Fat-free may be all the rage in packaged foods, but mice genetically engineered to lack the fat cells get diabetes with more severe symptoms than those obese mice. The findings, reported in two articles in the issue last week Genes and Development , may give clues to the riddle of adult onset diabetes, also known as type 2 diabetes or diabetes mellitus.
Obesity can lead to Type 2 diabetes, which affects at least 18 million Americans. But people born with a rare condition that nearly eliminates fat cells also get diabetes symptoms. To explore this link, Marc Reitman and the group of Charles Vinson at the National Institutes of Health in Bethesda, Maryland, inactivated genes for two transcription factors families that normally help the fat cells grow and develop. (Transcription factors are proteins that turn genes on or off.) A similar approach was taken by the Nobel Michael Brown and Joseph Goldstein and colleagues from the University of Texas Southwestern Medical Center in Dallas.
In both experiments, the mice are born with little or no white fat. Most animals died before reaching adulthood, but those who survived developed symptoms of adult onset diabetes in humans: high blood sugar, high insulin levels, and a fierce thirst and appetite. And like human diabetes, the animals also have elevated levels of triglycerides and other fat building blocks in their circulation and liver are saturated triglycerides. "These animals are really sick," says Reitman. "But they clearly do not get diabetes in the same way as the normal type 2 diabetes," in which excess body fat plays a role.
Reitman and Vinson may be able to explain why obesity and a total lack of fat can lead to diabetic symptoms. They propose that the acids and excess fatty triglycerides in the circulation and liver could somehow trigger the disease. the compounds could end up in traffic or because they spread from fat cells stuffed, in the case of obesity, or because there is no fat cells to store as fatless mice.
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