Department of Neuroscience and Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Diabetes, Obesity and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Biol Sex Differ. 2024 Jul 15;15(1):55. doi: 10.1186/s13293-024-00628-w.
Scientific evidence highlights the influence of biological sex on the relationship between stress and metabolic dysfunctions. However, there is limited understanding of how diet and stress concurrently contribute to metabolic dysregulation in both males and females. Our study aimed to investigate the combined effects of high-fat diet (HFD) induced obesity and repeated stress on fear-related behaviors, metabolic, immune, and hypothalamic outcomes in male and female mice.
To investigate this, we used a highly reliable rodent behavioral model that faithfully recapitulates key aspects of post-traumatic stress disorder (PTSD)-like fear. We subjected mice to footshock stressor followed by a weekly singular footshock stressor or no stressor for 14 weeks while on either an HFD or chow diet. At weeks 10 and 14 we conducted glucose tolerance and insulin sensitivity measurements. Additionally, we placed the mice in metabolic chambers to perform indirect calorimetric measurements. Finally, we collected brain and peripheral tissues for cellular analysis.
We observed that HFD-induced obesity disrupted fear memory extinction, increased glucose intolerance, and affected energy expenditure specifically in male mice. Conversely, female mice on HFD exhibited reduced respiratory exchange ratio (RER), and a significant defect in glucose tolerance only when subjected to repeated stress. Furthermore, the combination of repeated stress and HFD led to sex-specific alterations in proinflammatory markers and hematopoietic stem cells across various peripheral metabolic tissues. Single-nuclei RNA sequencing (snRNAseq) analysis of the ventromedial hypothalamus (VMH) revealed microglial activation in female mice on HFD, while male mice on HFD exhibited astrocytic activation under repeated stress.
Overall, our findings provide insights into complex interplay between repeated stress, high-fat diet regimen, and their cumulative effects on health, including their potential contribution to the development of PTSD-like stress and metabolic dysfunctions, emphasizing the need for further research to fully understand these interconnected pathways and their implications for health.
科学证据强调了生物性别对压力与代谢功能紊乱之间关系的影响。然而,对于饮食和压力如何共同导致男性和女性代谢失调,人们的理解有限。我们的研究旨在调查高脂饮食(HFD)诱导的肥胖和反复应激对雄性和雌性小鼠恐惧相关行为、代谢、免疫和下丘脑结果的综合影响。
为了研究这一点,我们使用了一种高度可靠的啮齿动物行为模型,该模型忠实地再现了创伤后应激障碍(PTSD)样恐惧的关键方面。我们让小鼠接受足底电击应激源,然后每周接受一次单一足底电击应激源或不接受应激源,同时给予 HFD 或标准饮食。在第 10 周和第 14 周,我们进行了葡萄糖耐量和胰岛素敏感性测量。此外,我们将小鼠放入代谢室进行间接量热测量。最后,我们收集大脑和外周组织进行细胞分析。
我们观察到 HFD 诱导的肥胖破坏了恐惧记忆的消退,导致雄性小鼠葡萄糖耐量受损,并影响了能量消耗。相反,HFD 喂养的雌性小鼠的呼吸交换率(RER)降低,仅在反复应激时才出现葡萄糖耐量显著缺陷。此外,反复应激和 HFD 的组合导致雄性和雌性小鼠的各种外周代谢组织中的促炎标志物和造血干细胞发生性别特异性改变。腹内侧下丘脑(VMH)的单细胞 RNA 测序(snRNAseq)分析显示,HFD 喂养的雌性小鼠中存在小胶质细胞激活,而 HFD 喂养的雄性小鼠在反复应激下表现出星形胶质细胞激活。
总的来说,我们的研究结果提供了关于反复应激、高脂肪饮食方案及其对健康的综合影响之间复杂相互作用的见解,包括它们对 PTSD 样应激和代谢功能紊乱发展的潜在贡献,强调需要进一步研究以充分了解这些相互关联的途径及其对健康的影响。