El intestino delgado, las incretinas y el metabolismo energético en la Diabetes mellitus

Cesar Ochoa

Texto completo:

PDF

Resumen

Las investigaciones completadas en años recientes han revelado el importante papel que juega el intestino delgado en la homeostasis energética del organismo por medio de las incretinas: enterohormonas que regulan el equilibrio entre las influencias de la insulina y el glucagon sobre el metabolismo glucídico, el vaciamiento gástrico, y el crecimiento y desarrollo de las células b presentes en los islotes pancreáticos. Las acciones biológicas de las incretinas han sido reconocidas en los sujetos en los que se ha observado remisión de la resistencia a la acción de la insulina tras la realización de cirugía bariátrica. El conocimiento íntimo de la biología y el efecto de las incretinas se ha traducido en nuevos enfoques terapéuticos y farmacológicos del tratamiento de la Diabetes mellitus.

Palabras clave

Intestino delgado; Incretinas; Insulina; Diabetes; Páncreas; Hígado

Referencias

DeFronzo RA. The Banting Lecture. From the triumvirate to the ominous octet: A new paradigm for the treatment of type 2 Diabetes mellitus. Diabetes 2009;58:773-95.

Del Prato S, Penno G, Miccoli R. Changing the treatment paradigm for type 2 diabetes. Diabetes Care 2009; 32(Suppl 2):S217-S222.

Wynne K, Stanley S, Bloom S. The gut and regulation of body weight. J Clin Endocrinol Metab 2004;89:2576-82.

Näslund E, Backman L, Juul Holst J, Theodorsson E, Hellström PM. Importance of small bowel peptides for the improved glucose metabolism 20 years after jejunoileal bypass for obesity. Obesity Surgery 1998;8:253-60.

Rubino F, Forgione A, Cummings DE, Vix M, Gnuli D, Mingrone G, et al. The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg 2006;244:741-9.

Drucker DJ. The biology of incretin hormones. Cell Metabolism 2006;3: 153-65.

Laferrère B. Gut feelings about diabetes. Endocrinol Nutr 2012;59:254-60.

Rubino F, Gagner M. Potential of surgery for curing Type 2 Diabetes mellitus. Ann Surg 2002;236:554-9.

Rubino F. Is type 2 diabetes an operable intestinal disease? A provocative yet reasonable hypothesis. Diabetes Care 2008;31(Suppl 2):S290-S296.

American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2006;29(Suppl 1):S43–S48.

Haller MJ, Atkinson MA, Schatz D. Type 1 diabetes mellitus: etiology, presentation, and management. Pediatr Clin North Amer 2005;52:1553-78.

Williamson DF, Thompson TJ, Thun M, Flanders D, Pamuk E, Byers T. Intentional weight loss and mortality among overweight individuals with diabetes. Diabetes Care 2000;23:1499-504.

Pi-Sunyer X, Blackburn G, Brancati FL, Bray GA, Bright R, Clark JM, et al. Reduction in weight and cardiovascular disease risk factors in individuals with type 2 diabetes: one-year results of the look AHEAD trial. Diabetes Care 2007;30:1374-83.

UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998;352(9131):854-65.

Nathan DM, Buse JB, Davidson MB, Ferrannini E, Holman RR, Sherwin R, Zinman B. Medical management of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy a consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2009;32:193-203.

Dockray GJ, Varro A, Dimaline R, Wang T. The gastrins: their production and biological activities. Annu Rev Physiol 2001;63:119-39.

Lam IP, Siu FK, Chu J, Chow BK. Multiple actions of secretin in the human body. Int Rev Cytol 2008;265:159-90.

Crawley JN, Corwin RL. Biological actions of cholecystokinin. Peptides 1994;15:731-55.

Van Der Lely AJ, Tschöp M, Heiman ML, Ghigo E. Biological, physiological, pathophysiological, and pharmacological aspects of ghrelin. Endocr Rev 2004; 25:426-57.

Cerdá Reverter JM, Larhammar D. cNeuropeptide Y family of peptides: structure, anatomical expression, function, and molecular evolution. Biochem Cell Biol 2000;78:371-92.

Larhammar D. Evolution of neuropeptide Y, peptide YY and pancreatic polypeptide. Regul Peptides 1996;62:1-11.

