Type 2 diabetes across generations: from pathophysiology to prevention and management
Abstract
Type 2 diabetes is now a pandemic and shows no signs of abatement. In this Seminar we review the pathophysiology of this disorder, with particular attention to epidemiology, genetics, epigenetics, and molecular cell biology. Evidence is emerging that a substantial part of diabetes susceptibility is acquired early in life, probably owing to fetal or neonatal programming via epigenetic phenomena. Maternal and early childhood health might, therefore, be crucial to the development of effective prevention strategies. Diabetes develops because of inadequate islet β-cell and adipose-tissue responses to chronic fuel excess, which results in so-called nutrient spillover, insulin resistance, and metabolic stress. The latter damages multiple organs. Insulin resistance, while forcing β cells to work harder, might also have an important defensive role against nutrient-related toxic effects in tissues such as the heart. Reversal of overnutrition, healing of the β cells, and lessening of adipose tissue defects should be treatment priorities.
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The liver does not seem to be a primary pathogenic driver of T2DM or GDM.
“Despite this, the liver does not seem to be a primary pathogenic driver of T2DM or GDM [123].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [123]
Attempts to directly reverse skeletal muscle insulin resistance, without reducing plasma glucose concentrations, could be detrimental.
“This is an important distinction when considering potential treatments for GDM: attempts to directly reverse skeletal muscle insulin resistance, without reducing plasma glucose concentrations, could be detrimental [123].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [123]
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- Authors
- Nolan, C. J., Damm, P., & Prentki, M.
- Affiliations
- Australian National University (AU)
- University of Copenhagen (DK)
- Université de Montréal (CA)
- Corresponding author
- Nolan, Christopher J
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 378
- Issue
- 9786
- Pages
- 169-181
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- OpenAlex
- W2156472431
- Cited by
- 923
- References
- 146
- Citations by year
- 2026: 13 · 2025: 23 · 2024: 43 · 2023: 42 · 2022: 54 · 2021: 60 · 2020: 57 · 2019: 58 · 2018: 58 · 2017: 55 · 2016: 93 · 2015: 86 · 2014: 104 · 2013: 90 · 2012: 78
- FWCI
- 13.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
- ANU Open Research (Australian National University) (submittedVersion)
- Funders
- Novo Nordisk
- Novo Nordisk Fonden
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- type 2 diabetes, pathophysiology, insulin resistance, beta-cell dysfunction, adipose tissue dysfunction, metabolic stress, epigenetics, fetal programming, neonatal programming, genetic susceptibility, diabetes prevention, diabetes management, overnutrition, maternal health, early childhood health
- MeSH terms
- Adipose Tissue, Animals, Blood Glucose, Diabetes Mellitus, Type 2, Diabetic Retinopathy, Female, Glucagon, Homeostasis, Humans, Insulin Resistance, Life Style, Liver, Myocardium, Obesity, Prediabetic State, Pregnancy, Diabetes, Gestational, Muscle, Skeletal, Genetic Predisposition to Disease, Epigenesis, Genetic, Fetal Development, Insulin-Secreting Cells, Glucagon-Like Peptide 1, Incretins
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