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J Diabetes Res. 2016;2016:1748065. doi: 10.1155/2016/1748065. Epub 2015 Dec 31.

Vitamin B6 Prevents Endothelial Dysfunction, Insulin Resistance, and Hepatic Lipid Accumulation in Apoe (-/-) Mice Fed with High-Fat Diet.

Author information

1
Department of Clinical Nutrition and Gastroenterology, The First Affiliated Hospital (People's Hospital of Hunan Province), Hunan Normal University, Changsha 430070, China.
2
College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China.
3
Division of Endocrinology, The Second Affiliated Hospital, Soochow University, Suzhou 215000, China.
4
College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, School of Medicine, Shandong University, Jinan 250012, China.

Abstract

BACKGROUNDS:

VitB6 deficiency has been associated with a number of adverse health effects. However, the effects of VitB6 in metabolic syndrome are poorly understood.

METHODS:

VitB6 (50 mg/kg/day) was given to Apoe (-/-) mice with hkdigh-fat diet (HFD) for 8 weeks. Endothelial dysfunction, insulin resistance, and hepatic lipid contents were determined.

RESULTS:

VitB6 administration remarkably increased acetylcholine-induced endothelium-dependent relaxation and decreased random blood glucose level in Apoe (-/-) mice fed with HFD. In addition, VitB6 improved the tolerance of glucose and insulin, normalized the histopathology of liver, and reduced hepatic lipid accumulation but did not affect the liver functions. Clinical and biochemical analysis indicated that the levels of VitB6 were decreased in patients with fatty liver.

CONCLUSIONS:

Vitamin B6 prevents endothelial dysfunction, insulin resistance, and hepatic lipid accumulation in Apoe (-/-) mice fed with HFD. Supplementation of VitB6 should be considered to prevent metabolic syndrome.

PMID:
26881239
PMCID:
PMC4735993
DOI:
10.1155/2016/1748065
[Indexed for MEDLINE]
Free PMC Article

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