Abstract
Background Diabetes is one of the common chronic diseases in which susceptibility is determined by a combination of genetic and environmental factors, and more than 90% of diabetic patients are diabetes mellitus type 2 (T2DM). The existing studies on the association between CDKAL1 rs10946398 gene polymorphism and susceptibility to type 2 diabetes are inconsistent across populations. Aim We aim to explore the association between CDKAL1 rs10946398 gene polymorphism and susceptibility to type 2 diabetes in different populations. Methods We examined all studies before June 12, 2021, that associated CDKAL1 rs10946398 with T2DM. Heterogeneity was assessed by meta-analysis of allelic inheritance models (A vs. C), dominant inheritance models (AA vs. AC+CC), and recessive inheritance model (AA+AC vs. CC); I2 was used to assess the heterogeneity (if I2 < 50%, the fixed-effects model was used; if I2 ≥ 50%, the random-effects model was used for data consolidation); correlation was judged by a forest map; potential publication bias was tested by the Egger test (p > 0.05 indicates that there is no publication bias). Results Fourteen data totaling 30288 subjects, including 19272 controls and 11016 patients with T2DM, met our inclusion criteria. In the Asian population, the differences were statistically significant (p < 0.01) for dominant genetic model (OR = 0.75, 95%CI = 0.64-0.88, p = 0.0003). But the allelic effect model (OR = 0.87, 95%CI = 0.75-1.02, p = 0.08) and the recessive genetic model (OR = 0.85, 95%CI = 0.66-1.10, p = 0.23) were not statistically significant (p > 0.01). In the non-Asian population, the differences were statistically significant (p < 0.01) for the allelic effect model (OR = 0.83, 95%CI = 0.77-0.88, p < 0.00001), the dominant model (OR = 0.79, 95%CI = 0.72-0.87, p < 0.00001), and the recessive model (OR = 0.78, 95%CI = 0.70-0.87, p < 0.0001). Conclusion In this study, CDKAL1 RS10946398 was positively associated with T2DM, but the association was different in Asian populations.
Highlights
According to the World Health Organization (WHO), approximately 3.4 million people died from developing diabetes in 2004, and it predicts that the number of diabetes deaths will double between 2005 and 2030
According to a large number of genome-wide association analyses (GWAS), CDK5 regulation-related protein 1LIAK 1 (CDKAL1) gene under the action of high glucose toxicity will increase the body’s demand for insulin, and pancreatic β cells continue to be activated, which may inhibit the activity of CDK5 in pancreatic β cells
Because mutations in CDKAL1 may lead to impaired insulin secretion, it increases the risk of Type 2 diabetes mellitus (T2DM), and CDK5 regulates the related protein 1-LIAK 1 (CDKAL1) gene which is one of the most repeatable risk genes in T2DM [20]
Summary
According to the World Health Organization (WHO), approximately 3.4 million people died from developing diabetes in 2004, and it predicts that the number of diabetes deaths will double between 2005 and 2030. Type 2 diabetes mellitus (T2DM), formerly known as non-insulin-dependent or adult-onset diabetes mellitus, is a type of diabetes mellitus It is caused by poor insulin action which is the relative lack of insulin in patients, and its susceptibility is determined by both genetic and environmental factors [2]. It is noteworthy that a variant of the CDKAL1 RS10946398 locus in the population of the Asian country of the United Arab Emirates may not be directly associated with the development of T2DM [1]. In the non-Asian population, the differences were statistically significant (p < 0:01) for the allelic effect model (OR = 0:83, 95%CI = 0:77-0.88, p < 0:00001), the dominant model (OR = 0:79, 95%CI = 0:72-0.87, p < 0:00001), and the recessive model (OR = 0:78, 95%CI = 0:70-0.87, p < 0:0001). CDKAL1 RS10946398 was positively associated with T2DM, but the association was different in Asian populations
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
