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Gastric Bypass Reduces Symptoms and Hormonal Responses in Hypoglycemia
Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
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2016 (Engelska)Ingår i: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 65, nr 9, s. 2667-2675Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Gastric bypass (GBP) surgery, one of the most common bariatric procedures, induces weight loss and metabolic effects. The mechanisms are not fully understood, but reduced food intake and effects on gastrointestinal hormones are thought to contribute. We recently observed that GBP patients have lowered glucose levels and frequent asymptomatic hypoglycemic episodes. Here, we subjected patients before and after undergoing GBP surgery to hypoglycemia and examined symptoms and hormonal and autonomic nerve responses. Twelve obese patients without diabetes (8 women, mean age 43.1 years [SD 10.8] and BMI 40.6 kg/m(2) [SD 3.1]) were examined before and 23 weeks (range 19-25) after GBP surgery with hyperinsulinemic-hypoglycemic clamp (stepwise to plasma glucose 2.7 mmol/L). The mean change in Edinburgh Hypoglycemia Score during clamp was attenuated from 10.7 (6.4) before surgery to 5.2 (4.9) after surgery. There were also marked postsurgery reductions in levels of glucagon, cortisol, and catecholamine and the sympathetic nerve responses to hypoglycemia. In addition, growth hormone displayed a delayed response but to a higher peak level. Levels of glucagon-like peptide 1 and gastric inhibitory polypeptide rose during hypoglycemia but rose less postsurgery compared with presurgery. Thus, GBP surgery causes a resetting of glucose homeostasis, which reduces symptoms and neurohormonal responses to hypoglycemia. Further studies should address the underlying mechanisms as well as their impact on the overall metabolic effects of GBP surgery.

Ort, förlag, år, upplaga, sidor
2016. Vol. 65, nr 9, s. 2667-2675
Nationell ämneskategori
Endokrinologi och diabetes
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URN: urn:nbn:se:umu:diva-126314DOI: 10.2337/db16-0341ISI: 000382099800021PubMedID: 27313315OAI: oai:DiVA.org:umu-126314DiVA, id: diva2:1044195
Tillgänglig från: 2016-11-02 Skapad: 2016-10-03 Senast uppdaterad: 2018-06-09Bibliografiskt granskad

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