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Hypoglycaemia breakthrough

Hormone causes hypoglycaemia after bypass surgery

Study focused specifically on blocking the gut hormone Glucagon-like Peptide 1 (GLP-1),

Blocking the action of one of the gut hormones can correct post-meal hypoglycaemia in gastric bypass patients, according to researchers at the University of Cincinnati (UC). The study, published the journal Gastroenterology, is part of an ongoing effort by UC researchers to better understand glucose metabolism after weight-loss surgery.

"Over the years we have recognised that gastric bypass is very effective for treatment of obesity and has an immediate and robust effect on glucose improvement in patients with Type 2 diabetes,” said Dr Marzieh Salehi, associate professor in the division of endocrinology, metabolism and diabetes, UC Health physician and lead investigator. “However, there is a subgroup of patients where gastric bypass surgery creates a situation of hypoglycaemia, associated with too much of insulin secretion after meal ingestion, several years after surgery."

Funded by a grant from the National Institutes of Health, this study focused specifically on blocking the gut hormone Glucagon-like Peptide 1 (GLP-1), which is enhanced after gastric bypass surgery.

Nine patients with recurrent hypoglycaemia after gastric bypass (H-GB), seven patients who were asymptomatic after gastric bypass (A-GB), and eight healthy control subjects underwent a mixed-meal tolerance test (350 kcal) using a dual glucose tracer method on two separate days.

On one day they received continuous infusion of the GLP-1 receptor antagonist exendin (9-39) (Ex-9), and on the other day they received a saline control. Glucose kinetics and islet and gut hormone responses were measured before and after the meal.

Outcomes

The results revealed that infusion of Ex-9 corrected hypoglycaemia in all patients with H-GB. The reduction in postprandial insulin secretion by Ex-9 was greater in the H-GB group than in the other groups (H-GB, 50% ± 8%; A-GB, 13% ± 10%; controls, 14% ± 10%) (p<0.05).

The meal-derived glucose appearance was significantly greater in subjects who had undergone gastric bypass compared to the controls and in the H-GB group compared to the A-GB group. Ex-9 shortened the time to reach peak meal-derived glucose appearance in all groups without a significant effect on overall glucose flux.

Postprandial glucagon levels were higher among patients who had undergone gastric bypass than controls and increased with administration of Ex-9.

The authors believe this study has implications for treatment of hyperinsulinemia hypoglycaemia after gastric bypass as well as better understanding of mechanisms by which this surgery alters glucose metabolism in general.

At this point there is no specific therapeutic option available for patients with this condition beyond dietary modification.

“In summary, we have shown that blocking the GLP-1R eliminates postprandial hypoglycemia in subjects who have undergone GB and are affected by the postprandial hypoglycemia syndrome,” they concluded.  “Our findings support enhanced beta cell sensitivity to GLP-1 in the hyperinsulinemia associated with symptomatic nadirs in postprandial glucose. The distinct pattern of ingested glucose appearance among subjects with H-GB suggests that altered GI function also contributes to glucose abnormalities in this syndrome.”

To access the article, please click here

http://www.gastrojournal.org/article/S0016-5085(13)01725-3/fulltext#tbl1

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