Diabetes Care：肥胖、缺维生素D可诱发胰岛素耐受

一个肥胖的人再加上缺乏维生素D，那么就会有更高的胰岛素耐受风险。而胰岛素耐受是2型糖尿病的主要危险因素，2型糖尿病是全球的第八大死因，困扰着2560万美国人和9240万中国人。相关论文发表在Diabetes Care杂志上。

“维生素D的缺乏和肥胖加重胰岛素耐受及个人罹患糖尿病危险程度，”流行病学博士，该文章首席作者Shaum Kabadi说：“我们的研究表明，这两个因素的结合增加胰岛素耐受的的可能性远大于其各自预计贡献值。”

在这项研究中，具有健康维生素D水平的肥胖个体，其具有胰岛素耐受的数量是平均水平的20倍，而具有较低维生素D水平的肥胖个体则是平均水平的32倍以上。

虽然并不清楚是否肥胖本身导致了低维生素D水平还是其他因素。维生素D容易在体内脂肪组织内堆积储存，储存在脂肪组织中的维生素D一般不容易被机体直接获取利用。因此，理论上来讲，肥胖的人可能因此出现血液中较低的维生素D水平。而维生素D又和糖尿病相关的心血管疾病、中风、抑郁症相联系。

这篇发表在Diabetes Care上的研究报道并不是第一个关注维生素D与糖尿病之间关联的文章，之前多伦多大学的Sheena Kayaniyil博士也认可这个结论。

为期三年的研究，涉及患有高血糖的2039人。在研究开始6个月，一年，两年，三年后，对他们的维生素D水平进行测定。

对于每增加5微克每毫升(ng / mL的)维生素D的水平，就下降了8%罹患糖尿病的风险。Pittas博士说，增加30微克每毫升或更高的水平都属正常。

学员们分成三组。组中的参与者中维生素D水平比最高水平高三分之一(约30毫微克/毫升的平均读数)比最低水平低三分之一的参与者(平均维生素D水平的13毫微克/毫升)发展为糖尿病的可能性要低38%。

该文章作者表示，补充维生素D或将是个廉价易取的预防糖尿病的手段，其困难程度要比让肥胖者减轻体重容易的多。

doi: 10.2337/dc12-0235
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Joint Effects of Obesity and Vitamin D Insufficiency on Insulin Resistance and Type 2 Diabetes

Shaum M. Kabadi, MPH?, Brian K. Lee, PHD and Longjian Liu, MD, PHD, MSC

OBJECTIVE The possible interaction of serum 25-hydroxyvitamin D [25(OH)D] and obesity in regard to type 2 diabetes and insulin resistance has not been well studied. To explore the effect modification of obesity on the association between 25(OH)D and insulin resistance/type 2 diabetes, data were examined from a nationally representative sample.

RESEARCH DESIGN AND METHODS The analytic sample for the type 2 diabetes analysis (n = 12,900) was limited to participants from the National Health and Nutrition Examination Survey (NHANES) 2001–2006 over 20 years of age. Participants >20 years of age assigned to the morning session and free of diabetes were limited to the insulin resistance analysis (n = 5,806). Multiplicative interaction was assessed through a cross-product interaction term in a multiple logistic regression model. The presence of additive interaction between insufficient 25(OH)D and obesity (indicated by BMI or waist circumference) was evaluated by calculation of the relative excess risk due to interaction (RERI) and attributable proportion due to interaction (AP).

RESULTS There was no multiplicative interaction of insufficient 25(OH)D and obesity on type 2 diabetes or insulin resistance. Furthermore, none of the RERI or AP values were statistically significant in the diabetes analysis. However, there was strong additive interaction between abdominal obesity and insufficient 25(OH)D (RERI 6.45 [95% CI 1.03–11.52]) in regard to insulin resistance. In addition, 47% of the increased odds of insulin resistance can be explained by interaction between insufficient 25(OH)D and high BMI (AP 0.47 [95% CI 0.08–0.87]).

CONCLUSIONS Within a cross-sectional, nationally representative sample, abdominal obesity and insufficient 25(OH)D interact to synergistically influence the risk of insulin resistance.