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Publications

Journal Article Review Ppublish 51 citations

PubMed: 39059357 DOI: 10.1016/j.cell.2024.06.029

Diabetes mellitus-Progress and opportunities in the evolving epidemic.

Cell 187(15):3789-3820

Authors: E Dale Abel, Anna L Gloyn, Carmella Evans-Molina, Joshua J Joseph, Shivani Misra, Utpal B Pajvani, Judith Simcox, Katalin Susztak, Daniel J Drucker

Affiliations

  • Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
  • Department of Pediatrics, Division of Endocrinology & Diabetes, Department of Genetics, Stanford Diabetes Research Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Division of Endocrinology, Diabetes and Metabolism, The Ohio State University College of Medicine, Columbus, OH, USA.
  • Department of Metabolism, Digestion and Reproduction, Imperial College London, and Imperial College NHS Trust, London, UK.
  • Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA.
  • Howard Hughes Medical Institute, Department of Biochemistry, University of Wisconsin-Madison, Madison, WI, USA.
  • Renal, Electrolyte, and Hypertension Division, Department of Medicine, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, USA.
  • Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, ON, Canada; Department of Medicine, University of Toronto, Toronto, ON, Canada.

Abstract

Diabetes, a complex multisystem metabolic disorder characterized by hyperglycemia, leads to complications that reduce quality of life and increase mortality. Diabetes pathophysiology includes dysfunction of beta cells, adipose tissue, skeletal muscle, and liver. Type 1 diabetes (T1D) results from immune-mediated beta cell destruction. The more prevalent type 2 diabetes (T2D) is a heterogeneous disorder characterized by varying degrees of beta cell dysfunction in concert with insulin resistance. The strong association between obesity and T2D involves pathways regulated by the central nervous system governing food intake and energy expenditure, integrating inputs from peripheral organs and the environment. The risk of developing diabetes or its complications represents interactions between genetic susceptibility and environmental factors, including the availability of nutritious food and other social determinants of health. This perspective reviews recent advances in understanding the pathophysiology and treatment of diabetes and its complications, which could alter the course of this prevalent disorder.

MeSH

Diabetes Mellitus, Cells, Food, Cell Biology, Environment, Epidemics

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