Female mice target deleted for the neuromedin B receptor have partial resistance to diet-induced obesity.

摘要: Previous studies have proposed a role for neuromedin B (NB), bombesin-like peptide, in the control of body weight homeostasis. However, nature this is unclear. The actions NB are mediated preferentially by NB-preferring receptors (NBRs). Here we examined consequences targeted deletion NBRs female mice on homeostasis fed normolipid diet (ND) or high-fat (HFD) 13 weeks. Body and food ingestion receptor knockout (NBR-KO) showed no difference relation to wild-type (WT). induced an 8.9- 4.8-fold increase WT NBR-KO, respectively, compared their controls maintained with diet, even though ingested same amount calories, regardless genotype. Comparing NBR-KO accumulated approximately 45% less fat depot mass than WT, exhibited lower percentage carcasses (19.2 vs. 31.3%), adipocytes were hypertrophied. Serum leptin mRNA inguinal perigonadal HFD serum adiponectin was similar among groups unaltered comparison ND-fed mice. HFD-fed developed glucose intolerance but not mice, although they had glycaemia insulinaemia. differences any parameters, except trend insulin levels. Therefore, disruption pathway did change diet; however, it result partial resistance diet-induced obesity.