Gómez FJ, Estrada-Villaseñor EG

Idioma: Español
Referencias bibliográficas: 43
Paginas: 33-40
Archivo PDF: 838.85 Kb.

RESUMEN

El concepto arcaico de considerar al tejido adiposo como un reservorio pasivo para el depósito de energía no es válido en la actualidad debido a que se ha demostrado que es un órgano endocrino esencial y altamente metabólico que no responde únicamente a señales aferentes de sistemas hormonales tradicionales y del sistema nervioso central, sino que también expresa y secreta factores con funciones endocrinas importantes. Estos factores incluyen leptina y otras citocinas. El tejido adiposo es también el sitio más importante en el metabolismo de esteroides sexuales y glucocorticoides. Su importante función endocrina se demuestra por las consecuencias metabólicas adversas asociadas a su exceso como a su deficiencia. El exceso de tejido adiposo principalmente en el compartimiento visceral se asocia a resistencia a la insulina, hiperglicemia, dislipidemia, hipertensión arterial y estados protrombóticos y pro inflamatorios. El hígado es uno de los órganos directamente afectados mediante mecanismos que involucran la activación de las vías de apoptosis por medio del factor de necrosis tumoral-α y activación de caspasas además del aumento de la formación de especies reactivas de oxígeno por activación del estrés oxidativo y cadenas enzimáticas como las que involucran el citocromo P450, CYP2E1 y CYP3A4 causando un espectro de lesiones que van desde un síndrome metabólico de hígado graso no relacionado a alcohol, esteatohepatitis no alcohólica con o sin fibrosis hasta cirrosis hepática.. Esta revisión presenta un panorama de las funciones endocrinas del tejido adiposo y su influencia en los mecanismos asociados al daño hepático.

REFERENCIAS (EN ESTE ARTÍCULO)

1. Eckel RH. Lipoprotein lipase. A multifunctional enzyme relevant to common metabolic diseases. N Engl J Med 1989;320:1060-8.

2. Donahoo WT, Jenses DR, Shepard TY, Eckel RH. Seasonal variation in lipoprotein lipase and plasma lipids in physically active, normal weight humans. J Clin Endocrinol Metab 2000;85:3065-8.

3. Lafontan M, Berlan M. Fat cell adrenergic receptors and the control of white and brown fat cell function. J Lipid Res 1993;34:1057-61.

4. Kissebah AH, Alfarsi S, Adams PW, Wynn V. Role of insulin resistance in adipose tissue and liver in the pathogenesis of endogenous hypertriglyceridaemia in man. Diabetologia 1976;12:563-71.

5. Linda RN, Serdar EB. Estrogen production and action. J Acad Dermatol 2001;45:S116-S124.

6. Lonn L, Kvist H, Ernest I, Sjostrom L. Changes in body composition and adipose tissue distribution after treatment of women with Cushing’s syndrome. Metabolism 1994;43:1517- 22.

7. Bengtsson B-A, Eden S, Lonn L. Treatment of adults with growth hormone (GH) deficiency with recombinant human GH. J Clin Endocrinol Metab 1993;76:309-17.

8. Johannsson G, Marin P, Lonn L. Growth hormone treatment of abdominally obese men reduces abdominal fat mass, improves glucose and lipoprotein metabolism and reduces diastolic blood pressure. J Clin Endocrinol Metab 1997;82:727-34.

9. Bjorntorp P. Visceral obesity: a “civilization syndrome”. Obesity Res 1993;1:206-22.

10. Divertie GD, Jensen MD, Miles JM. Stimulation of lipolysis in humans by physiological hypercortisolemia. Diabetes 1991;40:1228-32.

11. Reynisdottir S, Wahrenberg H, Bylin G, Arner P. Effect of glucocorticosteroid treatment on beta-adrenoceptor subtype function in adipocytes from patients with asthma. Clin Sci 1993;85:237-44.

12. Horber FF, Marsh HM, Haymond MW. Differential effects of prednisone and growth hormone on fuel metabolism and insulin antagonism in humans. Diabetes 1991;40:141-9.

13. Johannsson G, Marin P, Lonn L. Growth hormone treatment of abdominally obese men reduces abdominal fat mass, improves glucose and lipoprotein metabolism and reduces diastolic blood pressure. J Clin Endocrinol Metab 1997;82:727-34.

14. Krotkiewski M, Bjorntorp P, Sjostrom L, Smith U. Impact of obesity on metabolism in men and women. J Clin Invest 1983;72:1150-62.

15. Trayhurn P, Beattie, JH. Physiological role of adipose tissue: white adipose tissue as an endocrine and secretory organ. Proc Nutr Soc 2001;60:329-9.

16. Considine RV, Caro JF. Pleotropic cellular effects of leptin. Curr Opin Endocrinol Diabetes 1999;6:163-9.

17. Marshall S, Garvey WT, Traxinger RR. New insights into the metabolic regulation of insulin action and insulin resistance: role of glucose and amino acids. FASEB J 1991;5:3031-6.

