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J Biosci Bioeng. 2014 Oct;118(4):476-81. doi: 10.1016/j.jbiosc.2014.03.001. Epub 2014 Apr 8.

Dietary trimethylamine N-oxide exacerbates impaired glucose tolerance in mice fed a high fat diet.

Author information

1
College of Food Science and Engineering, Ocean University of China, No. 5, Yu Shan Road, Qingdao, Shandong Province 266003, China.
2
College of Food Science and Engineering, Ocean University of China, No. 5, Yu Shan Road, Qingdao, Shandong Province 266003, China. Electronic address: wangyuming@ouc.edu.cn.

Abstract

Trimethylamine N-oxide (TMAO) is an oxidation product of trimethylamine (TMA) and is present in many aquatic foods. Here, we investigated the effects of TMAO on glucose tolerance in high fat diet (HFD)-fed mice. Male C57BL/6 mice were randomly assigned to the control, high fat (HF), and TMAO groups. The HF group was fed a diet containing 25% fat, and the TMAO group was fed the HFD plus 0.2% TMAO for 4 weeks. After 3 weeks of feeding, oral glucose tolerance tests were performed. Dietary TMAO increased fasting insulin levels and homeostasis model assessment-estimated insulin resistance (HOMA-IR) and exacerbated the impaired glucose tolerance in HFD-fed mice. These effects were associated with the expression of genes related to the insulin signal pathway, glycogen synthesis, gluconeogenesis and glucose transport in liver. mRNA levels of the pro-inflammatory cytokine MCP-1 increased significantly and of the anti-inflammatory cytokine IL-10 greatly decreased in adipose tissue. Our results suggest that dietary TMAO exacerbates impaired glucose tolerance, obstructs the hepatic insulin signaling pathway, and causes adipose tissue inflammation in mice fed a high fat diet.

KEYWORDS:

Glucose tolerance; High fat diet; Inflammation; Insulin resistance; Trimethylamine N-oxide

PMID:
24721123
DOI:
10.1016/j.jbiosc.2014.03.001
[Indexed for MEDLINE]

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