ArticleHuman molecular genetics2018
A collective diabetes cross in combination with a computational framework to dissect the genetics of human obesity and Type 2 diabetes.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Transcriptomic Signature of Frailty in Older Patients With Cardiovascular Disease Undergoing Cardiac Surgery or TAVI.Journal of cachexia, sarcopenia and muscle · 2025Article
- Identification of a critical interval for type 2 diabetes QTL on chromosome 4 in DDD-AMammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Novel loci for hyperglycemia identified by QTL mapping of longitudinal phenotypes and congenic analysis.Scientific reports · 2023Article
- E96V Mutation in theInternational journal of molecular sciences · 2023Article
- Comparative genomic analyses of multiple backcross mouse populations suggest SGCG as a novel potential obesity-modifier gene.Human molecular genetics · 2022Article
- Alterations of Lipid Profile in Livers with Impaired Lipophagy.International journal of molecular sciences · 2022Article
- Heterogeneous Development of β-Cell Populations in Diabetes-Resistant and -Susceptible Mice.Diabetes · 2022Article
- Identification of Novel Genes Involved in Hyperglycemia in Mice.International journal of molecular sciences · 2022Article
- Multi-Omic Approaches to Identify Genetic Factors in Metabolic Syndrome.Comprehensive Physiology · 2021Article
- Alternative exon splicing and differential expression in pancreatic islets reveals candidate genes and pathways implicated in early diabetes development.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
- Immunity-related GTPase induces lipophagy to prevent excess hepatic lipid accumulation.Journal of hepatology · 2020Article
- A decade of experience with genetically tailored pig models for diabetes and metabolic research.Animal reproduction · 2020Review
- Polymorphisms in miRNA binding sites involved in metabolic diseases in mice and humans.Scientific reports · 2020Article
- Identification of Novel Potential Type 2 Diabetes Genes Mediating β-Cell Loss and Hyperglycemia Using Positional Cloning.Frontiers in genetics · 2020Article
- Two Novel Candidate Genes for Insulin Secretion Identified by Comparative Genomics of Multiple Backcross Mouse Populations.Genetics · 2018Article
Corrections and comments
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Authors and funding
22 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore the genetic determinants of obesity and Type 2 diabetes (T2D), the German Center for Diabetes Research (DZD) conducted crossbreedings of the obese and diabetes-prone New Zealand Obese mouse strain with four different lean strains (B6, DBA, C3H, 129P2) that vary in their susceptibility to develop T2D. Genome-wide linkage analyses localized more than 290 quantitative trait loci (QTL) for obesity, 190 QTL for diabetes-related traits and 100 QTL for plasma metabolites in the outcross populations. A computational framework was developed that allowed to refine critical regions and to nominate a small number of candidate genes by integrating reciprocal haplotype mapping and transcriptome data. The efficiency of the complex procedure was demonstrated for one obesity QTL. The genomic interval of 35 Mb with 502 annotated candidate genes was narrowed down to six candidates. Accordingly, congenic mice retained the obesity phenotype owing to an interval that contains three of the six candidate genes. Among these the phospholipase PLA2G4A exhibited an elevated expression in adipose tissue of obese human subjects and is therefore a critical regulator of the obesity locus. Together, our broad and complex approach demonstrates that combined- and comparative-cross analysis exhibits improved mapping resolution and represents a valid tool for the identification of disease genes.
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