Metabolism, Diabetes, and Cancer

This study shows that activating AMPK alpha2 T172 in skeletal muscle improves exercise performance and energy transduction, and its disruption mimics type 2 diabetes features.

This study shows that Parvin in skeletal muscle is essential for insulin-stimulated glucose uptake and mitochondrial function, while having little effect on liver insulin sensitivity.

This study shows TAS1R3 regulates glucose uptake in skeletal muscle via a Rac1 and phospho-cofilin pathway, independent of IRS1-AKT and Galphaq/11, and identifies it as a potential therapeutic target for T2D.

The paper shows that pyruvate metabolism affects cell growth in post-mitotic cells by altering redox balance and metabolic pathways, despite active growth signals.

This study identifies distinct roles of AMPKγ isoforms in glucose uptake in skeletal muscle, showing γ1 is required for ADaM site activator-stimulated uptake but not AMP-binding activators.

This study shows that aldometanib activates AMPK to enhance CD8+ T cell infiltration and control hepatocellular carcinoma growth in immune-competent mice.

This paper describes the mechanism and cellular effects of the potent AMPK inhibitor BAY-3827, showing it selectively blocks AMPK-dependent functions.

This study shows that Anxa6-/- mice have impaired fasting-induced hepatic gluconeogenesis, leading to hypoglycaemia and reliance on lipid oxidation.

This study shows miR-1 regulates metabolic flexibility in skeletal muscle by controlling pyruvate metabolism, with loss of miR-1 causing metabolic inflexibility and reduced endurance.

The paper uses proteomics to identify personalized signatures of insulin resistance and type 2 diabetes, showing that fasting proteome and phosphoproteome predict insulin sensitivity and reveal sex-specific differences.

This paper identifies rapaglutin E as a specific inhibitor of GLUT1 and explores its binding mechanism compared to rapaglutin A.

This study shows that mTORC2 and dietary potassium coordinate renal glucose reabsorption and gluconeogenesis through independent mechanisms, with implications for diabetes management.

This study shows MLX phosphorylation is required for ChREBP-MLX heterotetramer formation on ChoREs, regulating carbohydrate and lipid metabolism.

The paper describes an ELISA-based assay for measuring AMPK activity, offering a simple, sensitive alternative to radioactive and commercial methods.

This study identifies 166 differential proteins in rat urine after metformin treatment, revealing potential mechanisms and novel pathways associated with its effects.

This study integrates transcriptomic and metabolomic analyses to reveal novel regulatory functions of ChREBP in mitochondrial metabolism and cellular energy balance beyond its canonical roles in carbohydrate and lipid metabolism.

The paper uses multi-layered proteomics to show insulin increases EphA2 via ERK pathway, independent of insulin resistance, and dependent on low IGF1R levels.

This paper evaluates pioglitazone's effects on muscle fatigue and multi-omic profiles in breast cancer xenograft mice, finding partial restoration of lipid and mitochondrial transcriptomic dysregulation.

This study identifies ULK1-dependent AMPK activation mechanisms and shows MK8722 improves renal function in CKD.

This study identifies an HNF4-TET2-FBP1 axis that regulates gluconeogenesis and shows metformin's effect on this pathway in type 2 diabetes.

This study investigates whether MG53 interacts with the insulin receptor and affects Akt phosphorylation in muscle, heart, and liver tissues, finding low binding affinity and no effect on insulin signaling.

This study investigates how mechanical loading affects AMPK and mTOR signaling in myoblasts, showing that 10% static loading activates AMPK and inhibits mTOR, alters RNA/protein synthesis, and impacts mitochondrial biogenesis.

The paper links hyperinsulinemia to cancer progression by showing how reduced glucose storage capacity leads to insulin resistance and affects tumor response to therapy.

This study uses chemical imaging to show that metformin accumulates primarily in mitochondria within cells.

This study shows metformin induces different mitochondrial remodeling in rat skeletal muscle based on baseline aerobic capacity and muscle type.

This study uses phosphoproteomics to show how genetic background and diet influence insulin signalling in muscle, revealing key regulators of insulin responsiveness and glycolysis in insulin resistance.

The paper identifies small molecules that reverse insulin resistance in mouse skeletal muscle by integrating systems genetics and chemical screening.

The paper develops a genetic method to measure tissue-specific insulin signaling dynamics in Drosophila using phosphorylated Akt quantification.

This study examines the association between metformin use and DNA methylation profiles in blood samples to explore potential epigenetic mechanisms of aging and longevity.

This study uses multiomic analysis of skeletal muscle in obese and healthy mice to reveal differences in metabolic regulation by metabolites and genes after glucose administration.