Effects of SCFA on the DNA methylation pattern of adiponectin and resistin in high-fat-diet-induced obese male mice

Specific adipokines, such as adiponectin and resistin, are secreted from adipose tissue and are associated with the development of obesity. Supplementation of dietary SCFA can prevent and reverse high-fat-diet (HFD)-induced obesity. However, it is not clear whether SCFA ameliorate abnormal expressio...

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Bibliographic Details
Published in:British journal of nutrition 2018-08, Vol.120 (4), p.385-392
Main Authors: Lu, Yuanyuan, Fan, Chaonan, Liang, Aimin, Fan, Xiuqin, Wang, Rui, Li, Ping, Qi, Kemin
Format: Article
Language:English
Subjects:
Acetic acid
Adiponectin
Adipose tissue
Admixtures
Animal tissues
Binding
CpG islands
Deoxyribonucleic acid
Diet
Dietary supplements
DNA
DNA methylation
DNA methyltransferase
DNMT1 protein
Epigenetics
Fatty acids
Gene expression
High fat diet
Insulin resistance
Laboratory animals
Low fat diet
Metabolism
Mice
Microbiota
mRNA
Nutrient deficiency
Nutrition research
Obesity
Propionic acid
Proteins
Rodents
Sodium
Weight control
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Summary:Specific adipokines, such as adiponectin and resistin, are secreted from adipose tissue and are associated with the development of obesity. Supplementation of dietary SCFA can prevent and reverse high-fat-diet (HFD)-induced obesity. However, it is not clear whether SCFA ameliorate abnormal expression of adiponectin and resistin in the obese state. The aim of this study was to investigate the effects of SCFA on adiponectin and resistin's expressions in diet-induced obese mice, as well as the potential mechanisms associated with DNA methylation. C57BL/6J male mice were fed for 16 weeks with five types of HFD (34·9 % fat by wt., 60 % kJ) - a control HFD and four HFD with acetate (HFD-A), propionate (HFD-P), butyrate (HFD-B) and their admixture (HFD-SCFA). Meanwhile, a low-fat diet (4·3 % fat by wt., 10 % kJ) was used as the control group. The reduced mRNA levels of adiponectin and resistin in the adipose tissue of the HFD-fed mice were significantly reversed by dietary supplementation of acetate, propionate, butyrate or their admixture to the HFD. Moreover, the expressional changes of adiponectin and resistin induced by SCFA were associated with alterations in DNA methylation at their promoters, which was mediated by reducing the expressions of enzyme-catalysed DNA methyltransferase (DNMT1, 3a, 3b) and the methyl-CpG-binding domain protein 2 (MBD2) and suppressing the binding of these enzymes to the promoters of adiponectin and resistin. Our results indicate that SCFA may correct aberrant expressions of adiponectin and resistin in obesity by epigenetic regulation.
ISSN:0007-1145
1475-2662
DOI:10.1017/s0007114518001526