Background: Chronic kidney disease (CKD) is well known as a strong risk factor for both of end-stage renal disease and cardiovascular disease. To clarify the association of glucokinase and glucokinase regulatory protein (GCKR) polymorphisms with the risk of CKD in Japan, we examined this association among Japanese individuals using cross-sectional data.
Methods: The subjects for this analysis were 3,314 consecutively selected participants from the Japan Multi-Institutional Collaborative Cohort Study. Age- and sex- adjusted odds ratios (aORs) of CKD stages 3-5 were calculated for each genotype by logistic regression and the effects of genotype on estimated glomerular filtration rate were evaluated by linear regression. Gene-environment interaction was also investigated based on questionnaire information.
Results: When subjects with GCKR rs780094 G/A and G/G, or GCKR rs1260326 T/C and C/C were combined together and compared with the references (GCKR rs780094 A/A or GCKR rs1260326 T/T), the aORs were 0.84 (0.69-1.02) or 0.81 (0.67-0.99) (p = 0.075 or 0.037), respectively. A significant OR for interaction between GCKR rs1260326 T/T and current smoking (OR = 1.79, p = 0.041) was also observed.
Conclusion: The present study suggests a possible association of the T/T genotype of GCKR rs1260326 polymorphism with elevated risk of CKD and its interaction with current smoking, which may support the possibility of performing risk evaluation and prevention of this potentially life-threatening disease based on genetic traits in the near future.
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http://dx.doi.org/10.1007/s40620-013-0025-0 | DOI Listing |
Endocr Metab Immune Disord Drug Targets
January 2025
Department of Genetics, School of Biology and Basic Medical Sciences, Suzhou Medical College Soochow University, Suzhou 215123, China.
Background: There is still no conclusive understanding of whether the glucokinase regulator (GCKR) gene rs780094 and rs1260326 polymorphisms predispose to gestational diabetes mellitus (GDM).
Objective: This systematic review and meta-analysis aimed to determine the effect of the GCKR polymorphisms on GDM susceptibility.
Methods: Seven literature databases were searched (from inception to February 17, 2024) to locate relevant studies included in further meta-analysis.
Ther Adv Endocrinol Metab
September 2024
Department of Sports Medicine and Sportology, Graduate School of Medicine, Juntendo University, Bunkyo-ku, Tokyo, Japan.
Background: Metabolic syndrome involves health problems influenced by aging and genetics. The glucokinase regulatory protein () rs1260326 polymorphism (Leu446) is associated with metabolic traits. This study explores the impact of the GCKR rs1260326 polymorphism on metabolic traits in older Japanese with focusing on sex-specific differences.
View Article and Find Full Text PDFBiochem Pharmacol
November 2024
Biosciences Institute, Newcastle University, Newcastle upon Tyne NE2 4HH, UK. Electronic address:
Glucokinase activators (GKAs) have been developed as blood glucose lowering drugs for type 2 diabetes. Despite good short-term efficacy, several GKAs showed a decline in efficacy chronically during clinical trials. The underlying mechanisms remain incompletely understood.
View Article and Find Full Text PDFMol Biol Rep
July 2024
Life Science, and Biomedical Engineering Application and Research Center, Istanbul Gelisim University, Istanbul, 34310, Turkey.
Background: This study examines genetic variations in CYP2E1 (rs6413432, rs3813867), GCKR (rs780094, rs1260326), and PNPLA3 (rs738409) among Turkish patients to assess their influence on nonalcoholic steatohepatitis.
Methods: Allele and genotype frequencies were compared between 245 NASH patients and 120 healthy controls using SNP genotyping via polymerase chain reaction-restriction fragment length polymorphism. Additionally, the deviation of the observed genotype frequencies from Hardy-Weinberg proportion was examined.
J Hepatol
December 2024
Department of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland; Department for BioMedical Research, Visceral Surgery and Medicine, University of Bern, Switzerland. Electronic address:
Background & Aims: Regression of cirrhosis has been observed in patients with viral and non-viral etiologies of liver disease in whom the underlying cause of liver injury was effectively suppressed. However, the understanding of the factors contributing to reversibility of fibrosis and cirrhosis is limited. Our aims were to assess clinical factors, perform genotyping of known variants, and comprehensive metabolic phenotyping to characterize the regression of fibrosis in patients with compensated advanced chronic liver disease (cACLD).
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