on February 17th, 2015 No Comments
Why do some obese people develop Type 2 diabetes while others don’t? New evidence suggests the answer may lie just beneath the skin. A study published this month in the Journal of Lipid Research found metabolic anomalies in the subcutaneous fat of a group of people at risk for diabetes. Basically, fat cells under their skin weren’t very good at storing fat.
That’s a problem because fat that doesn’t get stored in these cells must go somewhere, and it often ends up in other organs, such as the liver, muscle, pancreas and heart. In those locations, there is evidence that too much fat causes “lipotoxicity,” in part by interfering with the messages of the sugar-handling hormone insulin.
The new research, a collaboration between Stanford’s Tracey McLaughlin, MD, and her colleagues here and at UC Berkeley and the National Institutes of Health, used a state-of-the-art technique developed by Berkeley’s Marc Hellerstein, MD, PhD, to monitor fat synthesis and storage in the subcutaneous fat cells of 15 people. All of the subjects were overweight or obese. Half were insulin resistant: Although their blood-sugar levels were normal, their bodies responded poorly to their own insulin, a state that precedes full-blown Type 2 diabetes. (Many scientists think that understanding insulin resistance could lead to preventive strategies for Type 2 diabetes.) The other subjects had normal insulin sensitivity.
Each day for four weeks, the subjects drank a few sips of heavy water, a non-radioactive substance labeled with “heavy” hydrogen atoms that have an extra neutron. After four weeks, the scientists took small samples of the subjects’ subcutaneous belly fat and measured how much heavy hydrogen had been incorporated into the cells’ stored fat molecules and their DNA.
The insulin-resistant subjects had less heavy hydrogen in their fat molecules than the insulin-sensitive subjects, suggesting that their subcutaneous fat cells made and stored less fat during the study. The amount of heavy hydrogen in the DNA of the two groups’ fat cells was the same. This means that the insulin-resistant people were making new subcutaneous fat cells at the same rate as the insulin-sensitive people. The bodies of the insulin-resistant people could generate new fat cells under the skin, but the cells didn’t work quite right.
“This is an important extension of limited static and nonhuman data supporting the hypothesis that dysfunctional fat storage in subcutaneous adipose tissue contributes to obesity-associated insulin resistance,” the scientists wrote, adding that future identification of the molecules that cause this problem may help researchers develop drugs that could treat insulin resistance and prevent Type 2 diabetes.
Previously: The role of nutrition in diabetes prevention and management, Preventing pre-diabetes from turning into diabetes and The importance of regular exercise in delaying and treating diabetes
Photo by Kim P