Laboratório de Genética Animal e Humana, Departamento de Genética, Ecologia e Evolução, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Laboratório de Genética Animal e Humana, Departamento de Genética, Ecologia e Evolução, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil; Center for Alcohol Research in Epigenetics, Department of Psychiatry, University of Illinois at Chicago, Chicago, IL, USA.
J Nutr Biochem. 2021 Jun;92:108622. doi: 10.1016/j.jnutbio.2021.108622. Epub 2021 Mar 8.
The high prevalence of obesity and associated metabolic disorders are one of the major public health problems worldwide. Among the main causal factors of obesity, excessive consumption of food rich in sugar and fat stands out due to its high energy density. The regulation of food intake relies on hypothalamic control by the action of several neuropeptides. Excessive consumption of hypercaloric diets has impact in the behavior and in the gut microbiota. In the present study, we used a high-sugar and fat (HSB) diet for 12 weeks to induce obesity in C57BL/6 mice and to investigate its effects on the gut microbiota, hypothalamic peptides, and behavior. We hypothesize that chronic consumption of HSB diet can change the behavior. Additionally, we also hypothesize that changes in gut microbiota can be associated with changes in the transcriptional regulation of hypothalamic peptides and behavior. To evaluate the gut microbiota, we performed the sequencing of 16S rRNA gene, which demonstrate that HSB diet modulates the gut microbiota with an increase in the Firmicutes and Actinobacteria phylum and a decrease of Bacteroidetes phylum. The real time qPCR revealed that HSB-fed mice presented changes in the transcriptional regulation of hypothalamic neuropeptides genes such as Npy, Gal and Galr1. The Marble-burying and Light/dark box tests also showed an alteration in anxiety and impulsive behaviors for the HSB-fed mice. Our data provides evidence that obesity induced by HSB diet consumption is associated with alterations in gut microbiota and behavior, highlighting the multifactorial characteristics of this disease.
肥胖症及其相关代谢紊乱的高发率是全球主要的公共卫生问题之一。在肥胖症的主要致病因素中，由于其高能量密度，过量摄入富含糖和脂肪的食物尤为突出。食物摄入的调节依赖于下丘脑通过几种神经肽的作用进行控制。过量摄入高热量饮食会对行为和肠道微生物群产生影响。在本研究中，我们使用高糖高脂肪（HSB）饮食喂养 12 周诱导 C57BL/6 小鼠肥胖，并研究其对肠道微生物群、下丘脑肽和行为的影响。我们假设慢性摄入 HSB 饮食会改变行为。此外，我们还假设肠道微生物群的变化可能与下丘脑肽和行为的转录调节变化有关。为了评估肠道微生物群，我们进行了 16S rRNA 基因测序，结果表明 HSB 饮食可通过增加厚壁菌门和放线菌门以及减少拟杆菌门来调节肠道微生物群。实时 qPCR 显示，HSB 喂养的小鼠下丘脑神经肽基因如 Npy、Gal 和 Galr1 的转录调控发生变化。大理石埋藏和明暗箱测试也显示 HSB 喂养的小鼠焦虑和冲动行为发生改变。我们的数据提供了证据，表明 HSB 饮食摄入诱导的肥胖与肠道微生物群和行为的改变有关，突出了这种疾病的多因素特征。
