ArticlePloS one2012
Deletion of CDKAL1 affects high-fat diet-induced fat accumulation and glucose-stimulated insulin secretion in mice, indicating relevance to diabetes.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.
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Who cites it
20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- Identification and Potential Clinical Utility of Common Genetic Variants in Gestational Diabetes among Chinese Pregnant Women.Diabetes & metabolism journal · 2025Pooled it
- Genome-Wide Association Analysis of Pancreatic Beta-Cell Glucose Sensitivity.The Journal of clinical endocrinology and metabolism · 2021Pooled it
- Molecular Genetics of β-Cell Compensation in Gestational Diabetes Mellitus: Insights from CDKAL1, SLC30A8 and HHEX.International journal of molecular sciences · 2026Review
- The Genetic Blueprint of Obesity: From Pathogenesis to Novel Therapies.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025Review
- Mechanisms and Physiological Roles of Polymorphisms in Gestational Diabetes Mellitus.International journal of molecular sciences · 2024Review
- Epitranscriptomics in metabolic disease.Nature metabolism · 2023Review
- Involvement of Cdkal1 in the etiology of type 2 diabetes mellitus and microvascular diabetic complications: a review.Journal of diabetes and metabolic disorders · 2022Review
- TheFrontiers in endocrinology · 2022Article
- Association of single nucleotide polymorphisms with insulin secretion, insulin sensitivity, and diabetes in women with a history of gestational diabetes mellitus.BMC medical genomics · 2021Article
- Dietary Protein and Fat Intake Affects Diabetes Risk withInternational journal of molecular sciences · 2020Article
- Insights into pancreatic islet cell dysfunction from type 2 diabetes mellitus genetics.Nature reviews. Endocrinology · 2020Review
- Role of Hepatic Glucocorticoid Receptor in Metabolism in Models of 5αR1 Deficiency in Male Mice.Endocrinology · 2019Article
- Cdkal1, a type 2 diabetes susceptibility gene, regulates mitochondrial function in adipose tissue.Molecular metabolism · 2017Article
- CDK5 Regulatory Subunit-Associated Protein 1-like 1 Negatively Regulates Adipocyte Differentiation through Activation of Wnt Signaling Pathway.Scientific reports · 2017Article
- An Isogenic Human ESC Platform for Functional Evaluation of Genome-wide-Association-Study-Identified Diabetes Genes and Drug Discovery.Cell stem cell · 2016Article
- The association analysis polymorphism of CDKAL1 and diabetic retinopathy in Chinese Han population.International journal of ophthalmology · 2016Article
- Erchen Decoction Prevents High-Fat Diet Induced Metabolic Disorders in C57BL/6 Mice.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Insights into the genetic basis of type 2 diabetes.Journal of diabetes investigation · 2013Review
- Article
- Metabolism Meets Translation: Dietary and Metabolic Influences on tRNA Modifications and Codon Biased Translation.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveThe CDKAL1 gene is among the best-replicated susceptibility loci for type 2 diabetes, originally identified by genome-wide association studies in humans. To clarify a physiological importance of CDKAL1, we examined effects of a global Cdkal1-null mutation in mice and also evaluated the influence of a CDKAL1 risk allele on body mass index (BMI) in Japanese subjects.
methodsIn Cdkal1-deficient (Cdkal1⁻/⁻) mice, we performed oral glucose tolerance test, insulin tolerance test, and perfusion experiments with and without high-fat feeding. Based on the findings in mice, we tested genetic association of CDKAL1 variants with BMI, as a measure of adiposity, and type 2 diabetes in Japanese. PRINCIPAL
findingsOn a standard diet, Cdkal1⁻/⁻ mice were modestly lighter in weight than wild-type littermates without major alterations in glucose metabolism. On a high fat diet, Cdkal1⁻/⁻ mice showed significant reduction in fat accumulation (17% reduction in %intraabdominal fat, P = 0.023 vs. wild-type littermates) with less impaired insulin sensitivity at an early stage. High fat feeding did not potentiate insulin secretion in Cdkal1⁻/⁻ mice (1.0-fold), contrary to the results in wild-type littermates (1.6-fold, P<0.01). Inversely, at a later stage, Cdkal1⁻/⁻ mice showed more prominent impairment of insulin sensitivity and glucose tolerance. mRNA expression analysis indicated that Scd1 might function as a critical mediator of the altered metabolism in Cdkal1⁻/⁻ mice. In accordance with the findings in mice, a nominally significant (P<0.05) association between CDKAL1 rs4712523 and BMI was replicated in 2 Japanese general populations comprising 5,695 and 12,569 samples; the risk allele for type 2 diabetes was also associated with decreased BMI.
conclusionsCdkal1 gene deletion is accompanied by modestly impaired insulin secretion and longitudinal fluctuations in insulin sensitivity during high-fat feeding in mice. CDKAL1 may affect such compensatory mechanisms regulating glucose homeostasis through interaction with diet.
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