Protection from obesity in mice lacking the VLDL receptor
JR Goudriaan, PJ Tacken, VEH Dahlmans… - … , and vascular biology, 2001 - Am Heart Assoc
Arteriosclerosis, thrombosis, and vascular biology, 2001•Am Heart Assoc
It has previously been reported that mice lacking the VLDL receptor (VLDLR−/−) exhibit
normal plasma lipid levels and a modest decrease in adipose tissue mass. In the present
study, the effect of VLDLR deficiency on profound weight gain was studied in mice. Obesity
was induced either by feeding of a high-fat, high-calorie (HFC) diet or by crossbreeding mice
onto the genetically obese ob/ob background. After 17 weeks of HFC feeding, VLDLR−/−
mice remained lean, whereas their wild-type littermates (VLDLR+/+) became obese …
normal plasma lipid levels and a modest decrease in adipose tissue mass. In the present
study, the effect of VLDLR deficiency on profound weight gain was studied in mice. Obesity
was induced either by feeding of a high-fat, high-calorie (HFC) diet or by crossbreeding mice
onto the genetically obese ob/ob background. After 17 weeks of HFC feeding, VLDLR−/−
mice remained lean, whereas their wild-type littermates (VLDLR+/+) became obese …
It has previously been reported that mice lacking the VLDL receptor (VLDLR−/−) exhibit normal plasma lipid levels and a modest decrease in adipose tissue mass. In the present study, the effect of VLDLR deficiency on profound weight gain was studied in mice. Obesity was induced either by feeding of a high-fat, high-calorie (HFC) diet or by crossbreeding mice onto the genetically obese ob/ob background. After 17 weeks of HFC feeding, VLDLR−/− mice remained lean, whereas their wild-type littermates (VLDLR+/+) became obese. Similarly, the weight gain of ob/ob mice was less profound in the absence of the VLDLR. Moreover, VLDLR deficiency led to increased plasma triglycerides after HFC feeding. The protection from obesity in VLDLR−/− mice involved decreased peripheral uptake of fatty acids, because VLDLR−/− mice exhibited a significant reduction in whole-body free fatty acid uptake, with no clear differences in food intake and fat absorption. These observations were supported by a strong decrease in average adipocyte size in VLDLR−/− mice of both obesity models, implying reduced adipocyte triglyceride storage in the absence of the VLDLR. These results suggest that the VLDLR plays a role in the delivery of VLDL-derived fatty acids into adipose tissue.
Am Heart Assoc