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The thrifty phenotype hypothesis revisited

Vaag, Allan LU ; Grunnet, L. G.; Arora, Geeti LU and Brons, C. (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)
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author
organization
publishing date
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 Verlag
external identifiers
  • wos:000306122600001
  • scopus:84866369211
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
2012-09-03 07:18:13
date last changed
2017-10-22 03:05:14
@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},
  keyword      = {Fetal programming,Intergenerational prevention,Metabolic syndrome,Thrifty phenotype,Type 2 diabetes},
  language     = {eng},
  number       = {8},
  pages        = {2085--2088},
  publisher    = {Springer Verlag},
  series       = {Diabetologia},
  title        = {The thrifty phenotype hypothesis revisited},
  url          = {http://dx.doi.org/10.1007/s00125-012-2589-y},
  volume       = {55},
  year         = {2012},
}