18. Wang J, Liu R, Hawkins M, Barzilai N, Rossetti L. A nutrientsensing pathway regulates leptin gene expression in muscle and fat. Nature 1998,;393:684-8.

19. Saad MF, Khan A, Sharma A. Physiological insulinemia acutely modulates plasma leptin. Diabetes 1998;47:544-9.

20. Utriainen T, Malmstrom R, Makimattila S, Yki-Jarvinen H. Supraphysiological hyperinsulinemia increases plasma leptin concentrations after 4 h in normal subjects. Diabetes 1996;45:1364-6.

21. Boden G, Chen X, Mozzoli M, Ryan I. Effect of fasting on serum leptin in normal human subjects. J Clin Endocrinol Metab 1996;81:3419-23.

22. McClain DA, Crook ED. Hexosamines and insulin resistance. Diabetes 1996;45:1003-9.

23. McClain DA, Alexander T, Cooksey RC, Considine RV. Hexosamines stimulate leptin production in transgenic mice. Endocrinology 2000;141:1999-2002.

24. Jensen MD, Haymond MW, Gerich JE, Cryer PE, Miles JM. Lipolysis during fasting. Decreased suppression by insulin and increased stimulation by epinephrine. J Clin Invest 1987;79:207-213.

25. Petruschke TH, Hauner H. Tumor necrosis factor-alpha prevents the differentiation of human adipocyte precursor cells and causes delipidation of newly developed fat cells. J Clin Endocrinol Metab 1993;76:742-7.

26. Prins JB, Niesler CU, Winterford CM, et al. Tumor necrosis factor-alpha induces apoptosis of human adipose cells. Diabetes 1997;46:1939-44.

27. Hotamisligil GS, Arner P, Caro JF, Atkinson RL, Spiegelman BM. Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. J Clin Invest 1995;95:2409-15.

28. Spiegelman BM, Hotamisligil GS. Through thick and thin: wasting, obesity, and TNFalpha. Cell 1993;73:625-7.

29. Escher G, Galli I, Vishwnanth BS, Frey BM, Frey FJ. Tumor necrosis factor alpha and interleukin 1beta enhance the cortison/cortisol shuttle. J Exp Med 1997;186:189-98.

30. Thornberry NA, Bull HG, Calacay JR. A novel heterodimeric cycteine protease is required for interleukin-1beta processing in monocytes. Nature 1992;356:768-74.

31. Wang L, Miura M, Bergeron B, Hzu H, Yuan J. Ich-1, an Ice/ced-3-related gene encodes both positive and negative regulators of programmed cell death. Cell 1994;78:739-750.

32. Sawdey MS, Loskutoff DJ. Regulation of murine type 1 plasminogen activator inhibitor gene expression in vivo. J Clin Invest 1991;88:1346-53.

33. Schneider DJ, Nordt TK, Sobel BE. Attenuated fibrinolysis and accelerated atherogenesis in type II diabetic patients. Diabetes 1993;42:1-7.

34. Bloomgarden Z. Obesity, hypertension, and insulin resistance. Diabetes Care 2002;25:2088-3007.

35. Marchesini G, Brizi M, Bianchi G, Tomassetti S, Bugianesi E, Lenzi M, McCullough AJ, Natale S, Forlani G, Melchionda N. Nonalcoholic fatty liver disease. Diabetes 2001;50:1844-50.

36. Falchuk KR, Fiske SC, Haggitt RC, Federman R, Trey C. Percentile hepatic fibrosis and intracellular hyalin in diabetes mellitus. Gastroenterology 1980;78:535-41.

37. Sheth SG, Gordon FD, Chopra S. Nonalcoholic steatohepatitis. Ann Intern Med 1997;126:137-45.

38. Brunt EM, Janney CJ, Di Bisceglie AM, Neuschwander-Tetri BA, Bacon BR. Non-alcoholic steatohepatitis: a proposal for grading and staging the histologic lesions. Am J Gastroenterol 1999;94:2467-74.

39. Clark J, Diehl AM. Nonalcoholic fatty liver disease an underrecognized cause of cryptogenic cirrhosis. JAMA 2003;289:3000-4.

40. Day CP. Non-alcoholic steatohepatitis (NASH): where are we now and where are we going? Gut 2002;50:585-8.

41. Pessayre D, Berson A, Fromenty B, Mansouri A. Mitochondria in steatohepatitis. Semin Liver Dis 2001;21:57-69.

42. Leclercq IA, Farrell GC, Field J, et al. CYP2E1 and CYP4A as microsomal catalysts of lipid peroxides in murine non-alcoholic steatohepatitis. J Clin Invest 2000;105:1067-75.

43. Tilg H, Dhiel AM. Mechanisms of disease: cytokines in alcoholic and non-alcoholic steatohepatitis. N Engl J Med 2000;343:1467-76.