FRIDAY, Feb. 5 (HealthDay News) -- The cell cycle protein cyclin D2 appears necessary for β-cell mass to expand in response to insulin resistance, suggesting that it may be useful in preventing or curing type 2 diabetes, according to research published online Jan. 26 in Diabetes.
Senta Georgia, Ph.D., of the David Geffen School of Medicine at the University of California in Los Angeles, and colleagues analyzed data from crossing cyclin D2 knockout mice with two types of mice that show insulin resistance and glucose intolerance but don't develop overt diabetes due to compensatory β-cell expansion.
The researchers found that each type of double knockout mice had insulin resistance and hyperinsulinemia, and didn't have compensatory β-cell hyperplasia. These findings suggest that lack of cyclin D2 during insulin resistance can directly affect β-cell function and proliferation, they write.
"The presence of an adequate functional β-cell mass is critical for maintaining euglycemia in mammals. In states of altered metabolic demand, e.g., pregnancy or high fat feeding, healthy β-cells maintain euglycemia either by increasing insulin secretion or by an elevated β-cell mass or both. Indeed, less than 20 percent of obese insulin-resistant individuals develop type 2 diabetes and a majority of insulin-resistant humans are capable of maintaining euglycemia by β-cell compensation," the authors write.
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