| First Author | Goudriaan JR | Year | 2001 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 21 |
| Issue | 9 | Pages | 1488-93 |
| PubMed ID | 11557677 | Mgi Jnum | J:102939 |
| Mgi Id | MGI:3608252 | Doi | 10.1161/hq0901.095147 |
| Citation | Goudriaan JR, et al. (2001) Protection from obesity in mice lacking the VLDL receptor. Arterioscler Thromb Vasc Biol 21(9):1488-93 |
| abstractText | 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. |