Stanley S, Wynne K, Bloom S. Gastrointestinal satiety signals III. Glucagon-like peptide 1, oxyntomodulin, peptide YY, and pancreatic polypeptide. Am J Physiol [Gastrointest Liver Physiol] 2004;286: G693-G697.

Phillips LK, Prins JB. Update on incretin hormones. Ann NY Acad Sci 2011; 1243:E55-E74.

Brubaker PL. Incretin-based therapies: mimetics versus protease inhibitors. Trends Endocrinol Metabol 2007;18:240-5.

Girard J. The incretins: from the concept to their use in the treatment of type 2 diabetes. Part A: Incretins: concept and physiological functions. Diabetes Metab 2008;34(6 Pt 1):550-9.

Gautier JF, Choukem SP, Girard J. Physiology of incretins (GIP and GLP-1) and abnormalities in type 2 diabetes. Diabetes Metabol 2008;34:S65-S72.

Holst J. Glucagon-like peptide-1 (GLP-1): an intestinal hormone, signaling nutritional abundance, with an unusual therapeutic potencial. Trends Endocrinol Metab 2005;90:359-65.

Mentlein R. Dipeptidyl-peptidase IV (CD26)-role in the inactivation of regulatory peptides. Regulator Peptides 1999;85:9-24.

Herman GA, Stein PP, Thornberry NA, Wagner JA. Dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes: focus on sitagliptin. Clin Pharmacol Ther 2007;81:761-7.

Ranganath LR. The entero-insular axis: implications for human metabolism. Clin Chem Lab Med 2008;46:43-56.

Holst JJ, Vilsbøll T, Deacon CF. The incretin system and its role in type 2 diabetes mellitus. Mol Cell Endocrinol 2009;297:127-36.

Rask E, Olsson T, Soderberg S, Johnson O, Seckl J, Holst J et al. Impaired incretin response after a mixed meal is associated with insulin resistence in nondiabetic men. Diabetes Care 2001; 24:1640-5.

Ranganath LR. Incretins: Patho-physiological and therapeutic implications of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1. J Clin Pathol 2008; 61:401-9.

Brubaker PL. Incretin-based therapies: Mimetics versus protease inhibitors. TIEM Trends Endocrinol Metabol 2007; 18:240-5.

Pories W, Swanson M, MacDonald K. Who would have thought it? An operation proves to be the most effective therapy for adult-onset Diabetes mellitus. Ann Surg 1995;222:339-50.

Buchwald H, Avidor Y, Braunwald E, Jensen M, Pories W, Fahrbach K, et al. Bariatric surgery: a systematic review and metaanalysis. JAMA 2004;292:1724-37.

Thaler JP, Cummings DE. Minireview: Hormonal and metabolic mechanisms of Diabetes remission after gastrointestinal surgery. Endocrinology 2009;150:2518-25.

Dixon J. Obesity and Diabetes: The impact of bariatric surgery on type-2 Diabetes. World J Surg 2009;10:2014-21.

Rubino F, Gagner M, Gentileschi P, Kini S, Fukuyama S, Feng J, et al. The early effect of the Roux-en-Y gastric bypass on hormones involved in body weight regulation and glucose metabolism. Ann Surg 2004;240:236-42.

Mingrone G, Castagneto-Gissey L. Mechanisms of early improvement/ resolution of type 2 diabetes after bariatric surgery. Diabetes Metab 2009; 35(6 Pt 2):518-23.

Rubino F, Marescaux J. Effect of duodenal-jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease. Ann Surg 2004;239:1-11.

Pacheco D, de Luis DA, Romero A, González Sagrado M, Conde R, Izaola O, et al. The effects of duodenal-jejunal exclusion on hormonal regulation of glucose metabolism in Goto-Kakizaki rats. Am J Surg 2007;194:221-4.

Wang TT, Hu SY, Gao HD, Zhang GY, Liu CZ, Feng JB, et al. Ileal transposition controls diabetes as well as modified duodenal jejunal bypass with better lipid lowering in a nonobese rat model of type II diabetes by increasing GLP-1. Ann Surg 2008;247:968-75.

Laferrère B. Do we really know why diabetes remits after gastric bypass surgery? Endocrine 2011;40:162-7.

American Diabetes Association. Standards of medical care in diabetes- 2009. Diabetes Care 2009;32(Suppl 1):S13-S61.

Enlaces refback

  • No hay ningún enlace refback.