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.
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Authors | J R Goudriaan, P J Tacken, V E Dahlmans, M J Gijbels, K W van Dijk, L M Havekes, M C Jong |
Journal | Arteriosclerosis, thrombosis, and vascular biology
(Arterioscler Thromb Vasc Biol)
Vol. 21
Issue 9
Pg. 1488-93
(Sep 2001)
ISSN: 1524-4636 [Electronic] United States |
PMID | 11557677
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Fatty Acids
- Receptors, LDL
- Triglycerides
- VLDL receptor
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Topics |
- Adipose Tissue
(metabolism, pathology)
- Animals
- Diet, Atherogenic
- Fatty Acids
(metabolism)
- Glucose Tolerance Test
- Insulin Resistance
- Mice
- Mice, Knockout
- Mice, Obese
- Mice, Transgenic
- Obesity
(blood, metabolism, pathology)
- Receptors, LDL
(genetics)
- Triglycerides
(blood)
- Weight Gain
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