Stolz D J, Martin R J
J Nutr. 1982 May;112(5):997-1002. doi: 10.1093/jn/112.5.997.
The role of insulin status in the development of obesity in Zucker rats was determined by equalization of available insulin. When streptozotocin-induced diabetic obese and lean rats received the same level of exogenous insulin, body weight gain and food intake per body weight were equalized. These types of observations are usually interpreted as proof for a role of insulin in genetically induced obesity. However, a more definitive examination of the composition of gain showed that the obese rat was still gaining significantly more lipid than the lean rat in spite of the equalization of available insulin. Further examination of liver enzymes involved in de novo lipogenesis indicated that increased heptic lipogenesis was not dependent on hyperinsulinemia. Protein gain in lean and obese rats was not significantly different. This study demonstrates that excessive weight gain and food intake of genetically obese rats is dependent on the differences in insulin status between lean and obese rats. The partitioning of more dietary energy toward lipid in the obese rat is independent of both food intake and insulin.