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A clinical trial showed that half of participants with type 2 diabetes achieved remission to a non-diabetic state after a weight-loss intervention delivered within 6 years of diagnosis, this is associated with the early and sustained improvement in the functioning of pancreatic beta cells. Presently, the early management of type 2 diabetes tends to involve a period of adjusting to the diagnosis plus pharmacotherapy with lifestyle changes. Substantial weight loss at the time of diagnosis is appropriate to rescue the beta cells.
According to the World Health Organization, diabetes affects about 420 million people across the globe. Approximately 90% of cases are type 2 diabetes, a condition in which the body does not produce enough or respond properly to insulin. This hormone, produced by beta cells in the pancreas, helps a sugar-glucose in the blood enter cells in muscle, fat, and liver to be used for energy. Type 2 diabetes has long been considered a lifelong condition that worsens over time.
Researchers at the United-Kingdom-based Diabetes Remission Clinical Trial (DiRECT) led by Taylor examined participants diagnosed with type 2 diabetes within 6 years of the start of the study, were randomly assigned to best-practice care (control group) or an intensive primary-care-led weight-management program (intervention group). One year later, 46% of the individuals in the intervention group successfully responded to weight loss in that they recovered and maintained control over blood glucose concentrations.
Some non-responders simply had not lost enough weight, but in those who had, it was not clear how their response differed from that of responders. Reseachers examined potentially relevant metabolic factors, such as liver fat content, pancreatic fat content, blood concentrations of fats called triglycerides, and beta-cell function, in a subset of DiRECT participants, including 64 individuals in the intervention group.
They discovered that responders to the weight loss program were similar to non-responders before the intervention but had a shorter duration of diabetes (2.7 years vs. 3.8 years). Both responders and non-responders had lost comparable amounts of weight, leading to similar reductions in liver fat content, pancreatic fat content, and blood concentrations of triglycerides.
However, only the responders demonstrated early and sustained improvement in beta-cell function. In particular, the most striking difference between responders and non-responders was the first-phase insulin response. Pancreatic beta cells secrete insulin in two phases in response to an increase in blood glucose concentration.
The first phase, which consists of a brief spike lasting approximately 10 minutes, is typically absent in patients with type 2 diabetes. First-phase insulin secretion increased in responders after weight loss but did not change in non-responders. Weight loss normalizes fat metabolism in individuals with type 2 diabetes, but the more rapid loss of the capacity of beta cells to recover prevents some individuals from returning to a non-diabetic state.