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      Cholecalciferol improves glycemic control in type 2 diabetic patients: a 6-month prospective interventional study

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          Abstract

          Background and purpose

          To investigate the effects of vitamin D supplementation on glucose homeostasis and lipid profile in type 2 diabetic patients who have vitamin D deficiency.

          Patients and methods

          One hundred twenty-five type 2 diabetic patients taking oral hypoglycemic agents as mono- or combination therapy were recruited from the diabetes and endocrinology clinic. Subject demographics, duration of diabetes, antidiabetic medication, body mass index (BMI), pulse, and blood pressure (BP) were assessed. Laboratory measurements of serum vitamin D3 level, hemoglobin A1c (HbA1c), fasting plasma glucose (FPG), and lipid profile were measured. Homeostatic model assessment-insulin resistance (HOMA-IR) was calculated whenever fasting insulin (FI) was available. Forty-one patients (27 males and 14 females) were started on cholecalciferol replacement–45,000 units once weekly for 8 weeks and then 22,500 units once weekly for 16 weeks. Calcium carbonate tablets 500 mg once daily were also prescribed for the initial 2 months of treatment. Measured variables were reassessed after 6 months of replacement therapy. During the trial, subjects were instructed not to change their diabetes drugs or lifestyle.

          Results

          No significant association was found between vitamin D3 level and any of the measured variables apart from a significant positive correlation with blood urea nitrogen. Vitamin D3 replacement was associated with a significant increase in its level (14.0±4.0 vs 31.0 vs 7.9 ng/mL, P<0.001). This was associated with a significant reduction of HbA1c (7.9±1.7 vs 7.4%±1.2%, P=0.001) and FPG (9.1±4.3 vs 7.9±2.4 mmol/L, P=0.034). Mean reduction of HbA1c was 0.54% and that of FPG was 1.22 mmol/L. FI, c-peptide and insulin resistance (IR) were reduced but this was statistically insignificant ( P=0.069, 0.376, 0.058, respectively). FI decreased by 22%, HOMA-IR by 27.6%, and c-peptide by 1.83%. Total cholesterol, low-density lipoprotein cholesterol, parathyroid hormone, alkaline phosphatase, serum creatinine, and pulse rate significantly decreased (4.3±0.9 vs 4.0±0.9 mmol/L, P=0.036; 2.5±0.8 vs 2.2±0.8 mmol/L, P=0.018; 4.6±2.1 vs 3.5±1.8 pmol/L, P=0.001; 82.1±26.2 vs 66.2±19.5 U/L, P<0.001; 74.6±15.6 vs 70.7±14.7 μmol/L, P=0.047; and 81.6±11.9 vs 77.5±12.0 bpm, P=0.045, respectively). Triglycerides and high-density lipoprotein cholesterol, both systolic and diastolic BP, and BMI did not show significant change.

          Conclusion

          Cholecalciferol helps improve blood glucose control and cholesterol profile in vitamin D3-deficient type 2 diabetic patients.

          Related collections

          Most cited references 27

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          1,25-Dihydroxyvitamin D(3) is a negative endocrine regulator of the renin-angiotensin system.

          Inappropriate activation of the renin-angiotensin system, which plays a central role in the regulation of blood pressure, electrolyte, and volume homeostasis, may represent a major risk factor for hypertension, heart attack, and stroke. Mounting evidence from clinical studies has demonstrated an inverse relationship between circulating vitamin D levels and the blood pressure and/or plasma renin activity, but the mechanism is not understood. We show here that renin expression and plasma angiotensin II production were increased severalfold in vitamin D receptor-null (VDR-null) mice, leading to hypertension, cardiac hypertrophy, and increased water intake. However, the salt- and volume-sensing mechanisms that control renin synthesis are still intact in the mutant mice. In wild-type mice, inhibition of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] synthesis also led to an increase in renin expression, whereas 1,25(OH)(2)D(3) injection led to renin suppression. We found that vitamin D regulation of renin expression was independent of calcium metabolism and that 1,25(OH)(2)D(3) markedly suppressed renin transcription by a VDR-mediated mechanism in cell cultures. Hence, 1,25(OH)(2)D(3) is a novel negative endocrine regulator of the renin-angiotensin system. Its apparent critical role in electrolytes, volume, and blood pressure homeostasis suggests that vitamin D analogues could help prevent or ameliorate hypertension.
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            Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.

