Abstract
Vitamin D has been suggested to play a role in glucose metabolism. However, previous findings are contradictory and mechanistic pathways remain unclear. We examined the relationship between plasma 25-hydroxyvitamin D (25(OH)D), insulin sensitivity, and insulin signaling in skeletal muscle and adipose tissue. Seventeen healthy adults (Body mass index: 26 ± 4; Age: 30 ± 12 years) underwent a hyperinsulinemic-euglycemic clamp, and resting skeletal muscle and adipose tissue biopsies. In this cohort, the plasma 25(OH)D concentration was not associated with insulin sensitivity (r = 0.19, p = 0.56). However, higher plasma 25(OH)D concentrations correlated with lower phosphorylation of glycogen synthase kinase-3 (GSK-3) αSer21 and βSer9 in skeletal muscle (r = −0.66, p = 0.015 and r = −0.53, p = 0.06, respectively) and higher GSK-3 αSer21 and βSer9 phosphorylation in adipose tissue (r = 0.82, p < 0.01 and r = 0.62, p = 0.042, respectively). Furthermore, higher plasma 25(OH)D concentrations were associated with greater phosphorylation of both protein kinase-B (AktSer473) (r = 0.78, p < 0.001) and insulin receptor substrate-1 (IRS-1Ser312) (r = 0.71, p = 0.01) in adipose tissue. No associations were found between plasma 25(OH)D concentration and IRS-1Tyr612 phosphorylation in skeletal muscle and adipose tissue. The divergent findings between muscle and adipose tissue with regard to the association between 25(OH)D and insulin signaling proteins may suggest a tissue-specific interaction with varying effects on glucose homeostasis. Further research is required to elucidate the physiological relevance of 25(OH)D in each tissue.
Highlights
Vitamin D, in its hydroxylated form, 25-hydroxyvitamin D (25(OH)D), and its biologically active form, 1,25-dihydroxyvitamin D (1,25(OH)2 D), is an important regulator of calcium, phosphorus, and bone metabolism [1]
Previous reports indicate that vitamin D supplementation in high-fat diet–fed mice attenuates weight gain and increases transcriptional activity of the insulin receptor substrate-1 (IRS-1) in skeletal muscle but not adipose tissue [18]
The aim of this study was to test the hypothesis that vitamin D status and 25(OH)D in humans is related to insulin signaling proteins in both skeletal muscle and adipose tissue
Summary
Vitamin D, in its hydroxylated form, 25-hydroxyvitamin D (25(OH)D), and its biologically active form, 1,25-dihydroxyvitamin D (1,25(OH) D), is an important regulator of calcium, phosphorus, and bone metabolism [1]. Potential cellular pathways are unclear, but may occur through direct binding of vitamin D to vitamin D receptors and activation of downstream signaling proteins; through increased gene expression of the insulin receptor; and indirectly through calcium regulation and subsequent downstream effects on glucose homeostasis signaling proteins [14,15,16,17]. Previous reports indicate that vitamin D supplementation in high-fat diet–fed mice attenuates weight gain and increases transcriptional activity of the insulin receptor substrate-1 (IRS-1) in skeletal muscle but not adipose tissue [18]. 1,25(OH) D participates in skeletal muscle cell proliferation and differentiation through a phosphoinositide 3-kinase/Akt-dependent signaling pathway [20] that is known to regulate glycemic control [21]. The aim of this study was to test the hypothesis that vitamin D status and 25(OH)D in humans is related to insulin signaling proteins in both skeletal muscle and adipose tissue
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