Obesity development in neuron-specific lipoprotein lipase deficient mice is not responsive to increased dietary fat content or change in fat composition.

摘要: We have previously reported that mice with neuron-specific LPL deficiency (NEXLPL-/-) become obese by 16weeks of age on chow. Moreover, these had reduced uptake triglyceride (TG)-rich lipoprotein-derived fatty acids and lower levels n-3 long chain polyunsaturated (n-3 PUFAs) in the hypothalamus. Here, we asked whether increased dietary fat content or altered composition could modulate obesity development NEXLPL-/- mice. Male littermate controls (WT) were randomly assigned one three synthetic diets; a high carbohydrate diet (HC, 10% fat), high-fat (HF, 45% HC supplemented PUFAs (HCn-3, fat, Lovaza, GSK®). After 42weeks feeding, body weight mass compared to WT. WT fed HF displayed typical diet-induced obesity, but gain was only marginal HF-fed mice, no significant difference composition. Dietary PUFA supplementation did not prevent associated differential modifications hypothalamic gene expression concentration Our findings suggest neuronal is involved regulation response either change quantity (HF feeding) quality PUFA-enriched) fat. The precise role lipid sensing brain requires further investigation.