Adipose tissue uncoupling protein 1 levels and function are increased in a mouse model of developmental obesity induced by maternal exposure to high-fat diet

Abstract

With brown adipose tissue (BAT) becoming a possible therapeutic target to counteract obesity, the prenatal environment could represent a critical window to modify BAT function and browning of white AT. We investigated if levels of uncoupling protein 1 (UCP1) and UCP1-mediated thermogenesis are altered in offspring exposed to prenatal obesity. Female CD-1 mice were fed a high-fat (HF) or standard-fat (SF) diet for 3 months before breeding. After weaning, all pups were placed on SF. UCP1 mRNA and protein levels were quantified using quantitative real-time PCR and Western blot analysis, respectively, in brown (BAT), subcutaneous (SAT) and visceral (VAT) adipose tissues at 6 months of age. Total and UCP1-dependent mitochondrial respiration were determined by high-resolution respirometry. A Student's t-test and Mann-Whitney test were used (significance: P<0.05). UCP1 mRNA levels were not different between the HF and SF offspring. UCP1 protein levels, total mitochondrial respiration and UCP1-dependent respiration were significantly higher in BAT from HF males (P=0.02, P=0.04, P=0.005, respectively) and females (P=0.01, P=0.04, P=0.02, respectively). In SAT, the UCP1 protein was significantly lower in HF females (P=0.03), and the UCP1-dependent thermogenesis was significantly lower from HF males (P=0.04). In VAT, UCP1 protein levels and UCP1-dependent respiration were significantly lower only in HF females (P=0.03, P=0.04, respectively). There were no differences in total respiration in SAT and VAT. Prenatal exposure to maternal obesity leads to significant increases in UCP1 levels and function in BAT in offspring with little impact on UCP1 levels and function in SAT and VAT.

Browning Effects of a Chronic Pterostilbene Supplementation in Mice Fed a High-Fat Diet

“…Protein levels of UCP1 were significantly increased by Pt in 3T3-L1 cells, although no differences were observed at the transcriptional level. This discrepancy between gene and protein expression was also observed by other groups in other models [42], and could be related, for example, to protein turnover regulation [43,44].…”

Gut Microbiota Interventions for the Management of Obesity: A Literature Review

“…There is increasing evidence revealing GM's relation with energy metabolism. Studies have suggested that GM is involved in preventing obesity by enhancing the uncoupling protein 1 (UCP-1)-dependent thermogenesis [ 14 , 15 ]. GM mediates the action of curcumin using the UCP-1 pathway to prevent and treat obesity [ 16 ].…”