Deficiency of Vitamin D, Immune System Function and Glucose Control in Non-Insulin Dependent Diabetic Patients

Fatwa M Al-Shred*

¹Department of Medical Laboratory Technology, King Abdulaziz University, Saudi Arabia

*Corresponding author: Fadwa M. Al-Shreef, Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia

Received: January 17, 2019; Accepted: February 21, 2019; Published: February 28, 2019

Abstract

Background: Recently, Vitamin D (25-OHD) deficiency is a global pandemic medical problem, which usually associated with high risk of osteoporosis, Non-Insulin Dependent Diabetes Mellitus (NIDDM), different types of cancer, autoimmune and cardiovascular disorders.

Objective: This study designed to measure the association between Vitamin D deficiency, immune system function and glucose control in non-insulin dependent diabetic patients. Material and Methods: Two hundred fifty seven noninsulin dependent diabetic Saudi patients (163 females and 94 males), treated with oral hypoglycemic medications (e.g. pioglitazone and/or metformin), their chronicity of diabetes was 11.68±2.97 years, the mean of their Body Mass Index (BMI) was 32.51±2.94 kg/m². However, smokers, pregnant women and patients with hepatic, renal, respiratory and heart failure were excluded. According to the level of 25-OHD levels, participants were enrolled in 3 groups: Vitamin D deficiency group (I) with 25-OHD less than 20 ng/ml (Vitamin D deficiency), group (II) with 25-OHD =20–30 ng/ml (Vitamin D insufficiency) and group (III) with 25-OHD greater than 30 ng/ml (normal Vitamin D).

Results: Concerning parameters of blood glucose control, results revealed higher significant values of the Quantitative Insulin-Sensitivity Check Index (QUICKI) in group (III) compared to group (II) and group (I) in addition to lower values of both Homeostasis Model Assessment (HOMA-IR) and glycosylated hemoglobin (HBA1c) in group (III) compared to group (II) and group (I). However, parameters of immune system results revealed higher significant values of the number of white blood cells, monocytes, total neutrophil count, CD3, CD4 and CD8 in group (I) compared to group (II) and group (III) (P‹0.05). However, there was a strong inverse relationship between 25-OHD & HOM-IR, HBA1c, WBCs, total neutrophil, monocytes, CD3, CD4 and CD8 count in addition to a strong direct relationship between 25-OHD & QUICKI in the three groups (P‹0.05).

Conclusion: This study provides evidence that Vitamin D deficiency adversely affects immune system and glucose control among non-insulin dependent diabetic patients.

Keywords: Glucose control; Immune system; Non-insulin dependent diabetes; Vitamin D

Introduction

Vitamin D (25-OHD) deficiency is global medical problem specially in Middle east and Asia [1]. Many studies confirmed the association between status of 25-OHD with cardiovascular diseases and diabetes-related out-comes [2-7] as there was a negative relation between diabetes prevalence and status of Vitamin D [8,9].

Insulin resistance and systemic inflammation are usually associated with diabetes [10], therefore 25-OHD improves islet-cell functions and as a result reduces insulin resistance and its antiinflammatory action [11-14] that means 25-OHD deficiency facilitates development of diabetes and reduce responses to medications [15- 18].

Vitamin D is important for many physiological processes regulation as homeostasis of calcium, muscle and bone health [19]. Therefore, this study aimed to measure the association between 25- OHD deficiency, immune system function and glucose control in patients with NIDDM.

Material and Methods

Subjects

Two hundred fifty seven NIDDM Saudi patients (164 females and 93 males), treated with oral hypoglycemic medications (e.g. pioglitazone and/or metformin), their chronicity of diabetes was 11.25±4.73 years, the mean of their Body Mass Index (BMI) was 32.86±2.94 kg/m2. However, smokers, pregnant women and patients with hepatic, renal, respiratory and heart failure were excluded. According to the level of 25-OHD levels, participants were enrolled in 3 groups: group (I) with 25-OHD less than 20 ng/ml (Vitamin D deficiency), group (II) with 25-OHD=20-30 ng/ml (Vitamin D insufficiency) and group (III) with 25-OHD greater than 30 ng/ml (normal Vitamin D). All participants signed informed consent before sharing in this study.

Measurements

A. Measurement of 25-hydroxyVitamin D (25-OHD) was undertaken using the commercial kit RIA (Elisa Kit; DiaSorin, Stillwater, MN, USA) [20,21].

B. Immune system parameters (CD3, CD4 and CD8): Flow cytometry using Cytomics FC500 and CXP software (Beckman Coulter) was used to measure the leukocyte differentiation antigens CD3, CD4 and CD8 (Beckman Coulter, Marseille, France). However, Beckman Coulter AcT 5diff hematology analyzer was used in analysis of peripheral blood cells (The number of white blood cells (WBCs), total neutrophil count and monocytes).

C. Serum glucose control: Concentration of plasma insulin and glucose undertaken using the commercial available kits (Roche Diagnostics GmbH, Mannheim, Germany). However, insulin resistance was detected using homeostasis model assessment (HOMA-IR). HOMA-IR = [fasting blood glucose (mmol/l)-fasting insulin (mIU/ml)]/22.5 [22]. Moreover, The Quantitative Insulin- Sensitivity Check Index (QUICKI) was the insulin sensitivity test using the formula: QUICKI=1/[log(insulin) + log(glucose)] [23].

