Laboratory of Molecular Genetics, National Institute of Nutrition, Hyderabad 500007, Telangana, India.
Laboratory of Molecular Genetics, National Institute of Nutrition, Hyderabad 500007, Telangana, India.
Steroids. 2020 Aug;160:108653. doi: 10.1016/j.steroids.2020.108653. Epub 2020 May 11.
Obesity is a multifactorial disorder, caused mainly due to lifestyle changes, and increased consumption of calorie dense diets is not just limited to developed countries anymore. Chronic physiological stress and oxidative stress are known to be implicated in the etiology of obesity. However, the role of stress response towards obesity manifestation in genetically different rat strains is poorly understood. In the current study we have used obesity susceptible & resistant rat models to understand the role of both glucocorticoid and oxidativestress in the pathophysiology of obesity. Upon challenge with calorie dense diets, WNIN showed an increased glucocorticoid stress, resulting in increased oxidative stress; whereas such a phenomenon was not noticed in F-344 and SD. However, there was an increase in the circulatory melatonin levels in calorie dense fed groups of both F-344 and SD animals, which might have contributed to reduced oxidative stress. The molecular switch in the activation of melatonin could be possibly attributed to the genetic differences among these strains. It will be interesting to explore other molecular mechanisms for melatonin regulation, albeit increased corticosterone is implicated in the enhanced production of melatonin.
肥胖是一种多因素疾病，主要是由于生活方式的改变引起的，而高热量饮食的增加不仅限于发达国家。慢性生理应激和氧化应激被认为与肥胖的发病机制有关。然而，不同遗传背景的大鼠对肥胖表现的应激反应的作用尚不清楚。在本研究中，我们使用肥胖易感和肥胖抵抗大鼠模型来了解糖皮质激素和氧化应激在肥胖发病机制中的作用。在高热量饮食的挑战下，WNIN 表现出糖皮质激素应激增加，导致氧化应激增加；而在 F-344 和 SD 中则没有观察到这种现象。然而，在 F-344 和 SD 动物的高热量饮食组中，循环褪黑素水平升高，这可能有助于减少氧化应激。褪黑素激活的分子开关可能归因于这些品系之间的遗传差异。尽管皮质酮的增加与褪黑素产量的增加有关，但探索褪黑素调节的其他分子机制将是有趣的。
