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http://dx.doi.org/10.1016/j.jcjd.2019.08.010 | DOI Listing |
Res Sq
March 2024
Hagey Laboratory for Pediatric Regenerative Medicine, Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University School of Medicine; Stanford, California, 94305, USA.
Front Vet Sci
February 2024
Tropical Crop Genetic Resource Research Institute, Chinese Academy of Tropical Agricultural Sciences, Haikou, China.
Diabetologia
March 2024
Metabolic Physiology Unit, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Gothenburg, Sweden.
Aims/hypothesis: Diabetes mellitus is associated with impaired insulin secretion, often aggravated by oversecretion of glucagon. Therapeutic interventions should ideally correct both defects. Glucagon-like peptide 1 (GLP-1) has this capability but exactly how it exerts its glucagonostatic effect remains obscure.
View Article and Find Full Text PDFJ Endocrinol
March 2024
Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK.
J Cell Sci
November 2023
Intracellular Trafficking Laboratory, Transdisciplinary Biology Research Program, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, Kerala 695014, India.
The rapid activation of the crucial kinase mechanistic target of rapamycin complex-1 (mTORC1) by insulin is key to cell growth in mammals, but the regulatory factors remain unclear. Here, we demonstrate that cholesterol plays a crucial role in the regulation of insulin-stimulated mTORC1 signaling. The rapid progression of insulin-induced mTORC1 signaling declines in sterol-depleted cells and restores in cholesterol-repleted cells.
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