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Protection from obesity in mice lacking the VLDL receptor

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Author: Goudriaan, J.R. · Tacken, P.J. · Dahlmans, V.E.H. · Gijbels, M.J.J. · Dijk, K.W. van · Havekes, L.M. · Jong, M.C.
Institution: Gaubius Instituut TNO
Source:Arteriosclerosis, Thrombosis, and Vascular Biology, 9, 21, 1488-1493
Identifier: 236326
Keywords: Adipose Tissue · Animals · Diet, Atherogenic · Fatty Acids · Glucose Tolerance Test · Insulin Resistance · Mice · Mice, Knockout · Mice, Obese · Mice, Transgenic · Obesity · Receptors, LDL · Triglycerides · Weight Gain


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. Chemicals/CAS: Fatty Acids; Receptors, LDL; Triglycerides; VLDL receptor