The Mechanisms of Surgical Treatment of Type 2 Diabetes

Mason, Edward E.

doi:10.1381/0960892053723330

Cited by 73 publications

(48 citation statements)

References 7 publications

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“…The improvement in diabetes following GBS is thought to result from decreased insulin resistance associated with caloric restriction and weight loss and enhanced insulin secretion through an altered enteroinsular axis (12,13,14), and even possibly through the activation of dormant b-cells (15). Reports of PHH following GBS first appeared in 2004 (3,16).…”

Section: Discussionmentioning

confidence: 99%

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

Myint

Greenfield²,

Farooqi³

et al. 2012

European Journal of Endocrinology

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Background: Spontaneous hyperinsulinaemic hypoglycaemia following gastric bypass surgery (GBS) is increasingly recognised. However, its pathophysiology remains unclear. Some patients require pancreatectomy. Medical therapy with calcium channel blockers, acarbose and diazoxide has been reported to be beneficial but has variable adherence and response. Method: We demonstrate the role of GLP1, counter-regulatory hormones and the subsequent response of GLP1 to somatostatin analogue therapy in a 42-year-old woman with persistent neuroglycopaenia 6 years after GBS. Plasma GLP1, insulin and glucose were measured for 5 h on three settings: i) a 75 g oral glucose tolerance test (OGTT); ii) a standard liquid test meal (LTM); and iii) an OGTT 30 min after a s.c. injection of 100 mg octreotide. Results: In comparison with obese non-diabetic controls, the patient had an elevated fasting and a markedly enhanced GLP1 response during the OGTT, followed by an exaggerated insulin response and a subsequent low glucose level. The GLP1 response to a LTM was similar but greater. Octreotide given prior to the OGTT attenuated both the GLP1 and insulin responses and abolished hypoglycaemia. Octreotide therapy significantly improved the patient's neuroglycopaenic symptoms. The hormone profile was reassessed after 6 months following the LTM preceded by octreotide injection. Peak GLP1 and insulin responses were less pronounced than pretreatment responses and without hypoglycaemia. The patient was treated with lanreotide and had remained symptom-free and euglycaemic for 4 years. Conclusion: An exaggerated incretin response following altered gastrointestinal anatomy was the likely cause of hypoglycaemia in our GBS patient. Somatostatin successfully suppressed this response acutely and in the long term, thereby avoiding pancreatectomy and its sequelae.

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Section: Discussionmentioning

confidence: 99%

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

Myint

Greenfield²,

Farooqi³

et al. 2012

European Journal of Endocrinology

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“…Interestingly, the majority of patients undergoing bariatric surgical procedures which include a bypass of the duodenum and proximal jejunum, as opposed to, for example, laparascopic adjustable gastric banding (LAGB), where only a restrictive change is introduced, experience resolution of diabetes within days postoperatively long before the surgical procedure has caused any significant weight loss [1]. At present two hypotheses have been proposed to explain this rapid resolution of type 2 diabetes: the 'hindgut hypothesis' [2] and the 'foregut hypothesis' [3]. The former is based upon the ability of expedited delivery of ingested nutrients to the distal part of the small intestine to enhance the secretion of factors improving glucose metabolism; whereas the latter advocates the glucose-lowering effect to depend on exclusion of the duodenum and proximal jejunum from transit of nutrients.…”

Section: Bariatric Surgery: Mechanisms Of Diabetes Resolutionmentioning

confidence: 99%

Resolution of type 2 diabetes following gastric bypass surgery: involvement of gut-derived glucagon and glucagonotropic signalling?

Knop

2009

Diabetologia

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Certain types of bariatric surgical procedures have proved not only to be effective with regard to treating obesity, but they also seem to be associated with endocrine changes which independently of weight loss give rise to remission of type 2 diabetes. Currently, it is speculated that surgical re-routing of nutrients triggers changes in the release of gastrointestine-derived hormones, which in turn cause amelioration of the diabetic state. The 'hindgut hypothesis' states that surgical re-routing of nutrients to the distal part of the small intestine results in increased secretion and concomitant glucose-lowering effects of glucagon-like peptide-1, whereas the 'foregut hypothesis' emphasises that surgical bypass of the foregut prevents the release of a hitherto unidentified nutrient-induced diabetogenic signal in susceptible individuals. Recent studies have shown that in patients with type 2 diabetes, glucagon is differentially secreted in response to oral and i.v. glucose, respectively, with lack of suppression (and initial net secretion) during oral glucose administration and a perfectly normal suppression during isoglycaemic i.v. glucose administration. These findings could point towards a role for glucagon or gut-derived glucagonotropic signalling as putative diabetogenic signals of the foregut hypothesis. In the present paper the hypotheses describing the glucoselowering mechanisms of bariatric surgical procedures sharing the common feature of a bypass of the duodenum and the proximal jejunum are outlined and a possible role for glucagon in these is proposed.

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“…Nutrients reach the distal ileum within 5 minutes of ingestion of food and this stimulates the secretion of GLP1 by L cells located in this area [5]. …”

Section: Mechanism Of Dm Control In Rygb (Roux-en-y Gastric Bypass)mentioning

confidence: 99%

Obesity Management-Bariatric Surgery vs Lifestyle Modification

Raman¹,

Banzal²

2013

OJEMD

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The Mechanisms of Surgical Treatment of Type 2 Diabetes

Cited by 73 publications

References 7 publications

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

Resolution of type 2 diabetes following gastric bypass surgery: involvement of gut-derived glucagon and glucagonotropic signalling?

Obesity Management-Bariatric Surgery vs Lifestyle Modification

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