Weight Loss Improves Beta Cell Function in Type 2 Diabetes

Weight Loss Improves Beta Cell Function in Type 2 Diabetes
Beta cell function can improve after just 12 weeks of weight loss in patients with type 2 diabetes, according to research presented here at the International Diabetes Federation World Diabetes Congress 2011.
For the first time, these changes have been shown to correlate with a decrease in pancreatic polypeptide, reported Hana Kahleova, MD, from the diabetes centre at the Institute for Clinical and Experimental Medicine in Prague, Czech Republic.

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Weight Loss Improves Beta Cell Function in Type 2 Diabetes

December 7, 2011 (Dubai, United Arab Emirates) — Beta cell function can improve after just 12 weeks of weight loss in patients with type 2 diabetes, according to research presented here at the International Diabetes Federation World Diabetes Congress 2011.

For the first time, these changes have been shown to correlate with a decrease in pancreatic polypeptide, reported Hana Kahleova, MD, from the diabetes centre at the Institute for Clinical and Experimental Medicine in Prague, Czech Republic.

"This is a novel suggestion of a mechanism through which weight loss might improve beta cell function. This is new, and it might help with therapeutic choices," said Dana Dabelea, MD, PhD, associate professor at the Colorado School of Public Health in Aurora, and cochair of the session in which the research was presented.

The study involved 74 subjects with type 2 diabetes who were treated with oral hypoglycemic agents. Mean age was 56.6 years, mean body mass index was 35.8 kg/m², and mean glycated hemoglobin level was 7.7%.

Subjects were prescribed 12 weeks of a weight-loss diet alone (a reduction of 500 kcal/day) followed by 12 weeks of the same diet but with aerobic exercise added.

At baseline, 12 weeks, and 24 weeks, insulin sensitivity was measured using a hyperinsulinemic isoglycemic clamp, plasma concentration of gastrointestinal peptides was measured during a fasting state and during clamp-induced hyperinsulinemia, beta cell function was assessed during standard meal tests, and the insulin secretory rate was calculated by C-peptide deconvolution.

In the cohort, mean weight loss was 5.0 kg (P = .001) after 12 weeks of dietary intervention; weight did not change significantly after the addition of exercise, said Dr. Kahleova.

Both fasting and stimulated plasma glucose and insulin concentrations decreased in response to the diet. In the case of glucose, there was no change after the addition of exercise, but plasma insulin decreased further with exercise.

Similarly, plasma concentrations of C-peptide decreased in response to the diet and further in response to exercise.

In addition, peripheral insulin sensitivity and insulin secretion increased, and glucose sensitivity of beta cells increased by 26% in response to the diet without a significant change after the addition of exercise.

"We also observed a marked decrease in both fasting and hyperinsulinemic concentrations of pancreatic polypeptide in response to dietary intervention," said Dr. Kahleova. There was no significant change in other gastrointestinal peptides.

"Pancreatic polypeptide is a novel marker, and the authors are showing for the first time in the context of caloric restriction that a reduction in pancreatic polypeptide correlated with an improvement in beta cell function," said John Sievenpiper, MD, PhD, from McMaster University in Hamilton, Ontario, Canada, who attended the presentation.

"But the bigger story for me is that they showed an improvement in beta cell function following a guidelines-based diet. Beta cell function is really an issue in type 2 diabetes in terms of the natural history and progression of the disease. Anything that can help delay the deterioration is really valuable."

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