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- Title
Deficiency of Adiponectin Receptor 2 Increases Adiposity in Mice Fed a High Fat Diet.
- Authors
Yanfang Liu; Otto, Keith A.; Miller, Anne Reifel
- Abstract
Adiponectin/adiponectin receptors are involved in energy homeostasis and inflammatory pathways. We have previously shown that AdipoR2 deletion diminishes high fat diet (HF) induced dyslipidemia and insulin resistance, yet deteriorates glucose homeostasis as HF feeding continues, resulting from the failure of pancreatic βcells to adequately compensate for moderate insulin resistance. In the present study, we first confirmed the body weight gain pattern observed in the previous study: both wild type (WT) and AdipoR2 deficient (KO) mice on HF rapidly became significantly heavier than their corresponding groups on standard chow diet (Std). The body weights of KO mice on HF (KO-HF) were significantly lower than that of the WT mice on HF (WT-HF) during the early stages of the study (8-13 weeks on diet) but became equivalent at later stages (14-23 weeks on diet). Although food intake was not different between genotypes, fecal fat content of KO-HF mice increased 27% compared to WT-HF mice, suggesting that decreased fat absorption contributed to the lower body weight found in KO-HF mice at the early stages of the study. Fecal fat contents in the two Std groups are comparable. Body temperatures were not different between genotypes. Body fat composition measured using quantitative nuclear magnetic resonance (qNMR.) showed that there was significantly less body fat mass in KO-HF mice at 8w on diet compared to WT-HF mice, and the body fat mass in KO-HF mice showed a trend of surpassing that of WT-HF mice beginning at 16w on diet. The body fat accumulation rate of KO-HF mice was 33% higher than that of WT-HF mice from 16w to 24w on diet. Interestingly, several adipogenic and lipogenic genes were significantly upregulated in the mesenteric, but not subcutaneous, fat pad of KO-HF mice. Indirect calorimetry using the OxyMax system showed that KO mice had higher respiratory quotient (RQ) values compared to their diet-matched WT mice. Consistently, detailed fuel utilization illustrated that KO mice burnt more carbohydrate and less fat, with the total energy expenditure comparable between diet-matched genotypes. Additionally, several plasma adipokines, including leptin, resistin, monocyte chemotactic protein-1 (MCP-1) and plasminogen activator inhibitor-1 (PAI-1), showed differential dynamic changes in KO-HF mice compared to WT-HF mice. Our study suggests new roles for AdipoR2 in overall metabolic control, including promotion of fat absorption and fat over carbohydrate oxidation and potentially suppression of mesenteric adipogenesis.
- Subjects
OBESITY; INSULIN resistance; DIABETES; BLOOD sugar; WEIGHT gain; LABORATORY mice
- Publication
Diabetes, 2007, Vol 56, pA350
- ISSN
0012-1797
- Publication type
Article