Exploring the interplay between DHCR7, vitamin D deficiency, and type 2 diabetes mellitus (T2DM): a systematic review.
Autor: | Mohammedsaeed W; Department of Clinical Laboratory Sciences, Faculty of Applied Medical Science, Taibah University, 344, Postal Code 3000, Al-Madinah, Saudi Arabia. wmohammedsaeed@taibahu.edu.sa. |
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Jazyk: | angličtina |
Zdroj: | Molecular biology reports [Mol Biol Rep] 2024 Nov 06; Vol. 51 (1), pp. 1123. Date of Electronic Publication: 2024 Nov 06. |
DOI: | 10.1007/s11033-024-10072-z |
Abstrakt: | Type 2 diabetes mellitus (T2DM) is a growing global health concern. The pathogenesis of T2DM is multifactorial and intricate, involving a complex interplay of genetic predisposition, environmental factors, and molecular interactions. Vitamin D (circulating 25-hydroxyvitamin D concentration) regulates factors crucial for T2DM, including insulin secretion, sensitivity, and inflammation. Thus, vitamin D deficiency has been linked to poor health outcomes in T2DM patients. The cholesterol-synthesizing enzyme 7-dehydrocholesterol reductase (DHCR7) represents a critical regulatory switch between cholesterol and vitamin D3 synthesis. Recent findings suggest that the enzyme DHCR7 may indicate T2DM glycolipid metabolic disorder and is associated with deficient circulating vitamin D (circulating 25-hydroxyvitamin D concentration) status. In this PRISMA-guided systematic review, articles were sourced from two databases, namely, PubMed and Cochrane Library, to evaluate the impact of vitamin D deficiency in patients with T2DM and to explore the emerging role of DHCR7 in T2DM pathogenesis. Our findings strongly indicate a positive correlation between deficient vitamin D status and poor health outcomes in T2DM patients. Finally, this systematic review presents a novel perspective on T2DM development, focusing on the interplay between T2DM-associated hyperglycemia, expression of DHCR7, and abrogation of vitamin D synthesis. (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.) |
Databáze: | MEDLINE |
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