The role of vitamin D in the development of type 2 diabetes

2021 ◽  
Vol 19 (1) ◽  
pp. 44-52
Author(s):  
A.P. Shumilov ◽  
◽  
M.Yu. Semchenkova ◽  
D.S. Mikhalik ◽  
T.G. Avdeeva ◽  
...  

Vitamin D plays an important role in decreasing the risk of developing type 2 diabetes by influencing calcium metabolism, thereby reducing β-cell dysfunction and preventing insulin resistance. The findings of research works are contradictory enough, although some of them demonstrated an inverse relationship between vitamin D levels and the incidence of type 2 diabetes. The article describes the biological mechanisms of relationships between vitamin D levels and type 2 diabetes, reviews the results of the studies conducted and summarizes the available data. Key words: vitamin D, type 2 diabetes mellitus, insulin resistance

Author(s):  
Froylan David Martínez-Sánchez ◽  
Valerie Paola Vargas-Abonce ◽  
Andrea Rocha-Haro ◽  
Romina Flores-Cardenas ◽  
Milagros Fernández-Barrio ◽  
...  

2007 ◽  
Vol 292 (6) ◽  
pp. E1694-E1701 ◽  
Author(s):  
Jane J. Kim ◽  
Yoshiaki Kido ◽  
Philipp E. Scherer ◽  
Morris F. White ◽  
Domenico Accili

Type 2 diabetes results from impaired insulin action and β-cell dysfunction. There are at least two components to β-cell dysfunction: impaired insulin secretion and decreased β-cell mass. To analyze how these two variables contribute to the progressive deterioration of metabolic control seen in diabetes, we asked whether mice with impaired β-cell growth due to Irs2 ablation would be able to mount a compensatory response in the background of insulin resistance caused by Insr haploinsufficiency. As previously reported, ∼70% of mice with combined Insr and Irs2 mutations developed diabetes as a consequence of markedly decreased β-cell mass. In the initial phases of the disease, we observed a robust increase in circulating insulin levels, even as β-cell mass gradually declined, indicating that replication-defective β-cells compensate for insulin resistance by increasing insulin secretion. These data provide further evidence for a heterogeneous β-cell response to insulin resistance, in which compensation can be temporarily achieved by increasing function when mass is limited. The eventual failure of compensatory insulin secretion suggests that a comprehensive treatment of β-cell dysfunction in type 2 diabetes should positively affect both aspects of β-cell physiology.


2020 ◽  
Vol 14 (1) ◽  
pp. 39-45
Author(s):  
Noor Thair Tahir ◽  
Hind SH. Ahmed ◽  
Rasha K. Hashim ◽  
Teba D. Soluiman

Background: Obesity and type 2 diabetes have both rapidly raised during the last periods and are ongoing to increase at a disturbing rate universal. Several clinical and epidemiological researches demonstrated a reverse association between circulating vitamin D levels, central adiposity and the progress of insulin resistance and diabetes. Objective: The target of this work was to elucidate the complex role of vitamin D and the clinical implications of diabetes on metabolic defects related with obesity. Subjects and Methods: This study encompassed 90 diabetic patients (45 obese and 45 non obese) who were attending the National Diabetic Center/ Al-Mustansiriyah University during the period from June 2019 to January 2020; their age range was (35-60) years. All participant underwent clinical and biochemical examinations. Results: A substantial rise (p= 0.01) in waist/hip ratio, body mass index, fasting serum glucose, total cholesterol, triacylglycerol, and low density lipoprotein cholesterol in obese diabetic patients as paralleled to non-obese group. Moreover, there was an elevation in glycated hemoglobin, serum insulin, and homeostasis model assessment for insulin resistance in obese group, but it was not significant. A substantial decrease (p= 0.01) in serum high density lipoprotein cholesterol and vitamin D3 were detected in obese diabetic patients as paralleled to non-obese group.       Also, obese diabetic patients had the higher percent (61%) of D3 deficiency as paralleled to non-obese patients. Conclusions: In the present study, it is found that there is significant increase in blood sugar in the individuals with decreased vitamin D levels, which was related with insulin resistance, decreased β-cell function, and obesity.  


Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2475
Author(s):  
Melvin R. Hayden

The novel coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was declared a pandemic by the WHO on 19 March 2020. This pandemic is associated with markedly elevated blood glucose levels and a remarkable degree of insulin resistance, which suggests pancreatic islet β-cell dysfunction or apoptosis and insulin’s inability to dispose of glucose into cellular tissues. Diabetes is known to be one of the top pre-existing co-morbidities associated with the severity of COVID-19 along with hypertension, cardiocerebrovascular disease, advanced age, male gender, and recently obesity. This review focuses on how COVID-19 may be responsible for the accelerated development of type 2 diabetes mellitus (T2DM) as one of its acute and suspected long-term complications. These observations implicate an active role of metabolic syndrome, systemic and tissue islet renin–angiotensin–aldosterone system, redox stress, inflammation, islet fibrosis, amyloid deposition along with β-cell dysfunction and apoptosis in those who develop T2DM. Utilizing light and electron microscopy in preclinical rodent models and human islets may help to better understand how COVID-19 accelerates islet and β-cell injury and remodeling to result in the long-term complications of T2DM.


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