Pantothenate protects against obesity via brown adipose tissue activation.
Huiqiao ZhouHanlin ZhangRongcai YeChunlong YanJun LinYuanyuan HuangXiaoxiao JiangShouli YuanLi ChenRui JiangKexin ZhengZiyu ChengZhi ZhangMeng DongWanzhu JinPublished in: American journal of physiology. Endocrinology and metabolism (2022)
Brown adipose tissue (BAT) is the primary site of adaptive thermogenesis, which is involved in energy expenditure and has received much attention in the field of obesity treatment. By screening a small-molecule compound library of drugs approved by the Food and Drug Administration, pantothenic acid was identified as being able to significantly upregulate the expression of uncoupling protein 1 (UCP1), a key thermogenic protein found in BAT. Pantothenate (PA) treatment decreased adiposity, reversed hepatic steatosis, and improved glucose homeostasis by increasing energy expenditure in C57BL/6J mice fed a high-fat diet. PA also significantly increased BAT activity and induced beige adipocytes formation. Mechanistically, the beneficial effects were mediated by UCP1 because PA treatment was unable to ameliorate obesity in UCP1 knockout mice. In conclusion, we identified PA as an effective BAT activator that can prevent obesity and may represent a promising strategy for the clinical treatment of obesity and related metabolic diseases. NEW & NOTEWORTHY PA treatment effectively and safely protected against obesity via the BAT-UCP1 axis. PA has therapeutic potential for treating obesity and type II diabetes.
Keyphrases
- insulin resistance
- adipose tissue
- high fat diet induced
- high fat diet
- metabolic syndrome
- type diabetes
- weight loss
- weight gain
- small molecule
- skeletal muscle
- glycemic control
- poor prognosis
- body mass index
- binding protein
- blood pressure
- long non coding rna
- drug induced
- combination therapy
- physical activity
- working memory
- nuclear factor
- climate change
- blood glucose
- high glucose
- amino acid
- diabetic rats
- nitric oxide synthase