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Mentorship in academic medicine: truth is in the eye of the beholder
Maria Fleseriu & Dawn Shao Ting LimÂ
doi : 10.1038/s41574-023-00846-z
Volume 19 Issue 7, July 2023
Artificial intelligence in diabetes mellitus and endocrine diseases � what can we expect?
Ioannis T. Oikonomakos, Charlotte Steenblock & Stefan R. BornsteinÂ
Approval of teplizumab: implications for patients
Cate Speake & Carla J. GreenbaumÂ
Gut microbiota influences effectiveness of anti-diabetic drug
Claire GreenhillÂ
Nonenzymatic prevention of insulin hyperresponsiveness by FBP1
Felicity TournantÂ
Glucocorticoid activation of macrophages protects against insulin resistance
Shimona StarlingÂÂ
Targeting senescent cells in ageing-related endocrine diseases
Joshua StokarÂÂ
Programming of metabolism by adipokines during development
Jose Donato JrÂ
doi : 10.1038/s41574-023-00828-1
The intrauterine and early postnatal periods represent key developmental stages in which an organism is highly susceptible to being permanently influenced by maternal factors and nutritional status. Strong evidence indicates that either undernutrition or overnutrition during development can predispose individuals to disease later in life, especially type 2 diabetes mellitus and obesity, a concept known as metabolic programming.
Adrenal cysts: an emerging condition
Jan Calissendorff, C. Christofer Juhlin, Anders Sundin, Irina Bancos & Henrik FalhammarÂ
doi : 10.1038/s41574-023-00835-2
Adrenal cysts are rare lesions representing approximately 1–2% of adrenal incidentalomas. The majority of these rare lesions are benign. Rarely, phaeochromocytomas and adrenal malignant masses can present as cystic lesions and can occasionally be difficult to distinguish from benign cysts.
The G protein-coupled oestrogen receptor GPER in health and disease: an update
Eric R. Prossnitz & Matthias BartonÂ
doi : 10.1038/s41574-023-00822-7
Oestrogens and their receptors contribute broadly to physiology and diseases. In premenopausal women, endogenous oestrogens protect against cardiovascular, metabolic and neurological diseases and are involved in hormone-sensitive cancers such as breast cancer.
Why does the immune system destroy pancreatic β-cells but not α-cells in type 1 diabetes?
Decio L. Eizirik, Florian Szymczak & Roberto MalloneÂ
doi : 10.1038/s41574-023-00826-3
A perplexing feature of type 1 diabetes (T1D) is that the immune system destroys pancreatic β-cells but not neighbouring α-cells, even though both β-cells and α-cells are dysfunctional. Dysfunction, however, progresses to death only for β-cells.
