Abbasi Fahim, Blasey Christine, Feldman David, Caulfield Michael P, Hantash Feras M, Reaven Gerald M
Divisions of Cardiovascular Medicine and
Department of Psychiatry, Stanford University School of Medicine, Stanford, CA; and.
J Nutr. 2015 Apr;145(4):714-9. doi: 10.3945/jn.114.209171. Epub 2015 Mar 4.
Individuals with prediabetes mellitus (PreDM) and low circulating 25-hydroxyvitamin D [25(OH)D] are at increased risk of type 2 diabetes mellitus (T2DM).
We aimed to determine whether low 25(OH)D concentrations are associated with defects in insulin action and insulin secretion in persons with PreDM.
In this cross-sectional study, we stratified 488 nondiabetic subjects as having PreDM or normal fasting glucose (NFG) and a 25(OH)D concentration ≤20 ng/mL (deficient) or >20 ng/mL (sufficient). We determined insulin resistance by steady state plasma glucose (SSPG) concentration and homeostasis model assessment of insulin resistance (HOMA-IR) and insulin secretion by homeostasis model assessment of β-cell function (HOMA-β). We compared insulin resistance and secretion measures in PreDM and NFG groups; 25(OH)D-deficient and 25(OH)D-sufficient groups; and PreDM-deficient, PreDM-sufficient, NFG-deficient, and NFG-sufficient subgroups, adjusting for age, sex, race, body mass index, multivitamin use, and season.
In the PreDM group, mean SSPG concentration and HOMA-IR were higher and mean HOMA-β was lower than in the NFG group (P < 0.001 for all comparisons). In the 25(OH)D-deficient group, mean SSPG concentration was higher (P < 0.001), but neither mean HOMA-IR nor HOMA-β was significantly different from that in the 25(OH)D-sufficient group. In the PreDM-deficient subgroup, mean (95% CI) SSPG concentration was higher (P < 0.01) than in the PreDM-sufficient, NFG-deficient, and NFG-sufficient subgroups [192 (177-207) mg/dL vs. 166 (155-177) mg/dL, 148 (138-159) mg/dL, and 136 (127-144) mg/dL, respectively]. Despite greater insulin resistance, mean HOMA-β was not significantly higher in the PreDM-deficient subgroup than in the PreDM-sufficient, NFG-deficient, and NFG-sufficient subgroups [98 (85-112) vs. 91 (82-101), 123 (112-136), and 115 (106-124), respectively].
Subjects with PreDM and low circulating 25(OH)D concentrations are the subgroup of nondiabetic individuals who are the most insulin resistant and have impaired β-cell function, attributes that put them at enhanced risk of T2DM.
患有糖尿病前期（PreDM）且循环25-羟基维生素D [25(OH)D]水平较低的个体患2型糖尿病（T2DM）的风险增加。
我们旨在确定25(OH)D浓度低是否与糖尿病前期患者的胰岛素作用和胰岛素分泌缺陷有关。
在这项横断面研究中，我们将488名非糖尿病受试者分为患有糖尿病前期或空腹血糖正常（NFG），且25(OH)D浓度≤20 ng/mL（缺乏）或>20 ng/mL（充足）。我们通过稳态血浆葡萄糖（SSPG）浓度和胰岛素抵抗稳态模型评估（HOMA-IR）来确定胰岛素抵抗，并通过β细胞功能稳态模型评估（HOMA-β）来确定胰岛素分泌。我们比较了糖尿病前期和NFG组；25(OH)D缺乏和25(OH)D充足组；以及糖尿病前期缺乏、糖尿病前期充足、NFG缺乏和NFG充足亚组的胰岛素抵抗和分泌指标，并对年龄、性别、种族、体重指数、复合维生素使用情况和季节进行了校正。
在糖尿病前期组中，平均SSPG浓度和HOMA-IR高于NFG组，平均HOMA-β低于NFG组（所有比较P<0.001）。在25(OH)D缺乏组中，平均SSPG浓度较高（P<0.001），但平均HOMA-IR和HOMA-β与25(OH)D充足组相比无显著差异。在糖尿病前期缺乏亚组中，平均（95%CI）SSPG浓度高于糖尿病前期充足、NFG缺乏和NFG充足亚组（P<0.01）[分别为192（177-207）mg/dL vs. 166（155-177）mg/dL、148（138-159）mg/dL和136（127-144）mg/dL]。尽管胰岛素抵抗更大，但糖尿病前期缺乏亚组的平均HOMA-β并不显著高于糖尿病前期充足、NFG缺乏和NFG充足亚组[分别为98（85-112）vs. 91（82-101）、123（112-136）和115（106-124）]。
患有糖尿病前期且循环25(OH)D浓度低的受试者是非糖尿病个体中胰岛素抵抗最强且β细胞功能受损的亚组，这些特征使他们患2型糖尿病的风险增加。
