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Pancreatic β-cell dysfunction contributes to type 2 diabetes mellitus (T2DM) pathogenesis. However, human islet studies have revealed few consistent molecular changes in T2DM, owing partly to technical and biological confounding factors. A new multi-omics study of islets from well-phenotyped living donors attempts to overcome these limitations to catalogue T2DM-associated molecular changes.
Immune checkpoint inhibitor therapies induce potent anti-tumour immunity as well as immune-related adverse events that manifest as autoimmune disease — particularly thyroiditis. Translational studies and preclinical models are beginning to unravel the molecular processes that mediate these adverse events; this knowledge might enable the development of ICIs with anti-tumour efficacy and improved safety margins.
Adipose tissue macrophages (ATMs) have important roles in the regulation of inflammatory responses and insulin resistance in obesity. A new study reports that a subpopulation of ATMs, TIM4+ resident ATMs, modulate adipocyte size via platelet-derived growth factor-CC production during development and diet-induced adipose tissue expansion.
The cellular consequences of dysfunctional autophagy contribute to numerous diseases. In this Review, Kitada and Koya consider the relationship between impaired autophagy and age-related metabolic derangements, including insulin resistance, type 2 diabetes mellitus and sarcopenic obesity, and discuss candidate autophagy-based therapies.
Although sexual dimorphism of the liver is well known, its contribution to non-alcoholic fatty liver disease (NAFLD) is often overlooked. Here, Lefebvre and Staels discuss liver sexual dimorphism in the context of increasingly accurate studies of cellular modifications in NAFLD.
Anterior pituitary tumours (APTs) are usually benign but sometimes exhibit aggressive behaviour. In very rare cases, they metastasize and are termed pituitary carcinomas. Here, the authors provide an overview of APTs and pituitary carcinomas, including their epidemiology, diagnosis, predictive markers, and current and emerging therapeutic approaches.
This Review outlines the pathogenesis of skeletal fragility in patients with type 2 diabetes mellitus, and discusses potential therapeutic approaches to the management of increased fracture risk in these patients. The evidence that skeletal fragility should now be included in the list of well-recognized diabetic complications is also summarized.
