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February 18, 2020
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Weight-loss that remits type 2 diabetes normalizes beta-cell function

Roy Taylor

Adults with type 2 diabetes who lose enough weight to enter diabetes remission are also able to recapture normal beta-cell capacity, according to findings published in Diabetes Care.

“The completeness of the return to normal maximal functional capacity of the beta cells was striking,” Roy Taylor, MD, FRCP, professor of medicine and metabolism at Newcastle University in the U.K., told Healio. “In the face of prevailing opinion that function had been irreversibly lost in developing type 2 diabetes, this is an important message of hope to convey to patients, especially as this may be motivating to take action.”

Taylor and colleagues analyzed data from 57 adults with type 2 diabetes from the Diabetes Remission Clinical Trial (DiRECT) who participated in an intensive weight-loss intervention (mean age, 52.9 years; 44% women), 26 adults who did not participate and 25 adults without diabetes. The intensive weight-loss intervention consisted of 16 weeks of a low-calorie liquid diet followed by gradual reintroduction of food. Participants in the intervention group who achieved an HbA1c below 6.5% were considered responders, whereas those who still had HbA1c of 6.5% or greater were considered nonresponders.

At 5 weeks, 1 year and 2 years, the researchers evaluated beta-cell function via first-phase insulin response and the maximal capacity for insulin response using the Stepped Insulin Secretion Test with Arginine (SISTA).

Weight loss scale and tape measure 2019 
Adults with type 2 diabetes who lose enough weight to enter diabetes remission are also able to recapture normal beta-cell capacity.
Source: Adobe Stock

Compared with baseline, the researchers found greater maximal rates of insulin response at 1 year (942 pmol/min/m2 vs. 581 pmol/min/m2; P = .028) and 2 years (936 pmol/min/m2 vs. 581 pmol/min/m2; P = .023) among responders, stating that “an almost linear increase was observed” and that the rate was similar to those without diabetes. The maximal rate of insulin response was also greater at 5 months (736 pmol/min/m2 vs. 491 pmol/min/m2; P = .002), 1 year (942 pmol/min/m2 vs. 485 pmol/min/m2; P = .001) and 2 years (936 pmol/min/m2 vs. 452 pmol/min/m2; P = .002) when the researchers compared responders with nonresponders.

“Type 2 diabetes is a reversible condition caused by excess triglyceride in the liver and pancreas,” Taylor said. “This [study] indicates that the beta cells in type 2 diabetes are not being apoptosed, but are unable to function normally under the triglyceride-induced stress. The time course of recovery is gradual, coming by 12 months after weight loss and remaining constant up to 2 years provided weight regain is avoided.”

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Compared with baseline, responders had greater first-phase insulin response at 5 months (107 pmol/min/m2 vs. 47 pmol/min/m2; P < .0001), 1 year (110 pmol/min/m2 vs. 42 pmol/min/m2; P < .0001) and 2 years (125 pmol/min/m2 vs. 42 pmol/min/m2; P < .0001), but this measure “remained substantially lower” compared with those without diabetes, according to the researchers.

“The first-phase insulin response did not completely normalize, although the degree of recovery was compatible with maintaining of nondiabetic blood glucose control,” the researchers wrote. “Not all beta-cells are required to achieve a normal first-phase insulin response, which can be achieved by rapid degranulation of some proportion of the whole. More detailed studies are required to determine the effect of an apparently adequate, but subnormal response during the postprandial period.” – by Phil Neuffer

For more information:

Roy Taylor, MD, FRCP, can be reached at roy.taylor@newcastle.ac.uk.

Disclosure: Taylor reports this work was supported by Diabetes UK and he has received lecture fees from Eli Lilly, Janssen and Novartis.