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

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Type 2 diabetes across generations: from pathophysiology to prevention and management. / Nolan, Christopher J; Damm, Peter; Prentki, Marc.

I: Lancet, Bind 378, Nr. 9786, 2011, s. 169-81.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Nolan, CJ, Damm, P & Prentki, M 2011, 'Type 2 diabetes across generations: from pathophysiology to prevention and management', Lancet, bind 378, nr. 9786, s. 169-81. https://doi.org/10.1016/S0140-6736(11)60614-4

APA

Nolan, C. J., Damm, P., & Prentki, M. (2011). Type 2 diabetes across generations: from pathophysiology to prevention and management. Lancet, 378(9786), 169-81. https://doi.org/10.1016/S0140-6736(11)60614-4

Vancouver

Nolan CJ, Damm P, Prentki M. Type 2 diabetes across generations: from pathophysiology to prevention and management. Lancet. 2011;378(9786):169-81. https://doi.org/10.1016/S0140-6736(11)60614-4

Author

Nolan, Christopher J ; Damm, Peter ; Prentki, Marc. / Type 2 diabetes across generations: from pathophysiology to prevention and management. I: Lancet. 2011 ; Bind 378, Nr. 9786. s. 169-81.

Bibtex

@article{d7032ffb4e1245ffb8b47de6eacbb3ba,

title = "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 {\ss}-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 {\ss} 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 {\ss} cells, and lessening of adipose tissue defects should be treatment priorities.",

author = "Nolan, {Christopher J} and Peter Damm and Marc Prentki",

year = "2011",

doi = "http://dx.doi.org/10.1016/S0140-6736(11)60614-4",

language = "English",

volume = "378",

pages = "169--81",

journal = "The Lancet",

issn = "0140-6736",

publisher = "TheLancet Publishing Group",

number = "9786",

}

RIS

TY - JOUR

T1 - Type 2 diabetes across generations: from pathophysiology to prevention and management

AU - Nolan, Christopher J

AU - Damm, Peter

AU - Prentki, Marc

PY - 2011

Y1 - 2011

N2 - 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 ß-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 ß 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 ß cells, and lessening of adipose tissue defects should be treatment priorities.

AB - 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 ß-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 ß 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 ß cells, and lessening of adipose tissue defects should be treatment priorities.

U2 - http://dx.doi.org/10.1016/S0140-6736(11)60614-4

DO - http://dx.doi.org/10.1016/S0140-6736(11)60614-4

M3 - Journal article

VL - 378

SP - 169

EP - 181

JO - The Lancet

JF - The Lancet

SN - 0140-6736

IS - 9786

ER -

ID: 40147894