Vitamin D supplementation improves SIRT1, Irisin, and glucose indices in overweight or obese type 2 diabetic patients: a double-blind randomized placebo-controlled clinical trial.

Peivasteh Safarpour, Milad Daneshi-Maskooni, Mohammadreza Vafa, Mitra Nourbakhsh, Leila Janani, Mohsen Maddah, Fatemeh-Sadat Amiri, Fereshteh Mohammadi, Homa Sadeghi

Journal: BMC family practice 2020;21(1):26

PMID: 32033527

Plain Language Summary

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Type 2 diabetes (T2D) is often preceded by a condition known as insulin resistance (IR). Recent studies have shown that low levels of vitamin D in the body are related to an increased incidence of IR and individuals with T2D have lower levels of vitamin D than healthy individuals. Vitamin D may have the ability to increase enzymes in the body that breakdown sugar and decrease IR. This 12-month double blind randomised control trial on 90 obese type 2 diabetics, aimed to assess the effects of vitamin D on these enzymes and blood sugar levels. The results showed that individuals on vitamin D had significantly increased enzymes which are involved in sugar breakdown and this translated into improved blood sugar levels, however this did not translate into improved markers for IR. It was concluded that compared to placebo, vitamin D supplementation improved blood sugar levels possibly due to the increase in enzymes involved in sugar breakdown. Healthcare professionals could use this study to recommend vitamin D supplementation to obese type 2 diabetics to improve their blood sugar levels.

Abstract

BACKGROUND

Vitamin D (VD) may increase sirtuin 1 (SIRT1) and subsequently PPAR-γ coactivator 1α (PGC-1α) and irisin levels and these improvements may reduce insulin resistance (IR). The aim was to assess the effects of vitamin D supplementation on SIRT1, irisin, and IR in overweight/obese type 2 diabetes (T2D) patients.

METHODS

Ninety T2D males and females were recruited as a clinical trial study (mean of age and body mass index (BMI) of intervention and placebo groups were 50.05 ± 10.17 and 50.36 ± 10.2 yrs. and 31.37 ± 3.4 and 30.43 ± 3.2 kg/m, respectively). The inclusion criteria were T2D, VD deficient, BMI > 25 kg/m, and serum HbA1c < 8.5%. The exclusion criteria were using vitamin and mineral supplements, having any acute disease, recent modifying dose or type of drugs. The supplementation was 50,000 IU/week VD or placebo for 8 weeks. The demographic characteristics, anthropometrics, dietary intakes and physical activity status, sun exposure status, fasting blood sugar (FBS) and insulin, glycosylated hemoglobin (HbA1c), irisin, SIRT1, 25-hydroxy D3 (25(OH)VD), homeostasis model assessment of insulin resistance (HOMA-IR), and quantitative insulin sensitivity check index (QUICKI) were determined. The significant P-value was ≤0.05.

RESULTS

The increase of serum VD, SIRT1, and irisin in the intervention group was significant (p < 0.001). HbA1c was decreased significantly by 1%. The changes in the other glucose indices (FBS, insulin, and IR) were non-significant.

CONCLUSIONS

VD supplementation may improve T2D by decreasing HbA1c and increasing SIRT1 and irisin in VD deficient T2D patients. Further trials are suggested.

TRIAL REGISTRATION

Iranian Registry of Clinical Trials, IRCT201604202365N11. Registered 21/08/2016, http://en.irct.ir/trial/2019.

Address: Department of Nutrition, School of Public Health, Iran University of Medical Sciences, Tehran, Iran.; Department of Nutrition, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Kerman, Iran.; Department of Nutrition, School of Public Health, Iran University of Medical Sciences, Tehran, Iran. [email protected].; Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.; Department of Biostatistics, School of Public Health, Preventive Medicine and Public Health Research Center, Iran University of Medical Sciences, Tehran, Iran.; Department of Medicine, School of Medicine, Guilan University of Medical Sciences, Guilan, Iran.; Department of Epidemiology, University of Massachusetts Lowell, Lowell, MA, USA.
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