The thrifty phenotype hypothesis revisited
(2012) In Diabetologia 55(8). p.2085-2088- Abstract
- Twenty years ago, Hales and Barker along with their co-workers published some of their pioneering papers proposing the 'thrifty phenotype hypothesis' in Diabetologia (4;35:595-601 and 3;36:62-67). Their postulate that fetal programming could represent an important player in the origin of type 2 diabetes, the metabolic syndrome and cardiovascular disease (CVD) was met with great scepticism. More recently, their observations have been confirmed and expanded in many epidemiological and animal experimental studies, and human integrative physiological studies have provided insights into some of the underlying molecular mechanisms. Type 2 diabetes is a multiple-organ disease, and developmental programming, with its idea of organ plasticity, is a... (More)
- Twenty years ago, Hales and Barker along with their co-workers published some of their pioneering papers proposing the 'thrifty phenotype hypothesis' in Diabetologia (4;35:595-601 and 3;36:62-67). Their postulate that fetal programming could represent an important player in the origin of type 2 diabetes, the metabolic syndrome and cardiovascular disease (CVD) was met with great scepticism. More recently, their observations have been confirmed and expanded in many epidemiological and animal experimental studies, and human integrative physiological studies have provided insights into some of the underlying molecular mechanisms. Type 2 diabetes is a multiple-organ disease, and developmental programming, with its idea of organ plasticity, is a plausible hypothesis for a common basis for the widespread organ dysfunctions in type 2 diabetes and the metabolic syndrome. Only two among the 45 known type 2 diabetes susceptibility genes are associated with low birthweight, indicating that the association between low birthweight and type 2 diabetes is mainly non-genetic. Prevention programmes targeting adult lifestyle factors seems unable to stop the global propagation of type 2 diabetes, and intensive glucose control is inadequate to reduce the excess CVD mortality in type 2 diabetic patients. Today, the thrifty phenotype hypothesis has been established as a promising conceptual framework for a more sustainable intergenerational prevention of type 2 diabetes. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2994875
- author
- Vaag, Allan LU ; Grunnet, L. G. ; Arora, Geeti LU and Brons, C.
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Fetal programming, Intergenerational prevention, Metabolic syndrome, Thrifty phenotype, Type 2 diabetes
- in
- Diabetologia
- volume
- 55
- issue
- 8
- pages
- 2085 - 2088
- publisher
- Springer
- external identifiers
-
- wos:000306122600001
- scopus:84866369211
- pmid:22643933
- ISSN
- 1432-0428
- DOI
- 10.1007/s00125-012-2589-y
- language
- English
- LU publication?
- yes
- id
- 97748b9a-d120-4b02-9495-f45ab454fab6 (old id 2994875)
- date added to LUP
- 2016-04-01 10:01:36
- date last changed
- 2024-04-06 23:01:07
@article{97748b9a-d120-4b02-9495-f45ab454fab6,
abstract = {{Twenty years ago, Hales and Barker along with their co-workers published some of their pioneering papers proposing the 'thrifty phenotype hypothesis' in Diabetologia (4;35:595-601 and 3;36:62-67). Their postulate that fetal programming could represent an important player in the origin of type 2 diabetes, the metabolic syndrome and cardiovascular disease (CVD) was met with great scepticism. More recently, their observations have been confirmed and expanded in many epidemiological and animal experimental studies, and human integrative physiological studies have provided insights into some of the underlying molecular mechanisms. Type 2 diabetes is a multiple-organ disease, and developmental programming, with its idea of organ plasticity, is a plausible hypothesis for a common basis for the widespread organ dysfunctions in type 2 diabetes and the metabolic syndrome. Only two among the 45 known type 2 diabetes susceptibility genes are associated with low birthweight, indicating that the association between low birthweight and type 2 diabetes is mainly non-genetic. Prevention programmes targeting adult lifestyle factors seems unable to stop the global propagation of type 2 diabetes, and intensive glucose control is inadequate to reduce the excess CVD mortality in type 2 diabetic patients. Today, the thrifty phenotype hypothesis has been established as a promising conceptual framework for a more sustainable intergenerational prevention of type 2 diabetes.}},
author = {{Vaag, Allan and Grunnet, L. G. and Arora, Geeti and Brons, C.}},
issn = {{1432-0428}},
keywords = {{Fetal programming; Intergenerational prevention; Metabolic syndrome; Thrifty phenotype; Type 2 diabetes}},
language = {{eng}},
number = {{8}},
pages = {{2085--2088}},
publisher = {{Springer}},
series = {{Diabetologia}},
title = {{The thrifty phenotype hypothesis revisited}},
url = {{http://dx.doi.org/10.1007/s00125-012-2589-y}},
doi = {{10.1007/s00125-012-2589-y}},
volume = {{55}},
year = {{2012}},
}