Inhibition of glucocorticoid synthesis alleviates cognitive impairment in high-fat diet-induced obese mice

Comprehensive Psychoneuroendocrinology

Sutin Kingtong¹  Yoottana Janthakhin²  Sirikran Juntapremjit³ 

[1] Corresponding author. College of Research Methodology and Cognitive Science, Burapha University, 169 Long had Bangsaen road, Saensook, Chonburi, 20131, Thailand.;Cognitive Science and Innovation Research Unit (CSIRU), College of Research Methodology and Cognitive Science, Burapha University, Chonburi, 20131, Thailand;Department of Biology, Faculty of Science, Burapha University, Chonburi, 20131, Thailand;

关键词: High-fat diet;    Obesity;    Memory impairments;    Glucocorticoid;    Synaptic plasticity;   

DOI  :  

来源: DOAJ

【 摘 要 】

In addition to cardiovascular diseases, metabolic syndrome and type 2 diabetes mellitus, obesity is associated with cognitive deficits. In rodents, it has been shown that long-term high-fat diet (HFD) consumption leads to the alteration of hypothalamic-pituitary-adrenal (HPA) axis resulting in increased corticosterone release. However, mechanisms underpinning cognitive impairments induced by long-term HFD intake are unclear. Herein we evaluated the effects of systemic administration of glucocorticoid synthesis inhibitor metyrapone on cognitive performance assessed by novel object recognition test and plasma corticosterone levels evaluated by enzyme-linked immunosorbent assay in HFD-induced obese mice. We found that metyrapone treatment alleviated recognition memory impairments in HFD-induced obese mice. Furthermore, glucocorticoid synthesis inhibitor also lowered plasma corticosterone levels in HFD-induced obese mice. Our findings indicate that hyperactivation of HPA axis resulting in elevated circulating glucocorticoid levels leads to memory impairments in HFD-induced obese mice. We identify glucocorticoid system as a potential therapeutic target for treating cognitive deficits associated with obesity condition.

【 授权许可】

Unknown