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The Capital Region of Denmark - a part of Copenhagen University Hospital
E-pub ahead of print

Vitamin D supplementation improves fasting insulin levels and HDL cholesterol in infertile men

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CONTEXT: Vitamin D has been linked with glucose and lipid metabolism. Men with impaired gonadal function have a higher risk of metabolic syndrome and mortality, and vitamin D status may be a reversible modulator.

OBJECTIVE: Determine the effect of daily vitamin D and calcium supplementation for 150 days on glucose and lipid homeostasis in infertile men.

DESIGN: A single-center, double-blinded, randomized clinical trial (NCT01304927), 307 infertile men were randomized (1:1) to a single dose of 300,000 IU cholecalciferol followed by 1,400 IU cholecalciferol + 500 mg of calcium daily (n=151) or placebo (n=156) for 150 days. Reported metabolic parameters including fasting plasma glucose, HbA1c, fasting serum insulin, homeostatic model assessment of insulin resistance (HOMA-IR), fasting plasma cholesterols and triglyceride were secondary endpoints. The primary endpoint semen quality has previously been reported.

RESULTS: Men receiving vitamin D supplementation improved their vitamin D status, while vitamin D status was aggravated in the placebo group characterized by higher serum parathyroid hormone (PTH). At end of trial, men receiving vitamin D supplementation had 13% lower fasting serum insulin concentrations compared with the placebo-treated group (65 vs. 74 pmol/L, P = 0.018) and 19% lower HOMA-IR (2.2 vs. 2.7, P = 0.025). Moreover, men in the vitamin D group had higher high-density lipoprotein (HDL) cholesterol levels (1.38 vs. 1.32 mmol/L, P = 0.008) compared with the placebo group.

CONCLUSION: High-dose vitamin D supplementation had beneficial effects on glucose homeostasis and HDL cholesterol levels in infertile men.

Original languageEnglish
JournalThe Journal of clinical endocrinology and metabolism
ISSN0021-972X
DOIs
Publication statusE-pub ahead of print - 11 Sep 2021

Bibliographical note

© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

ID: 67899131