Association of vitamin D and vitamin D receptor gene polymorphisms with chronic inflammation, insulin resistance and metabolic syndrome components in type 2 diabetic Egyptian patients

Autor: Mohammed E.H. Badawi, Amal M.H. Mackawy
Jazyk: angličtina
Rok vydání: 2014
Předmět:
NHANES III
National Health and Examination Survey
medicine.medical_treatment
BMI
body mass index
HPLC
High performance liquid chromatography
Type 2 diabetes
Calcitriol receptor
HDL-C
high density lipoprotein cholesterol
DM
diabetes mellitus
WC
waist circumference
X2
Chi-square
PTH
parathyroid hormone
Vitamin D
Genetics (clinical)
Vitamin D Receptor gene
biology
TG
triglyceride
Metabolic syndrome
FokI
PGs
pro-inflammatory prostaglandins
CRP
C-reactive protein
LDL-C
low density lipoprotein cholesterol
medicine.medical_specialty
IL-6
interleukin -6
FBG
fasting blood glucose
Pro-inflammatory cytokines
DBP
diastolic blood pressure
Article
Insulin resistance
IRS
insulin receptor substrates
Internal medicine
Genetics
medicine
Vitamin D and neurology
SOCS
suppressors of cytokine signaling
VitD
Vitamin D
FPI
fasting plasma insulin
HOMA
Homeostasis of Metabolic Assessment
Type 2 diabetes mellitus (DM)
business.industry
Insulin
SBP
systolic blood pressure
medicine.disease
OR
odds ratio
TC
total cholesterol
Endocrinology
CI
confidence intervals
Interleukin-6 (IL-6)
biology.protein
MetSyn
metabolic syndrome
Gene polymorphism
HbA1c
glycated hemoglobin
business
SD
standard deviation
Polymorphisms
VDR
Vit D receptor
Zdroj: Meta Gene
ISSN: 2214-5400
Popis: Background To date the published data concerning the possible interplay between vitamin D (VitD) and Vit D receptor (VDR) gene polymorphism with the immune/inflammatory mediators in type 2 diabetes mellitus (DM) is insufficient. Some of the immune non-classical actions of vitamin D may point to its role in the pathogenesis of type 2 DM through down-regulation of cytokines (IL-6). Although there is evidence to support a relationship among vitamin D status, chronic inflammation and insulin resistance, the underlying mechanism requires further exploration. We aimed to investigate the role of vitamin D in chronic inflammation and insulin resistance in type 2 DM. Moreover, to examine the association of VDR gene polymorphisms [VDR 2228570 C > T (FokI); VDR 1544410 A > G (BsmI)] with the components of metabolic syndrome (MetSyn) in type 2 diabetic Egyptian patients . Subjects and methods A total of 190 subjects were enrolled in this study, 60 controls and 130 type 2 diabetic patients (Group II). Group II was subdivided into 63 patients without MetSyn (subgroup IIa) and 67 patients with MetSyn (subgroup IIb). Genetic analysis for VDR gene polymorphisms was done in all subjects. VitD and IL-6 plasma levels were estimated. Results The TT genotype for the VDR FokI was significantly more frequent in subgroup IIb than in subgroup IIa and controls ( X 2 = 6.83, P = 0.03 and X 2 = 16.592, P = 0.000) respectively. The T allele was more frequent in the MetSyn group as compared to diabetics without MetSyn (p = 0.001), odds ratio (OR) and 95% CI for the T allele of C > T (FokI) = 2.30 (1.37–3.86). We did not detect any significant difference in VDR BsmI genotypes between patients and control groups (P = 0.947). FokI VDR was significantly associated with the lipid profile parameters, VitD and IL-6 plasma levels in subgroup IIa and associated with HOMA-IR, insulin, VitD, IL-6 levels, waist circumference (WC) and body mass index (BMI) in subgroup IIb while BsmI VDR variant was associated only with VitD values in both subgroups. Conclusion The present study suggests an interaction between VDR polymorphisms and important components of MetSyn, VitD and pro-inflammatory cytokines (IL-6). FokI VDR polymorphisms may be linked to mild inflammation and insulin resistance and might represent a genetic determinant for developing MetSyn in type 2 diabetic Egyptian patients. The challenge is determining the mechanisms of VitD action for recommendation of VitD supplementation that reduces the risks of MetSyn, insulin resistance and progression to type 2 diabetes.
Databáze: OpenAIRE
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