ArticleScientific reports2016
High fat diet-induced TGF-β/Gbb signaling provokes insulin resistance through the tribbles expression.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- Review
- Influence of high-fat diet and sex on connective tissue in carpal tunnel syndrome.Scientific reports · 2026Article
- Myostatin in Obesity: A Molecular Link Between Metabolic Dysfunction and Musculotendinous Remodeling.International journal of molecular sciences · 2026Review
- Obesity promotes conserved inflammatory and metabolic transcriptional programs in colon tumors: evidence from mouse models and the ColoCare Study Patient Cohort.The American journal of clinical nutrition · 2025Article
- From Lab to Clinic and Farm: LeveragingBiology · 2025Review
- Microemulsion-based drug delivery system identifies pepper alkaloids as anti-obesity compounds.Acta pharmacologica Sinica · 2025Article
- The Drosophila pseudokinase Tribbles translocates to the fat body membrane in response to fasting to modulate insulin sensitivity.Development (Cambridge, England) · 2025Article
- Dual signaling pathways of TGF-β superfamily cytokines in hepatocytes: balancing liver homeostasis and disease progression.Frontiers in pharmacology · 2025Review
- Review
- Regulation of protein O-GlcNAcylation by circadian, metabolic, and cellular signals.The Journal of biological chemistry · 2024Review
- Obesity and Insulin Resistance in Asthma Pathogenesis and Clinical Outcomes.Biomedicines · 2024Review
- Convergent insulin and TGF-β signalling drives cancer cachexia by promoting aberrant fat body ECM accumulation in a Drosophila tumour model.EMBO reports · 2023Article
- Upregulation of Tribbles decreases body weight and increases sleep duration.Disease models & mechanisms · 2023Article
- Utility of Hypoglycemic Agents to Treat Asthma with Comorbid Obesity.Pulmonary therapy · 2023Review
- The Role of Gut Microbiota in High-Fat-Diet-Induced Diabetes: Lessons from Animal Models and Humans.Nutrients · 2023Review
- A genetic strategy to measure insulin signaling regulation and physiology in Drosophila.PLoS genetics · 2023Article
- A protein restricted diet induces a stable increased fat storage phenotype in flies.Toxicology reports · 2023Article
- Exploring a novel therapeutic strategy: the interplay between gut microbiota and high-fat diet in the pathogenesis of metabolic disorders.Frontiers in nutrition · 2023Review
- Protein acylation: mechanisms, biological functions and therapeutic targets.Signal transduction and targeted therapy · 2022Review
- Genetic variation of macronutrient tolerance in Drosophila melanogaster.Nature communications · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia, hyperlipidemia, and insulin resistance are hallmarks of obesity-induced type 2 diabetes, which is often caused by a high-fat diet (HFD). However, the molecular mechanisms underlying HFD-induced insulin resistance have not been elucidated in detail. In this study, we established a Drosophila model to investigate the molecular mechanisms of HFD-induced diabetes. HFD model flies recapitulate mammalian diabetic phenotypes including elevated triglyceride and circulating glucose levels, as well as insulin resistance. Expression of glass bottom boat (gbb), a Drosophila homolog of mammalian transforming growth factor-β (TGF-β), is elevated under HFD conditions. Furthermore, overexpression of gbb in the fat body produced obese and insulin-resistant phenotypes similar to those of HFD-fed flies, whereas inhibition of Gbb signaling significantly ameliorated HFD-induced metabolic phenotypes. We also discovered that tribbles, a negative regulator of AKT, is a target gene of Gbb signaling in the fat body. Overexpression of tribbles in flies in the fat body phenocopied the metabolic defects associated with HFD conditions or Gbb overexpression, whereas tribbles knockdown rescued these metabolic phenotypes. These results indicate that HFD-induced TGF-β/Gbb signaling provokes insulin resistance by increasing tribbles expression.
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