Laboratory of Endocrine and Metabolic Physiology, Biosciences and Health, Postgraduate, University of West Parana, Cascavel, PR, Brazil.
Institute of Basic Health Sciences. Biological Sciences: Physiology, postgraduate. Department of Physiology, Room 337-7, Laboratory of Neurophysiology of Cognition and Development of the Brain, Federal University of Rio Grande do Sul, 500, Sarmento Leite - Farroupilha, Porto Alegre, RS, 90050-170, Brazil.
Sci Rep. 2021 Jan 13;11(1):1158. doi: 10.1038/s41598-020-80104-8.
Maternal obesity induced by cafeteria diet (CAF) predisposes offspring to obesity and metabolic diseases, events that could be avoided by maternal bariatric surgery (BS). Herein we evaluated whether maternal BS is able to modulate brown adipose tissue (BAT) morphology and function in adult male rats born from obese female rats submitted to Roux-en-Y gastric bypass (RYGB). For this, adult male rat offspring were obtained from female rats that consumed standard diet (CTL), or CAF diet, and were submitted to simulated operation or RYGB. Analysis of offspring showed that, at 120 days of life, the maternal CAF diet induced adiposity and decreased the expression of mitochondrial Complex I (CI) and Complex III (CIII) in the BAT, resulting in higher accumulation of lipids than in BAT from offspring of CTL dams. Moreover, maternal RYGB increased UCP1 expression and prevented excessive deposition of lipids in the BAT of adult male offspring rats. However, maternal RYGB failed to reverse the effects of maternal diet on CI and CIII expression. Thus, maternal CAF promotes higher lipid deposition in the BAT of offspring, contributing to elevated adiposity. Maternal RYGB prevented obesity in offspring, probably by increasing the expression of UCP1.
饮食诱导的母体肥胖(CAF)使后代易患肥胖和代谢疾病,而母体减重手术(BS)可以避免这些疾病的发生。在此,我们评估了肥胖女性接受 Roux-en-Y 胃旁路术(RYGB)后,母体 BS 是否能够调节雄性大鼠成年后代棕色脂肪组织(BAT)的形态和功能。为此,雄性大鼠后代来自于食用标准饮食(CTL)或 CAF 饮食的雌性大鼠,并接受模拟手术或 RYGB。对后代的分析表明,在 120 天龄时,母体 CAF 饮食导致肥胖,并降低了 BAT 中线粒体复合物 I(CI)和复合物 III(CIII)的表达,导致 BAT 中脂质的积累高于 CTL 母鼠后代。此外,母体 RYGB 增加了 UCP1 的表达,并防止了成年雄性后代大鼠 BAT 中脂质的过度沉积。然而,母体 RYGB 未能逆转母体饮食对 CI 和 CIII 表达的影响。因此,母体 CAF 促进了后代 BAT 中更高的脂质沉积,导致肥胖。母体 RYGB 预防了后代肥胖,可能是通过增加 UCP1 的表达。