In the earlier study, the mice ate a regular diet. In this new study, the researchers fed PKC beta-deficient and normal mice either a diet in which 60 percent of calories were derived from fat the high-fat diet or a standard diet in which 15 percent of calories came from fat. In the typical American diet, about 40 percent of calories are derived from fat.
The normal mice on the high-fat diet showed weight gain within three weeks, a trend that continued throughout the 12-week study. The PKC beta-deficient mice on the same diet gained less weight even while appearing to be extra hungry and eating more calories than the normal mice meaning their lower body weight was not the result of eating less.
Of animals eating the high-fat diet, the fat tissue and livers in the normal mice were larger than those in the PKC beta-deficient mice, as well. The livers of the normal mice were on average about 50 percent larger than the livers in mice lacking the gene. And the white fat tissue the tissue in which PKC beta was expressed as a result of the high-fat diet was almost three times as heavy in the normal mice as in the PKC beta-deficient mice.
The protein-deficient mice were able to clear insulin to regulate blood sugar more rapidly than normal mice after eating the high-fat diet, meaning avoiding obesity also allowed them to avoid development of insulin resistance associated with diabetes, said Mehta, also an investigator in Ohio State's Davis Heart and Lung Research Institute.
"Obesity leads to liver damage and to diabetes. So if we can take care of obesity associated with a high-fat diet, we can also take care of most of the related disorders," Mehta said.
A separate component of the current study further showed that mice engineered to be obese als
|Contact: Kamal Mehta|
Ohio State University