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Bioscience Metabolism

As seen in: Nature, Wiley Online Library, Frontiers, JoVE- Journal of Visualized Experiments, Journal of Pharmacology and Experimental Therapeutics
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Articles

Insulin-stimulated glucose uptake is impaired in senescent human adipocytes

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By Bioscience Metabolism, Bioscience Renal
| Frontiers
Abstract Background: Cell senescence, a state of cell cycle arrest induced by intrinsic or extrinsic stress, is linked to aging and aging-associated diseases. Senescence markers are elevated in adipose tissue with age and in obesity. Recently, it was shown that human mature adipocytes can undergo senescence in response to hyperinsulinemia. However, the functional consequences of adipocyte cell senescence remain poorly understood.
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Preclinical Evaluation and First-In-Human Phase 1 Trial of AZD0186, a Novel, Oral Small Molecule Glucagon-Like Peptide-1 Receptor Agonist

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By Alessandro Boianelli, Bioscience Metabolism, Sara Lundqvist
| Journal of Pharmacology and Experimental Therapeutics
ArticleArticles in Press103683Open access 1Translational Sciences and Clinical Development, Early Cardiovascular, Renal and Metabolism, BioPharmaceuticals, R&D, AstraZeneca, Gaithersburg, MD, USA 2Biometrics, Early Oncology, AstraZeneca, Gaithersburg, Maryland, USA 3DMPK, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden 4Bioscience Metabolism, Research and Early Development, Cardiovascular, Renal and Metabolism,...
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Targeting PNPLA3 to Treat MASH and MASH Related Fibrosis and Cirrhosis

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By Bioscience Metabolism, Sahlgrenska Academy, Gregory J. Tesz
| Wiley Online Library Verified
PNPLA3 rs738409, 148M, is the strongest genetic risk allele variant for MASLD, MASH and metALD related fibrosis and cirrhosis. PNPLA3 148M induces liver steatosis, inflammation and fibrosis in preclinical experimental studies. Silencing of PNPLA3 148M improves MASH and liver fibrosis in liver cellular systems and humanised transgenic mouse models.
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