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

被引:48
|
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
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