            Low serum 25-hydroxyvitamin D (25(OH)D) has been shown to correlate with increased risk of type 2 diabetes. Small, observational studies suggest an action for vitamin D in improving insulin sensitivity and/or insulin secretion. The objective of the present study was to investigate the effect of improved vitamin D status on insulin resistance (IR), utilising randomised, controlled, double-blind intervention administering 100 microg (4000 IU) vitamin D(3) (n 42) or placebo (n 39) daily for 6 months to South Asian women, aged 23-68 years, living in Auckland, New Zealand. Subjects were insulin resistant - homeostasis model assessment 1 (HOMA1)>1.93 and had serum 25(OH)D concentration 25 microg (1000 IU)/d. The HOMA2 computer model was used to calculate outcomes. Median (25th, 75th percentiles) serum 25(OH)D(3) increased significantly from 21 (11, 40) to 75 (55, 84) nmol/l with supplementation. Significant improvements were seen in insulin sensitivity and IR (P = 0.003 and 0.02, respectively), and fasting insulin decreased (P = 0.02) with supplementation compared with placebo. There was no change in C-peptide with supplementation. IR was most improved when endpoint serum 25(OH)D reached > or = 80 nmol/l. Secondary outcome variables (lipid profile and high sensitivity C-reactive protein) were not affected by supplementation. In conclusion, improving vitamin D status in insulin resistant women resulted in improved IR and sensitivity, but no change in insulin secretion. Optimal vitamin D concentrations for reducing IR were shown to be 80-119 nmol/l, providing further evidence for an increase in the recommended adequate levels. Registered Trial No. ACTRN12607000642482.
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              Selective vitamin D receptor activation with paricalcitol for reduction of albuminuria in patients with type 2 diabetes (VITAL study): a randomised controlled trial.

              Despite treatment with renin–angiotensin–aldosterone system (RAAS) inhibitors, patients with diabetes have increased risk of progressive renal failure that correlates with albuminuria. We aimed to assess whether paricalcitol could be used to reduce albuminuria in patients with diabetic nephropathy. In this multinational, placebo-controlled, double-blind trial, we enrolled patients with type 2 diabetes and albuminuria who were receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Patients were assigned (1:1:1) by computer-generated randomisation sequence to receive 24 weeks’ treatment with placebo,1 μg/day paricalcitol, or 2 μg/day paricalcitol. The primary endpoint was the percentage change in geometric mean urinary albumin-to-creatinine ratio (UACR) from baseline to last measurement during treatment for the combined paricalcitol groups versus the placebo group. Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00421733. Between February, 2007, and October, 2008, 281 patients were enrolled and assigned to receive placebo(n=93), 1 μg paricalcitol (n=93), or 2 μg paricalcitol (n=95); 88 patients on placebo, 92 on 1 μg paricalcitol, and 92 on2 μg paricalcitol received at least one dose of study drug, and had UACR data at baseline and at least one timepoint during treatment, and so were included in the primary analysis. Change in UACR was: –3% (from 61 to 60 mg/mmol;95% CI –16 to 13) in the placebo group; –16% (from 62 to 51 mg/mmol; –24 to –9) in the combined paricalcitol groups, with a between-group difference versus placebo of –15% (95% CI –28 to 1; p=0.071); –14% (from 63 to 54 mg/mmol; –24 to –1) in the 1 μg paricalcitol group, with a between-group difference versus placebo of –11%(95% CI –27 to 8; p=0.23); and –20% (from 61 to 49 mg/mmol; –30 to –8) in the 2 μg paricalcitol group, with a between-group difference versus placebo of –18% (95% CI –32 to 0; p=0.053). Patients on 2 μg paricalcitol showed a nearly, sustained reduction in UACR, ranging from –18% to –28% (p=0.014 vs placebo). Incidence of hypercalcaemia,adverse events, and serious adverse events was similar between groups receiving paricalcitol versus placebo. Addition of 2 μg/day paricalcitol to RAAS inhibition safely lowers residual albuminuria in patients with diabetic nephropathy, and could be a novel approach to lower residual renal risk in diabetes. Abbott.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2017
                07 July 2017
                : 13
                : 813-820
                Affiliations
                [1 ]Faculty of Medicine, Department of Internal Medicine
                [2 ]Faculty of Medicine, Department of Medical Biochemistry, Mansoura University, Mansoura, Egypt
                Author notes
                Correspondence: Aml Mohamed Nada, Faculty of Medicine, Department of Internal Medicine, Mansoura University, El Gomhouria St, Mansoura, Dakahlia 35516, Egypt, Email aml_nadanoha@ 123456yahoo.com
                Article
                tcrm-13-813
                10.2147/TCRM.S132344
                5508814
                © 2017 Nada and Shaheen. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Medicine

                parathyroid hormone, creatinine, cholesterol, hba1c, type 2 diabetes, vitamin d

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