Gastric Banding Equals Metformin in Slowing Diabetes Onset

A new study shows that gastric banding and metformin have a similar effect on β-cell function in adults with impaired glucose tolerance (IGT) or mild type 2 diabetes (T2D).

Researchers at the University of Southern California (USC; Los Angeles, USA), Kaiser Permanente Southern California (KPSC; Pasadena, USA), and other institutions conducted a study involving 88 adults with a body mass index (BMI) of 30–40 kg/m2 and known IGT or T2D for less than one year in order to compare gastric banding and metformin impact on β-cell function. Arginine injection at maximally potentiating glycemia was performed at baseline, 12 months, and at 24 months to measure steady-state C-peptide (SSCP), acute C-peptide response (ACPRmax), and insulin sensitivity (M/I).

The results revealed that at 24 months, the band group lost 10.7 kg, while the metformin group lost just 1.7 kg. Insulin sensitivity increased 45% in the band group and 25% in the metformin group, and SSCP--adjusted for insulin sensitivity--fell slightly, but not significantly in each group. ACPRmax adjusted for insulin sensitivity fell significantly in the metformin group, but not in the band group. Normoglycemia was present in 22% and 15% of band and metformin groups, respectively, at 24 months. The study was presented at the European Association for the Study of Diabetes annual meeting, held during October 2018 in Berlin (Germany).

“Gastric banding and metformin offered approximately equal approaches for improving insulin sensitivity in adults with mild to moderate obesity and impaired glucose tolerance or early, mild T2D,” said senior author and study presenter Tom Buchanan, MD, chief of the division of endocrinology and diabetes at USC. “The predominant β-cell response was a reduction in secretion to maintain a relatively constant compensation for insulin resistance, with only a small improvement in glucose; whether these interventions will have different effects on β-cell function over the long-term remains to be determined.”

In healthy individuals, pancreatic β-cells release regular pulses of insulin into the bloodstream that restrict the amount of glucose released by the liver, as well as propel body tissues to absorb the released glucose. However, in hyperglycemia, a hallmark of T2D, the excess glucose suppresses the "inner clock" of beta cells that controls the rhythm of insulin pulses, reducing insulin production.

Related Links:
University of Southern California
Kaiser Permanente Southern California