Cited by 924Birth, Development, and HealthPancreatic function and diabetesDiabetes, Cardiovascular Risks, and Lipoproteins

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Type 2 diabetes across generations: from pathophysiology to prevention and management

Nolan, Christopher J, Damm, Peter, Prentki, Marc·2011·The Lancet

DOI 10.1016/s0140-6736(11)60614-4

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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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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
ORCID: Nolan, Christopher J
Damm, Peter
Prentki, Marc
Venue: The Lancet
Publisher: Elsevier BV
Published: 2011-07
Volume: 378
Issue: 9786
Pages: 169-181
ISSN: 0099-5355 (ISSN-L)
0140-6736
DOI: 10.1016/s0140-6736(11)60614-4
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
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 › Endocrinology, Diabetes and Metabolism › 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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Type 2 diabetes across generations: from pathophysiology to prevention and management

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