Nirali Rathwa1, Roma Patel1, Sayantani Pramanik Palit1, Shahnawaz D Jadeja1, Mahendra Narwaria2, A V Ramachandran3, Rasheedunnisa Begum4. 1. Department of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara 390002, Gujarat, India. 2. Asian Bariatrics Hospital, Ahmedabad 380015, Gujarat, India. 3. Department of Zoology, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara 390002, Gujarat, India. 4. Department of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara 390002, Gujarat, India. Electronic address: rasheedunnisab@yahoo.co.in.
Abstract
OBJECTIVE: Omentin-1, an anti-inflammatory protein, is secreted by the visceral adipose tissue. Altered levels of Omentin-1 are associated with obesity and Type 2 Diabetes (T2D). Although Omentin-1 is implicated in the insulin signaling pathway, the relationship between the genetic variants of Omentin-1 and T2D is not yet explored. The current study evaluates the association of Omentin-1 polymorphisms (rs2274907 A/T and rs1333062 G/T), its transcript and protein levels, and genotype-phenotype correlation with metabolic parameters and T2D susceptibility. METHODS: Plasma and Peripheral Blood Mononuclear Cells (PBMCs) were separated from venous blood taken from 250 controls and 250 T2D patients recruited from Gujarat, India. Genomic DNA was isolated from PBMCs and genotyping of Omentin-1 variants was performed by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP). RNA was isolated from Visceral Adipose Tissue (VAT) samples of 12 controls and 10 patients, and transcript levels of Omentin-1 were assessed by qPCR. Plasma Omentin-1 levels were estimated by ELISA. Fasting Blood Glucose, Body Mass Index (BMI) and plasma lipid profile were considered for the genotype-phenotype correlation analysis. RESULTS: Our study revealed no association of Omentin-1 genetic variants with T2D risk (p > 0.05). However, the AT genotype of Omentin-1 rs2274907 A/T polymorphism was associated with increased BMI (p = 0.0247). Plasma Omentin-1 levels were significantly decreased (p < 0.0001) however, increased VAT Omentin-1 transcript levels (p = 0.0127) were observed in T2D patients. CONCLUSION: Our findings suggest that decreased circulatory Omentin-1 levels could pose a risk towards T2D susceptibility.
OBJECTIVE:Omentin-1, an anti-inflammatory protein, is secreted by the visceral adipose tissue. Altered levels of Omentin-1 are associated with obesity and Type 2 Diabetes (T2D). Although Omentin-1 is implicated in the insulin signaling pathway, the relationship between the genetic variants of Omentin-1 and T2D is not yet explored. The current study evaluates the association of Omentin-1 polymorphisms (rs2274907 A/T and rs1333062 G/T), its transcript and protein levels, and genotype-phenotype correlation with metabolic parameters and T2D susceptibility. METHODS: Plasma and Peripheral Blood Mononuclear Cells (PBMCs) were separated from venous blood taken from 250 controls and 250 T2D patients recruited from Gujarat, India. Genomic DNA was isolated from PBMCs and genotyping of Omentin-1 variants was performed by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP). RNA was isolated from Visceral Adipose Tissue (VAT) samples of 12 controls and 10 patients, and transcript levels of Omentin-1 were assessed by qPCR. Plasma Omentin-1 levels were estimated by ELISA. Fasting Blood Glucose, Body Mass Index (BMI) and plasma lipid profile were considered for the genotype-phenotype correlation analysis. RESULTS: Our study revealed no association of Omentin-1 genetic variants with T2D risk (p > 0.05). However, the AT genotype of Omentin-1 rs2274907 A/T polymorphism was associated with increased BMI (p = 0.0247). Plasma Omentin-1 levels were significantly decreased (p < 0.0001) however, increased VAT Omentin-1 transcript levels (p = 0.0127) were observed in T2D patients. CONCLUSION: Our findings suggest that decreased circulatory Omentin-1 levels could pose a risk towards T2D susceptibility.
Authors: Chandan K Jha; Rashid Mir; Imadeldin Elfaki; Jamsheed Javid; Abdullatif Taha Babakr; Shaheena Banu; S M S Chahal Journal: J Pers Med Date: 2020-10-26