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

Effects of GCK, GCKR, G6PC2 and MTNR1B variants on glucose metabolism and insulin secretion.

PloS one - 23 Jul 2010

Hu Cheng, Zhang Rong, Wang Congrong, Yu Weihui, Lu Jingyi, Ma Xiaojing, Wang Jie, Jiang Feng, Tang Shanshan, Bao Yuqian, Xiang Kunsan, Jia Weiping

Abstract excerpt

BACKGROUND: Single nucleotide polymorphisms (SNPs) from GCK, GCKR, G6PC2 and MTNR1B were found to modulate the fasting glucose levels. The current study aimed to replicate this association in the Chinese population and further analyze their effects on biphasic insulin secretion. METHODS/PRINCIPAL FINDINGS: SNPs from GCK, GCKR, G6PC2 and MTNR1B were genotyped in the Shanghai Chinese, including 3,410 type 2...

Read the complete abstract on PubMed

Topics

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

Share to Adaptor Proteins, Signal Transducing
Share to Diabetes Mellitus, Type 2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Germinal Center Kinases

Share to Glucose

Share to Glucose-6-Phosphatase

Share to Insulin

Share to Insulin Secretion

Share to Protein Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 20668700
DOI: 10.1371/journal.pone.0011761
PMCID: PMC2909258

Genes

GCK
GCKR

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

Effects of GCK, GCKR, G6PC2 and MTNR1B variants on glucose metabolism and insulin secretion.PMID 20668700Read ↗

Common polymorphisms in MTNR1B, G6PC2 and GCK are associated with increased fasting plasma glucose and impaired beta-cell function in Chinese subjects.Semantic proximity Read ↗

Large scale meta-analyses of fasting plasma glucose raising variants in GCK, GCKR, MTNR1B and G6PC2 and their impacts on type 2 diabetes mellitus risk.Semantic proximity Read ↗

Association of GCKR rs780094, alone or in combination with GCK rs1799884, with type 2 diabetes and related traits in a Han Chinese population.Semantic proximity Read ↗

Additive effects of genetic variation in GCK and G6PC2 on insulin secretion and fasting glucose.Semantic proximity Read ↗

Additive genetic effect of GCKR, G6PC2, and SLC30A8 variants on fasting glucose levels and risk of type 2 diabetes.Semantic proximity Read ↗

A Genome-Wide Association Study of IVGTT-Based Measures of First-Phase Insulin Secretion Refines the Underlying Physiology of Type 2 Diabetes Variants.Semantic proximity Read ↗

Detailed physiologic characterization reveals diverse mechanisms for novel genetic Loci regulating glucose and insulin metabolism in humans.Semantic proximity Read ↗

A genetic variant of G6PC2 is associated with type 2 diabetes and fasting plasma glucose level in the Chinese population.Semantic proximity Read ↗

The GCKR rs780094 polymorphism is associated with susceptibility of type 2 diabetes, reduced fasting plasma glucose levels, increased triglycerides levels and lower HOMA-IR in Japanese population.Semantic proximity Read ↗

Common variants at the GCK, GCKR, G6PC2-ABCB11 and MTNR1B loci are associated with fasting glucose in two Asian populations.Semantic proximity Read ↗

Associations of common polymorphisms in GCKR with type 2 diabetes and related traits in a Han Chinese population: a case-control study.Semantic proximity Read ↗

Combined effects of single-nucleotide polymorphisms in GCK, GCKR, G6PC2 and MTNR1B on fasting plasma glucose and type 2 diabetes risk.Semantic proximity Read ↗

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