Title
Protection from obesity in mice lacking the VLDL receptor
Author
Goudriaan, J.R.
Tacken, P.J.
Dahlmans, V.E.H.
Gijbels, M.J.J.
van Dijk, K.W.
Havekes, L.M.
Jong, M.C.
Gaubius Instituut TNO
Publication year
2001
Abstract
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
Subject
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
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TNO identifier
236326
ISSN
1079-5642
Source
Arteriosclerosis, Thrombosis, and Vascular Biology, 21 (9), 1488-1493
Document type
article