Changing the way that cells burn fat might not lead to a cure for obesity as previously thought, according to new research.
The study, conducted at the Johns Hopkins University, Baltimore, and published in Cell Reports, sheds new light on the process of fat oxidation and insulin resistance, potentially affecting the development of type 2 diabetes.
Brown fat – the “good fat” found more abundantly in thinner people – burns white fat for warmth and energy in a process called oxidation. Research has suggested that the by-products of oxidation may trigger inflammation in fat cells, which has a strong association with insulin resistance and type 2 diabetes.
Based on this idea, previous attempts to develop an effective weight loss drug have focused on disrupting the oxidation of fat in all of an animal’s cells. This new study allowed oxidation in all cells except the fat cells by modifying the genomes of mice. Having been fed a high-calorie diet for a few, the mice were not protected from diabetes symptoms, suggesting that oxidation of fatty acid is not the only cause of insulin resistance.
The mice with the disrupted fat oxidation gene were around the same weight as normal mice, even after being fed high-fat diets for months. The brown fat cells in the normal mice, which would have to burn fat to keep the body warm, did not make them any leaner than the mice with the dysfunctional fat oxidation gene, who could not burn fat.
Michael Wolfgang, Ph.D., associate professor of biological chemistry at Johns Hopkins University School of Medicine’s Institute for Basic Biomedical Sciences, explained: “It’s been suggested that if we could make the process of breaking down fat into useful energy less efficient inside fat cells, they would burn more fat to compensate – sort of like leaving the windows open while the heat is on.
“Our experiment looked at the opposite scenario: would mice be more prone to obesity if their fat cells couldn’t burn fat? The answer, surprisingly, was no.
“We expected the brown fat cells in the normal mice would burn lots of fat to stay warm, and they would end up thinner than that couldn’t burn fat. It seems there’s some other systems that’s compensating when fat cells can’t burn fat, though we don’t know yet what it is.
“Keep your sweater on: Staying warm probably doesn’t lead to weight gain.”
Last week, researchers from the Basic Biomedical Sciences at Johns Hopkins University School of Medicine found several clues as to how diabetes is triggered by a combination of genetics and environmental factors.

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