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Nutrition. 2016 Jul-Aug;32(7-8):732-9. doi: 10.1016/j.nut.2016.01.011. Epub 2016 Jan 25.

Beneficial role of vitamin K supplementation on insulin sensitivity, glucose metabolism, and the reduced risk of type 2 diabetes: A review.

Author information

1
Biotechnology Division, CSIR-North East Institute of Science and Technology, Jorhat, Assam, India. Electronic address: pmanna2012@gmail.com.
2
Biotechnology Division, CSIR-North East Institute of Science and Technology, Jorhat, Assam, India.

Abstract

Micronutrients are gaining acceptance as an important nutritional therapy for the prevention and/or management of diabetes and its associated health risks. Although a very small quantity of micronutrients are required for specific functions in our bodies, moderate deficiencies can lead to serious health issues. Impaired insulin sensitivity and glucose intolerance play a major role in the development of diabetic pathophysiology. Vitamin K is well known for its function in blood coagulation. Moreover, several human studies reported the beneficial role of vitamin K supplementation in improving insulin sensitivity and glucose tolerance, preventing insulin resistance, and reducing the risk of type 2 diabetes (T2 D). Both animal and human studies have suggested that vitamin K-dependent protein (osteocalcin [OC]), regulation of adipokine levels, antiinflammatory properties, and lipid-lowering effects may mediate the beneficial function of vitamin K in insulin sensitivity and glucose tolerance. This review for the first time provides an overview of the currently available preclinical and clinical evidences on the effect of vitamin K supplementation in the management of insulin sensitivity and glucose tolerance. The outcome of this review will increase understanding for the development of a novel adjuvant therapy to achieve better control of glycemia and improve the lives of diabetic patients.

KEYWORDS:

Anti-inflammatory; Glucose tolerance; Insulin sensitivity; Lipid lowering; Reduced risk of T2 D; Vitamin K

PMID:
27133809
DOI:
10.1016/j.nut.2016.01.011
[Indexed for MEDLINE]
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