Evidence map›Paper›PMID 37746545›Full record

ArticleIndian journal of clinical biochemistry : IJCB2023

Association of the Human Leptin Receptor Gene (rs1137101; Gln223Arg) Polymorphism and Circulating Leptin in Patients with Metabolic Syndrome in the Indian Population.

Deepak Parchwani, Sagar Dholariya, Digishaben D Patel, Ashishkumar Agravatt, Jayant Uperia, Tanishk Parchwani, Ragini Singh, Madhuri Radadiya, Yash Desai

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Article in Indian journal of clinical biochemistry : IJCB, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Deepak ParchwaniAll India Institute of Medical Sciences, Rajkot, Gujarat India.ORCID 0000-0001-5024-970X
Sagar DholariyaAll India Institute of Medical Sciences, Rajkot, Gujarat India.
Digishaben D PatelAll India Institute of Medical Sciences, Rajkot, Gujarat India.
Ashishkumar AgravattBJ Medical College, Ahmedabad, Gujarat India.
Jayant UperiaGMERS Medical College, Himmatnagar, Gujarat India.
Tanishk ParchwaniSMS Medical College, Jaipur, Rajasthan India.
Ragini SinghAll India Institute of Medical Sciences, Rajkot, Gujarat India.
Madhuri RadadiyaTutor PDU Medical College, Rajkot, Gujarat India.
Yash DesaiBJ Medical College, Ahmedabad, Gujarat India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenotypic expression of metabolic syndrome is precipitated by environmental variables along with the individual genetic susceptibility to the obesogenic environment and growing body of evidence suggest a paramount role of adipocytokines. Therefore, identifying the genetic influence on circulation leptin levels and clarifying genotype-phenotype correlation of rs1137101 {Leptin receptor gene (LEPR) Gln223Arg (Q223R; A668G)} in metabolic syndrome were the primary objective of this study. A total of 447 adult participants, including 214 metabolic syndrome patients and 233 healthy controls, were genotyped using polymerase chain reaction-restriction fragment length polymorphism method to unravel the effects of genetic risk loci {Leptin receptor gene; Gln223Arg (Q223R; A668G); rs1137101} on the occurrence of metabolic syndrome in consort with circulation leptin levels. Suitable descriptive statistics was used for different variables. The genotype frequencies were found to be in Hardy-Weinberg equilibrium for both cases (p > 0.2722) as well as in controls (p > 0.2331). However, genotype (x2: 11.26, 2 d.f. p = 0.0036) and allele distribution (x2: 10.51, 2 d.f. p: 0.0012) of the LEPR Gln223Arg (Q223R; A668G) differed significantly between cases and controls. Gln/Arg genotype (OR = 1.6099; 95% CI = 1.0847-2.3893; p value = 0.0181), Arg/Arg genotype (OR = 2.8121; 95% CI = 1.4103-5.6074; p value = 0.0033) and R allele (OR = 1.5875; 95% CI = 1.1996-2.1008; p value = 0.0012) were significantly associated with increased risk of metabolic syndrome in univariate analysis. Further a multivariate logistic regression adjusted for potential confounders showed that Arg/Arg genotype (OR = 1.9; 95% CI = 1.271-2.639; p-value < 0.05) and Gln/Arg (OR: 1.3; 95% CI = 0.873-2.034; p value < 0.05) have a significant risk for the occurrence of the metabolic syndrome. A progressive increase in the serum leptin levels from major homozygous alleles to minor homozygous alleles were observed indicating that rs1137101 modify the serum leptin concentrations in patients with metabolic syndrome. These findings provide enough evidence of a significant association of LEPR Gln223Arg (Q223R; A668G) polymorphism in the LepR gene in Indian patients with increased risk of metabolic syndrome for R allele and Arg/Arg homozygote. Thus, rs1137101 might be a pleiotropic locus for metabolic syndrome and its components in studied population.

Indexed as

Gln223ArgLeptinLeptin receptorSingle nucleotide polymorphism

Identifiers

PMID37746545
PMCPMC10516842

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