Statistical analysis

All variables were analyzed using SPSS version 17(Chicago, IL, USA) and described as mean ± SD. However, ANOVA was used for comparing variables between the three groups. Moreover, Pearson’s correlation coefficients was used for testing correlation between 25- OHD, HBA1c, QUICKI, serum insulin, HOM-IR, the number of WBCs, total neutrophil count and monocytes (P‹0.05).

Results

Comparison between the three groups regarding baseline variables revealed no significant differences except values of fasting and postprandial blood sugar levels were significantly greater in group (I) than both group (II) and group (III) (Table 1).

Table 1: Baseline criteria for participants of the three groups.




  
    Variables
    Group (I)
    Group (II)
    Group (III)
    Significance
  
  
    Age (year)
    53.25 ± 5.37
    54.36 ± 7.94
    51.81 ± 6.12
    0.16
  
  
    Gender (Female: Male)
    102(62%):61(38%)
    33(65%):18(35%)
    29(68%):14(32%)
    0.081
  
  
    BMI (kg/m²)
    31.98 ± 3.67
    32.72 ± 2.85
    32.64 ± 2.31
    0.172
  
  
    Waist hip ratio
    0.87 ± 0.18
    0.88 ± 0.21
    0.88 ± 0.19
    0.215
  
  
    Chronicity of diabetes (year)
    11.74 ± 3.83
    10.95 ± 2.14
    12.36 ± 3.25
    0.079
  
  
    Fasting blood sugar (mg/dL)
    177.36 ± 31.72
    151.53 ± 22.67
    128.12 ± 16.84
    0.011*
  
  
    Postprandial blood sugar    (mg/dl)
    268.17 ± 42.65
    197.56 ± 33.24
    172.35 ± 20.91
    0.005*
  
  
    Insulin (mU/L)
    15.81 ± 2.87
    14.12 ± 2.93
    12.41 ± 2.15
    0.024*
  
  
    BMI:    Body Mass Index; (*) indicates a significant difference between groups, P    <0.05.



Table 1: Baseline criteria for participants of the three groups.

Concerning parameters of blood glucose control, results revealed higher significant values of QUICKI in group (III) compared to group (II) and group (I) in addition to lower values of both HBA1c and HOM-IR in group (III) compared to group (II) and group (I). However, parameters of immune system results revealed higher significant values of the number of WBCs, monocytes, total neutrophil count, CD3, CD4 and CD8 in group (I) compared to group (II) and group (III) (Table 2).

Download PDF

Citation: Al-Shred FM. Deficiency of Vitamin D, Immune System Function and Glucose Control in Non-Insulin Dependent Diabetic Patients. Austin J Clin Immunol. 2019; 6(1):1034.ISSN : 2381-9138

Instruction for Authors

Submit Your Article

Variable	Group (I)	Group (II)	Group (III)	Significance
WBCs count (10⁹/µL)	9.47 ±3.28	7.95 ± 3.16	6.13 ± 2.45	0.012*
Total neutrophil count (10⁹/µL)	6.32 ± 2.54	5.14 ± 2.27	4.25 ± 1.98	0.005*
Monocytes (10⁹/µL)	0.67 ± 0.26	0.49 ± 0.24	0.31 ± 0.17	0.031*
CD3 count (10⁹/L)	1.95 ±0.83	1.63 ± 0.84	1.36 ± 0.65	0.016*
CD4 count (10⁹/L)	1.57 ± 0.72	1.41 ± 0.65	1.19 ± 0.52	0.029*
CD8 count (10⁹/L)	0.89 ± 0.26	0.74 ± 0.23	0.53 ± 0.18	0.042*
HBA1c (%)	9.41 ± 3.12	8.15 ± 2.34	7.24 ±2.85	0.011*
HOMA-IR	5.78 ±1.85	4.23 ±1.61	3.97 ± 1.42	0.015*
QUICKI	0.119 ±0.06	0.155 ± 0.08	0.186 ±0.09	0.022*
WBCs: White Blood Cells; HOMA-IR: Homeostasis Model Assessment-Insulin Resistance (HOMA-IR) Index; HBA1c: Glycosylated Hemoglobin; QUICKI: The Quantitative Insulin-Sensitivity Check Index; (*) indicates a significant difference between groups, P <0.05.

Variable	Group (I)	Group (II)	Group (III)
WBCs count (10⁹/µL)	-0.681**	-0.573*	-0.614*
Total neutrophil count (10⁹/µL)	-0.537*	-0.638*	-0.642*
Monocytes (10⁹/µL)	-0.732**	-0.663*	-0.519*
CD3 count (10⁹/L)	-0.651*	-0.592*	-0.711**
CD4 count (10⁹/L)	-0.583*	-0.675**	-0.634*
CD8 count (10⁹/L)	-0.672**	-0.723**	-0.586*
HBA1c (%)	-0.684**	-0.618*	-0.734**
HOMA-IR	-0.756**	-0.724**	-0.567*
QUICKI	0.691**	0.638*	0.718**
WBCs: White Blood Cells; HOMA-IR: Homeostasis Model Assessment-Insulin Resistance (HOMA-IR) Index; HBA1c: Glycosylated Hemoglobin; QUICKI: The Quantitative Insulin-Sensitivity Check Index; Spearman's correlation was used: P <0.05 *: P <0.01