Background and objectives: Vitamin D is involved in insulin resistance through genomic and non-genomic mechanisms. Several observational and randomized studies have discrepant results; some of them showed an improved insulin resistance (IR), and others a neutral effect after vitamin D deficiency is corrected. Materials and Methods: We designed a retrospective observational study that included all women who presented for 33 months in an outpatient clinic in Bucharest, Romania. Results: We analyzed 353 patients with a mean age of 58.5 ± 13.7 years, a mean body mass index (BMI) of 27.36 ± 4.87 kg/m-2, and a mean level of 25-hydroxyvitamin D (25OHD) of 39.53 ± 15.73 ng/mL. There were no differences in the calculated Homeostatic Model Assessment of Insulin Resistance variants 1 and 2 (HOMA-IR) and the Quantitative Insulin Sensitivity Check Index (QUICKI) between women with vitamin D deficit versus normal values. In multivariate analysis, there was no significant relation between 25OHD and the response variables considered by us. Conclusions: We observed a small positive correlation between a higher level of 25OHD and increased glycosylated hemolobin (HbA1c) or IR indices without clinical significance. Other modifiable or non-modifiable factors override 25OHD influence on IR in adult women with a normal serum level and may contribute to the remainder of the variability observed.
Background and objectives: Vitamin D is involved in insulin resistance through genomic and non-genomic mechanisms. Several observational and randomized studies have discrepant results; some of them showed an improved insulin resistance (IR), and others a neutral effect after vitamin D deficiency is corrected. Materials and Methods: We designed a retrospective observational study that included all women who presented for 33 months in an outpatient clinic in Bucharest, Romania. Results: We analyzed 353 patients with a mean age of 58.5 ± 13.7 years, a mean body mass index (BMI) of 27.36 ± 4.87 kg/m-2, and a mean level of 25-hydroxyvitamin D (25OHD) of 39.53 ± 15.73 ng/mL. There were no differences in the calculated Homeostatic Model Assessment of Insulin Resistance variants 1 and 2 (HOMA-IR) and the Quantitative Insulin Sensitivity Check Index (QUICKI) between women with vitamin D deficit versus normal values. In multivariate analysis, there was no significant relation between 25OHD and the response variables considered by us. Conclusions: We observed a small positive correlation between a higher level of 25OHD and increased glycosylated hemolobin (HbA1c) or IR indices without clinical significance. Other modifiable or non-modifiable factors override 25OHD influence on IR in adult women with a normal serum level and may contribute to the remainder of the variability observed.
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