Journal
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Volume 26, Issue 12, Pages 1678-1684Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2015.08.014
Keywords
Betaine; N6-methyladenosine methylation; AMP-activated protein kinase; Adipose tissue; Fatty acid oxidation
Funding
- National Basic Research Program of China [2012CB124705]
- Special Fund for Cultivation and Breeding of New Transgenic Organism [2014ZX0800949B]
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The current study was conducted to determine whether betaine could improve fatty acid oxidation, mitochondrial function and N6-methyladenosine (m(6)A) mRNA methylation in adipose tissue in high-fat-induced mice and how AMP-activated protein kinase al subunit (AMPK alpha 1) was involved. AMPKal knockout mice and wild-type mice were fed either a low-fat diet, high-fat diet or high-fat diet supplemented with betaine in the drinking water for 8 weeks. Our results showed that mitochondrial genes (PGC1 alpha) and beta-oxidation-related genes (CPT1a) at protein level were increased in wild-type mice supplemented with betaine when compared with those in mice with high-fat diet. Betaine also decreased FTO expression and improved m(6)A methylation in adipose tissue of wild-type mice with high-fat diet. However, betaine failed to exert the abovementioned effects in AMPK alpha 1 knockout mice. In adipocytes isolated from mice with high-fat diet, betaine treatment increased lipolysis and lipid oxidation. Moreover, betaine decreased FTO expression and increased m(6)A methylation. However, while AMPK alpha 1 was knockdown, no remarkable changes in adipocytes were observed under betaine treatment. Our results indicated that betaine supplementation rectified mRNA hypomethylation and high FTO expression induced by high-fat diet, which may contribute to its beneficial effects on impaired adipose tissue function. Our results suggested that the AMPK alpha 1 subunit is required for the beneficial effects of betaine on dysfunctional adipose tissue and m(6)A methylation. These results may provide the foundation for a mechanism that links m(6)A methylation status in RNA, AMPK alpha 1 phosphorylation and dysfunctional adipose tissue induced by high-fat diet. (C) 2015 Elsevier Inc. All rights reserved.
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