Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A polymorphism in the promoter of UCP2 gene modulates lipid levels in patients with type 2 diabetes.

Molecular genetics and metabolism - 1 Aug 2004

Reis André F, Dubois-Laforgue Danièle, Bellanné-Chantelot Christine, Timsit José, Velho Gilberto

Abstract excerpt

A G/A single nucleotide polymorphism (SNP) in the position -866 of the UCP2 promoter modulates UCP2 expression in adipose tissue and pancreatic beta-cell, and is associated with variations of body mass index (BMI) and insulin secretion in nondiabetic subjects. We investigated associations of this SNP with traits related to obesity, dyslipidemia, and hyperglycemia in patients with type 2 diabetes. The -866 G/A SNP...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Diabetes Mellitus, Type 2
Share to France

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Ion Channels

Share to Lipid Metabolism

Share to Lipids

Share to Membrane Transport Proteins

Share to Mitochondrial Proteins

Share to Uncoupling Protein 2

Source

Identifiers

PMID: 15308133
DOI: 10.1016/j.ymgme.2004.06.008

Genes

UCP2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A polymorphism in the promoter of UCP2 gene modulates lipid levels in patients with type 2 diabetes.PMID 15308133Read ↗

Association study of the -866G/A UCP2 gene promoter polymorphism with type 2 diabetes and obesity in a Tehran population: a case control study.Semantic proximity Read ↗

A common polymorphism in the promoter of UCP2 is associated with obesity and hyperinsulenemia in northern Indians.Semantic proximity Read ↗

The common -866G/A polymorphism in the promoter region of the UCP-2 gene is associated with reduced risk of type 2 diabetes in Caucasians from Italy.Semantic proximity Read ↗

The common -866G/A polymorphism of the UCP2 gene in healthy Iranians compared with world populations.Semantic proximity Read ↗

Mitochondrial uncoupling protein 2 (UCP2) gene polymorphism - 866 G/A in the promoter region is associated with type 2 diabetes mellitus among Kashmiri population of Northern India.Semantic proximity Read ↗

Uncoupling protein-2 polymorphisms in type 2 diabetes, obesity, and insulin secretion.Semantic proximity Read ↗

The frequent UCP2 -866G>A polymorphism protects against insulin resistance and is associated with obesity: a study of obesity and related metabolic traits among 17 636 Danes.Semantic proximity Read ↗

Mitochondrial uncoupling protein 2 (UCP2) gene polymorphism -866 G/A in the promoter region is associated with Type 2 Diabetes Mellitus among Kashmiri population of Northern IndiaSemantic proximity Read ↗

Genetic Variance in<i>Uncoupling Protein 2</i>in Relation to Obesity, Type 2 Diabetes, and Related Metabolic Traits: Focus on the Functional −866G>A Promoter Variant (rs659366)Semantic proximity Read ↗

Uncoupling protein 2 promoter polymorphism -866G/A affects its expression in beta-cells and modulates clinical profiles of Japanese type 2 diabetic patients.Semantic proximity Read ↗

Variation in the UCP2 and UCP3 genes associates with abdominal obesity and serum lipids: the Finnish Diabetes Prevention Study.Semantic proximity Read ↗

An association between -866G/A polymorphism in the promoter of UCP2 and obesity: a meta-analysis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.