Influence of Vitamin D Status on Insulin Secretion and Glucose Tolerance in the Rabbit*

Endocrinology ◽  
1984 ◽  
Vol 115 (1) ◽  
pp. 191-197 ◽  
Author(s):  
BULANGU L. NYOMBA ◽  
ROGER BOUILLON ◽  
PIETER DE MOOR
1998 ◽  
Vol 79 (4) ◽  
pp. 315-327 ◽  
Author(s):  
B. J. Boucher

Environmental factors are important in the aetiology of glucose intolerance, type II diabetes and IHD. The lack of vitamin D, which is necessary for adequate insulin secretion, relates demographically to increased risk of myocardial infarction. These disorders are connected, degenerative vascular disease increasing with glucose intolerance and diabetes and, with its risk factors, comprising syndrome ‘X’. Evidence is presented suggesting that vitamin D deficiency may be an avoidable risk factor for syndrome ‘X’, adding another preventative measure to current recommendations which are aimed at reducing the worldwide epidemic of these disorders. Experimentally, vitamin D deficiency progressively reduces insulin secretion; glucose intolerance follows and becomes irreversible. Relationships between vitamin D status, glucose tolerance and 30 min insulin secretion during oral glucose tolerance tests are reported in British Asians; insulin secretion, but not glycaemia, improving with short-term supplementation. Studies showing reduction in blood pressure and in risk of heart attack and diabetes with exercise (usually outdoor), rarely consider the role of vitamin D status. Glycaemia and insulin secretion in elderly European men, however, relate to vitamin D status, independent of season or physical activity. Prolonged supplementation can improve glycaemia. Hypertension improves with vitamin D treatment with or without initial deficiency. Vitamin D status and climate are reviewed as risk factors for myocardial infarction; the risk reducing with altitude despite increasing cold. Glycaemia and fibrinogenaemia improve and insulin secretion increases in summer. Variation in vitamin D requirements could arise from genetic differences in vitamin D processing since bone density can vary with vitamin D-receptor genotype. Vitamin D receptors are present in islet β cells and we report insulin secretion in healthy Asians differing profoundly with the Apa I genotype, being independent of vitamin D status. Those at risk of vitamin D deficiency include the elderly, those living indoors or having a covered-up style of dress, especially dark-skinned immigrants, and pregnant women, and these are groups recognized as being at increased risk of diabetes.


2013 ◽  
Vol 33 (5) ◽  
pp. 349-357 ◽  
Author(s):  
Vanessa M. Kobza ◽  
James C. Fleet ◽  
Jing Zhou ◽  
Travis B. Conley ◽  
Munro Peacock ◽  
...  

Endocrine ◽  
2009 ◽  
Vol 36 (2) ◽  
pp. 205-210 ◽  
Author(s):  
Hataikarn Nimitphong ◽  
Suwannee Chanprasertyothin ◽  
Wallaya Jongjaroenprasert ◽  
Boonsong Ongphiphadhanakul

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Anna Pleskačová ◽  
Vendula Bartáková ◽  
Lukáš Pácal ◽  
Katarína Kuricová ◽  
Jana Bělobrádková ◽  
...  

Of many vitamin D extraskeletal functions, its modulatory role in insulin secretion and action is especially relevant for gestational diabetes mellitus (GDM). The aims of the present study were to determine midgestational and early postpartum vitamin D status in pregnant women with and without GDM and to describe the relationship between midgestational and postpartum vitamin D status and parallel changes of glucose tolerance. A total of 76 pregnant women (47 GDM and 29 healthy controls) were included in the study. Plasma levels of 25(OH)D were measured using an enzyme immunoassay. Vitamin D was not significantly decreased in GDM compared to controls during pregnancy; however, both groups of pregnant women exhibited high prevalence of vitamin D deficiency. Prevalence of postpartum 25(OH)D deficiency in post-GDM women remained significantly higher and their postpartum 25(OH)D levels were significantly lower compared to non-GDM counterparts. Finally, based on the oGTT repeated early postpartum persistent glucose abnormality was ascertained in 15% of post-GDM women; however, neither midgestational nor postpartum 25(OH)D levels significantly differed between subjects with GDM history and persistent postpartum glucose intolerance and those with normal glucose tolerance after delivery.


2019 ◽  
Vol 104 (9) ◽  
pp. 3785-3794
Author(s):  
Karen M Switkowski ◽  
Carlos A Camargo, ◽  
Patrice Perron ◽  
Sheryl L Rifas-Shiman ◽  
Emily Oken ◽  
...  

Abstract Context Vitamin D may be important for prenatal programming of insulin and glucose regulation, but maternal vitamin D deficiency during pregnancy is common. Objective We examined associations of early vitamin D status with markers of fetal insulin secretion: cord blood insulin and c-peptide. We hypothesized that maternal 25-hydroxyvitamin D (25(OH)D) during pregnancy and cord blood 25(OH)D would both be positively associated with cord blood insulin and c-peptide. Methods We studied mother-newborn pairs from two cohorts: Project Viva (n = 862 pairs included) and Genetics of Glucose Regulation in Gestation and Growth (Gen3G; n = 660 pairs included). We analyzed associations of the cord blood hormones with maternal 25(OH)D using generalized additive models with nonlinear spline terms, and with cord blood 25(OH)D using multivariable linear regression models. Results The 25(OH)D levels were <75 nmol/L in >70% of mothers and 85% of newborns. Maternal and cord blood 25(OH)D levels were correlated (Project Viva, r = 0.58; Gen3G, r = 0.37). Maternal 25(OH)D had an inverted-U–shaped relationship with cord blood insulin and c-peptide in both cohorts. Cord blood 25(OH)D had a linear relationship with the cord blood hormones. In fully adjusted models, each 10-nmol/L increase in cord blood 25(OH)D was associated with higher cord blood insulin and c-peptide concentrations: 3.7% (95% CI, 0.09 to 7.5) and 3.2% (95% CI, 0.8 to 5.6), respectively, in Project Viva; 2.2% (95% CI, −0.1 to 4.6) and 3.6% (95% CI, 1.0 to 6.3), respectively, in Gen3G. Conclusion Vitamin D may play a role in regulating fetal insulin secretion, potentially affecting glucose regulation and growth.


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