Hepatic Acetyl CoA Links Adipose Tissue Inflammation to Hepatic Insulin Resistance and Type 2 Diabetes
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Summary
It is shown that the major mechanism by which insulin suppresses HGP is through reductions in hepatic acetyl CoA by suppression of lipolysis in white adipose tissue (WAT) leading to reductions in pyruvate carboxylase flux.
- Type
- article
- Published
- 2015-02-05
- Cited by
- 667
- References
- 64
- Access
- Open access
- OpenAlex
- https://openalex.org/W25662011
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:8696479
Keywords
Computer science, Multimedia
References
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- Mechanism by which arylamine N-acetyltransferase 1 ablation causes insulin resistance in mice
- Elevated triglyceride-glucose (TyG) index predicts incidence of Prediabetes: a prospective cohort study in China
- Type 2 diabetes mellitus
- Impact of Reduced ATGL-Mediated Adipocyte Lipolysis on Obesity-Associated Insulin Resistance and Inflammation in Male Mice.
- Adipocyte lipolysis and insulin resistance.
- Metabolism: Hepatic insulin resistance—missing link identified
- Hypophagia and metabolic adaptations in mice with defective ATGL-mediated lipolysis cause resistance to HFD-induced obesity
- The TZD insulin sensitizer clue provides a new route into diabetes drug discovery
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- Second‐generation antisense oligonucleotides against β‐catenin protect mice against diet‐induced hepatic steatosis and hepatic and peripheral insulin resistance
- Mesenteric Fat Lipolysis Mediates Obesity-Associated Hepatic Steatosis and Insulin Resistance
- Retinol as a cofactor for PKCδ‐mediated impairment of insulin sensitivity in a mouse model of diet‐induced obesity
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- Model-Based Quantification of the Systemic Interplay between Glucose and Fatty Acids in the Postprandial State
- The Role of PDE3B Phosphorylation in the Inhibition of Lipolysis by Insulin
- Membrane and nuclear estrogen receptor a collaborate to suppress adipogenesis but not triglyceride content