Role of the incretin system in the remission of type 2 diabetes following bariatric surgery

被引:49
作者
Mingrone, G. [1 ]
机构
[1] Univ Cattolica Sacro Cuore, Dept Internal Med, Rome, Italy
关键词
Morbid obesity; Incretins; Bariatric surgery;
D O I
10.1016/j.numecd.2008.07.004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims: It has been observed, as a collateral outcome of bariatric surgery, that morbidly obese patients with frank type 2 diabetes mellitus or impaired glucose tolerance undergone Roux-en-Y Gastric Bypass (RYGB) or bilio-pancreatic diversion (BPD) became and remained euglycemic since surgery. But, most interestingly, the conversion to euglycemia happened within few days from the operation, tong before a significant weight loss could intervene. The purpose of this viewpoint is to try to elucidate the mechanisms involved in the resolution/remission of diabetes after bariatric surgery, in particular highlighting the role played by the modifications in incretin secretion. Data synthesis: The effect of purely restrictive procedures in improving glucose control is directly proportional to the degree of weight loss. In contrast, either RYGB or BPD, the first a mainly restrictive and the second a quite purely malabsorptive bariatric technique, operate through a different mechanism, as a probable consequence of the small intestine bypass. The bypass of different intestinal portions covers a central rote in the mechanisms of action of these two surgical procedures. In fact, white RYGB does not affect insulin resistance but increases insulin secretion via the stimulation of nutrient-mediated incretin secretion, BPD induces a full normalization of insulin resistance and, consequently, a significant reduction of insulin secretion. The insulin resistance reversion is only partially explained by the incretin level changes after BPD. Conclusion: A role of incretins in type 2 diabetes improvement or resolution is ascertained although it is possible that other, not yet identified, hormone(s) can cooperate with them. (C) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:574 / 579
页数:6
相关论文
共 54 条
[1]   Laparoscopic spleen-preserving distal pancreatectomy as treatment for nesidioblastosis after gastric bypass surgery [J].
Alvarez, Glauco C. ;
Faria, Everton N. ;
Beck, Maristela ;
Girardon, Dener T. ;
Machado, Ana Cristina .
OBESITY SURGERY, 2007, 17 (04) :550-552
[2]   Bariatric surgery: A systematic review and meta-analysis [J].
Buchwald, H ;
Avidor, Y ;
Braunwald, E ;
Jensen, MD ;
Pories, W ;
Fahrbach, K ;
Schoelles, K .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2004, 292 (14) :1724-1737
[3]   Restoration of adiponectin pulsatility in severely obese subjects after weight loss [J].
Calvani, M ;
Scarfone, A ;
Granato, L ;
Mora, EV ;
Nanni, G ;
Castagneto, M ;
Greco, AV ;
Manco, M ;
Mingrone, G .
DIABETES, 2004, 53 (04) :939-947
[4]   β-cell function in morbidly obese subjects during free living -: Long-term effects of weight loss [J].
Camastra, S ;
Manco, M ;
Mari, A ;
Baldi, S ;
Gastaldelli, A ;
Greco, AV ;
Mingrone, G ;
Ferrannini, E .
DIABETES, 2005, 54 (08) :2382-2389
[5]   β-cell function in severely obese type 2 diabetic patients -: Long-term effects of bariatric surgery [J].
Camastra, Stefania ;
Manco, Melania ;
Mari, Andrea ;
Greco, Aldo V. ;
Frascerra, Silvia ;
Mingrone, Geltrude ;
Ferrannini, Ele .
DIABETES CARE, 2007, 30 (04) :1002-1004
[6]   Post-gastric bypass hyperinsulinism with nesidioblastosis: Subtotal or total pancreatectomy may be needed to prevent recurrent hypoglycemia [J].
Clancy, Thomas E. ;
Moore, Franci's D., Jr. ;
Zinner, Michael J. .
JOURNAL OF GASTROINTESTINAL SURGERY, 2006, 10 (08) :1116-1119
[7]   INCRETIN CONCEPT TODAY [J].
CREUTZFELDT, W .
DIABETOLOGIA, 1979, 16 (02) :75-85
[8]   Adjustable gastric banding and conventional therapy for type 2 diabetes - A randomized controlled trial [J].
Dixon, John B. ;
O'Brien, Paul E. ;
Playfair, Julie ;
Chapman, Leon ;
Schachter, Linda M. ;
Skinner, Stewart ;
Proietto, Joseph ;
Bailey, Michael ;
Anderson, Margaret .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2008, 299 (03) :316-323
[9]   Glucagon-like peptide-1 and the islet β-cell:: Augmentation of cell proliferation and inhibition of apoptosis [J].
Drucker, DJ .
ENDOCRINOLOGY, 2003, 144 (12) :5145-5148
[10]   Glucagon-like peptides: Regulators of cell proliferation, differentiation, and apoptosis [J].
Drucker, DJ .
MOLECULAR ENDOCRINOLOGY, 2003, 17 (02) :161-171