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Glucocorticoid-induced bone loss linked with marrow adipocyte senescence
Shimona StarlingÂÂ
Succinate signalling regulates leptin production in adipocytes
Olivia TysoeÂÂ
Urban built environments: interventions for reducing cardiometabolic risks
Chinmoy Sarkar & Ka Yan LaiÂ
Adipose tissue boosts muscle regeneration by supplying mesenchymal stromal cells
Akiyoshi UezumiÂÂ
Large study on hormone therapy for transgender youth provides reassurance amid treatment politicization
Ximena Lopez & Laura E. KuperÂ
Revisiting the role of glucagon in health, diabetes mellitus and other metabolic diseases
Sofie Hædersdal, Andreas Andersen, Filip K. Knop & Tina VilsbøllÂ
doi : 10.1038/s41574-023-00817-4
Insulin and glucagon exert opposing effects on glucose metabolism and, consequently, pancreatic islet β-cells and α-cells are considered functional antagonists. The intra-islet hypothesis has previously dominated the understanding of glucagon secretion, stating that insulin acts to inhibit the release of glucagon. By contrast, glucagon is a potent stimulator of insulin secretion and has been used to test β-cell function. Over the past decade, α-cells have received increasing attention due to their ability to stimulate insulin secretion from neighbouring β-cells, and α-cell–β-cell crosstalk has proven central for glucose homeostasis in vivo.
The role of ChREBP in carbohydrate sensing and NAFLD development
Marion Régnier, Thaïs Carbinatti, Lucia Parlati, Fadila Benhamed & Catherine PosticÂ
doi : 10.1038/s41574-023-00809-4
Excessive sugar consumption and defective glucose sensing by hepatocytes contribute to the development of metabolic diseases including type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD). Hepatic metabolism of carbohydrates into lipids is largely dependent on the carbohydrate-responsive element binding protein (ChREBP), a transcription factor that senses intracellular carbohydrates and activates many different target genes, through the activation of de novo lipogenesis (DNL).
Mammalian models of diabetes mellitus, with a focus on type 2 diabetes mellitus
Thomas A. LutzÂÂ
doi : 10.1038/s41574-023-00818-3
Although no single animal model replicates all aspects of diabetes mellitus in humans, animal models are essential for the study of energy balance and metabolism control as well as to investigate the reasons for their imbalance that could eventually lead to overt metabolic diseases such as type 2 diabetes mellitus.
A perspective on treating type 1 diabetes mellitus before insulin is needed
Danijela Tatovic, Parth Narendran & Colin M. DayanÂ
doi : 10.1038/s41574-023-00816-5
Type 1 diabetes mellitus (T1DM) is a progressive autoimmune disease that starts long before a clinical diagnosis is made. The American Diabetes Association recognizes three stages: stage 1 (normoglycaemic and positive for autoantibodies to β-cell antigens); stage 2 (asymptomatic with dysglycaemia); and stage 3, which is defined by glucose levels consistent with the definition of diabetes mellitus. This Perspective focuses on the management of the proportion of individuals with early stage 3 T1DM who do not immediately require insulin; a stage we propose should be termed stage 3a.
Author Correction: A perspective on treating type 1 diabetes mellitus before insulin is needed
Danijela Tatovic, Parth Narendran & Colin M. DayanÂ
