Journal
JOURNAL OF BIOSCIENCE AND BIOENGINEERING
Volume 118, Issue 4, Pages 476-481Publisher
SOC BIOSCIENCE BIOENGINEERING JAPAN
DOI: 10.1016/j.jbiosc.2014.03.001
Keywords
Glucose tolerance; Insulin resistance; Inflammation; High fat diet; Trimethylamine N-oxide
Funding
- National Key Technology RD Program [2012BAD33B07]
- National Natural Science Foundation of China [31371757]
- Program for Changjiang Scholars and Innovative Research Team in University (PCSIRT) [IRT1188]
- Taishan Scholars Programme of Shandong Province
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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. mEtNA 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. (c) 2014, The Society for Biotechnology, Japan. All rights reserved.
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