Boffins have found that the absence of CD38 gene prevented mice on high-fat diets from gaining weight.
The study was conducted by a team of researchers led by Eduardo Chini at Mayo Clinic.
As part of the study, researchers studied two groups of mice - one with the gene CD38 and the other without. Each group was fed a high-calorie diet with 60 percent of calories from fat. In a second test, each group was fed a standard diet in which 4 percent of calories came from fat.
Researchers found that the body fat of mice that carried CD38 and were on a high-fat diet nearly quadrupled and their body weight almost doubled. After eight weeks on a high-fat diet, mice with CD38 began to show signs of glucose intolerance, one of the first indicators of diabetes onset.
In addition, this group of mice lived for only four-to-six months compared to the second group of mice that lived for 12 months.
The study noted that for the group of mice that had no CD38, the body fat and weight did not change even though they were on a high fat diet. These mice burned more energy, were leaner and otherwise healthy. he researchers also examined the effects of resveratrol in mice.
Resveratrol is a naturally occurring substance found in some plants such as mulberries, peanuts and red grapes used to make wine. It has been marketed as a drug that mimics the effects of moderate exercise without the physical act of exercising and also as a longevity drug, despite the lack of evidence that resveratrol is safe and effective in humans.
Researchers treated mice with CD38 with 30 milligrams of resveratrol per day and to determine the effects of the SIRT genes on obesity, mice without CD38 received the same dose of sirtinol, a drug that shuts down the SIRT genes.
Researchers found that mice with CD38 that were treated with resveratrol for two weeks were protected from high-fat, diet-induced obesity. By contrast, the protective effect against high-fat, diet-induced obesity in the absence of CD38 in mice was invalidated by sirtinol.
Mice without CD38 that were treated with sirtinol gained a statistically significant amount of weight when compared with mice without the gene who were not treated with sirtinol.
"Together these results identify a novel pathway regulating body weight and clearly show that CD38 is a nearly obligatory component of the cellular cascade that led to diet-induced obesity," the authors write.
The findings of the study were published in the online issue of The FASEB Journal, the journal of the Federation of American Societies for Experimental Biology. The study will appear in the November 2007 print issue of the journal.