Résumé:
Type 2 diabetes (T2D) is amongst the most highly prevalent diseases in the world, and it is caused mostly by a combination of two fundamental factors: Insulin insufficiency is caused by a lack of pancreatic β-cell secretion and insulin-responsive tissue sensitivity. Vitamin D is a prehormone that is mostly produced at the epidermal level by ultraviolet B radiation action from its precursor, 7-dehydrocholestérol. It has lately attracted extensive attention in diabetes causation and prevention. Through its active form, calcitriol, vitamin D may play an important role in maintaining pancreatic β-cell function. There may be different explanations for this effect. It can be induced by activating VDR located on the phospholipid layer of the plasma membrane of pancreatic β-cells, muscle cell and adipocyte. Significant evidence exists to suggest the relationship between vitamin D insufficiency and T2D. This relationship is mediated by vitamin D's direct and indirect effects on insulin production, insulin sensitivity, and systemic inflammation.
The goal of this study is to determine if there is a link between vitamin D and T2D. A total of 55 people with T2D, aged 40 to 84 years, who attended analysis medical laboratory of Dr. Ettalhi for a diabetic examination between March and June 2022. We primarily attempted to link vitamin D levels with glycated hemoglobin (HbA1c) levels. The results showed that 72.7% of the 55 patients had a deficient vitamin D level and 27.3% had a vitamin D level in the insufficiency range, while HbA1C levels were found to be greater than normal in all T2D patients. We observed an inverse relationship between HbA1c and vitamin D. whereas, we concluded that Vitamin D was found to be strongly associated to glycemic control. Thus, when deficient or insufficient levels of vitamin D are identified in T2D patients, supplementation should be investigated since it may assist to improve glycemic control.
