Abstract
Close

Current Research in Nutrition and Food Science - An open access, peer reviewed international journal covering all aspects of Nutrition and Food Science

lock and key

Sign in to your account.

Account Login

Forgot your password?

Review on Potential Vitamin D Mechanism with Type 2 Diabetes Mellitus Pathophysiology in Malaysia


Nurliyana Najwa bt Md Razip, Huzwah bt Khaza'ai*


Dept. of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia.

Corresponding Author Email: huzwah@upm.edu.my


Abstract:

Evidences on vitamin D deficiency suggest there is increasing risk of diabetes. To date, some cohort, observation, cross-sectional studies on populations and randomized controlled trials in vitamin D supplements highlighting the potential of vitamin D are essentially in modifying Type 2 Diabetes Mellitus (T2DM) pathophysiology. Relevant literature sought in a various databases focus on the discovery of vitamin D studies in Malaysia, particularly in dietary, health status and disease study. However, recent data in Malaysia, the scope of the literature focuses on the deficient vitamin D mediated insulin impairment. The development of literary findings encompasses on the etiology of diabetes which highly correlates with decreased mechanism of action of vitamin D. It is important to understand diabetes etiology before explaining more about insulin resistance mechanisms which is strongly correlated with the involvement of c-Jun N-terminal kinase (JNK) pathways in insulin signalling. Furthermore, the vitamin D works synergistically with calcium homeostasis which is believed to have interaction with insulin. The purpose of this article is to illustrate the potential of vitamin D in modulating T2DM pathophysiology. Existing evidence showing the biochemical function of vitamin D is strongly involved in the pathogenesis of T2DM which requires considerable attention.


Keywords:

Calcium homeostasis; Vitamin D Type 2 diabetes mellitus; Insulin


[ HTML Full Text]


Back to TOC