![]() of cholecalciferol or placebo daily for 4 weeks. In one trial, 92 early type 2 diabetics (defined by glycosylated hemoglobin ≥5.8% and 2-hour postprandial glucose ≥140 mg/dL) were randomized to receive 2,000 i.u. Of four recently published randomized trials, two demonstrate improvements in glycemic control. The use of vitamin D in patients already diagnosed with type 2 diabetes has also been investigated. Based on the results these five studies, patients at risk for development of type 2 diabetes may benefit from vitamin D supplementation. daily) that may not have been adequate over 89% of participants did not achieve normal levels of vitamin D by the end of the trial. One of these used only low doses of vitamin D (400 i.u. ![]() Two trials failed to show effect of vitamin D supplementation. ![]() of cholecalciferol compared to an increase in fasting glucose in the placebo group. In the third trial, subjects with impaired fasting glucose showed stability in fasting glucose levels after three years of daily supplementation of 700 i.u. A second trial showed improvement in insulin sensitivity and decreased fasting insulin levels in 81 vitamin D deficient subjects with baseline insulin resistance given 4,000 i.u. of cholecalciferol or placebo every 2 weeks after 6 weeks of followup. One study showed improved oral glucose tolerance and insulin sensitivity in 71 obese males supplementation with 120,000 i.u. Three of five randomized trials demonstrate improvements in insulin sensitivity with vitamin D supplementation in subjects with insulin resistance or impaired fasting glucose. Recent reviews and metaanalyses of clinical trials suggest a potential effect of vitamin D supplementation on the development of type 2 diabetes in high-risk individuals. Seasonal fluctuations in glycemic control in type 2 diabetics may also be due in part to fluctuations in vitamin D levels, though behavioral differences may also explain these findings. Many epidemiologic studies demonstrate an inverse relationship between 25-hydroxyvitamin D level and prevalence of type 2 diabetes. ![]() In vitamin D deficient animals, pancreatic β-cell dysfunction is noted, which is restored with vitamin D supplementation. Preclinical evidence for the role of vitamin D in insulin secretion and function includes the presence of vitamin D receptors in human pancreatic β-cells, the detection of 1- α-hydroxylase activity, and insulin gene transcription responsiveness to vitamin D in pancreatic β-cells. While some controversy exists over treatment targets in individuals with mild insufficiency of vitamin D especially for the purported extraskeletal effects of vitamin D supplementation, a significant amount of evidence suggests there may be some beneficial effect in using vitamin D supplementation for improvement in glucose metabolism and insulin signaling in patients with type 2 diabetes or impaired glucose tolerance. The prevalence of vitamin D insufficiency (defined as <30 mg/dL) in obese individuals ranges from 80–90%. High rates of vitamin D insufficiency and frank deficiency have been reported in obese individuals and in diabetics. Specific micronutrient deficiencies in obese individuals may also influence the development of type 2 diabetes. Increased insulin resistance, incretin hormone resistance, oxidative stress, pancreatic β-cell dysfunction, and genetic and behavioral factors all contribute to the development of diabetes in obese individuals. The causal relationship of obesity and diabetes is complex. The risk of type 2 diabetes is increased 4-fold in obese patients. The importance of certain micronutrients as cofactors in glucose metabolic pathways, pancreatic β-cell function and in the insulin signaling cascade suggests that deficiency in these micronutrients may play a role in the development of type 2 diabetes. Despite an excess of dietary calorie intake, obese individuals have relatively high rates of micronutrient deficiencies. Modern agriculture and food processing techniques lead to a relative reduction in the micronutrient content of common foods. The increased availability of low-cost, high-calorie, nutrient-poor foods over the past four decades is a key component to the rise in obesity worldwide. Multiple genetic, environmental and behavioral factors contribute to the increasing trend in obesity. ![]() Obesity is highly prevalent both in the United States and worldwide and is projected to surpass tobacco use as the most economically important modifiable risk factor in public health and disease. ![]()
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