Impact of fetal and neonatal environment on beta cell function and development of diabetes
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Impact of fetal and neonatal environment on beta cell function and development of diabetes. / Nielsen, Jens H; Haase, Tobias N; Jaksch, Caroline; Nalla, Amarnadh; Søstrup, Birgitte; Nalla, Anjana A; Larsen, Louise; Rasmussen, Morten; Dalgaard, Louise T; Gaarn, Louise W; Thams, Peter; Kofod, Hans; Billestrup, Nils.
In: Acta Obstetricia et Gynecologica Scandinavica, Vol. 93, No. 11, 11.2014, p. 1109-22.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Impact of fetal and neonatal environment on beta cell function and development of diabetes
AU - Nielsen, Jens H
AU - Haase, Tobias N
AU - Jaksch, Caroline
AU - Nalla, Amarnadh
AU - Søstrup, Birgitte
AU - Nalla, Anjana A
AU - Larsen, Louise
AU - Rasmussen, Morten
AU - Dalgaard, Louise T
AU - Gaarn, Louise W
AU - Thams, Peter
AU - Kofod, Hans
AU - Billestrup, Nils
N1 - © 2014 Nordic Federation of Societies of Obstetrics and Gynecology.
PY - 2014/11
Y1 - 2014/11
N2 - The global epidemic of diabetes is a serious threat against health and healthcare expenses. Although genetics is important it does not explain the dramatic increase in incidence, which must involve environmental factors. Two decades ago the concept of the thrifty phenotype was introduced, stating that the intrauterine environment during pregnancy has an impact on the gene expression that may persist until adulthood and cause metabolic diseases like obesity and type 2 diabetes. As the pancreatic beta cells are crucial in the regulation of metabolism this article will describe the influence of normal pregnancy on the beta cells in both the mother and the fetus and how various conditions like diabetes, obesity, overnutrition and undernutrition during and after pregnancy may influence the ability of the offspring to adapt to changes in insulin demand later in life. The influence of environmental factors including nutrients and gut microbiota on appetite regulation, mitochondrial activity and the immune system that may affect beta cell growth and function directly and indirectly is discussed. The possible role of epigenetic changes in the transgenerational transmission of the adverse programming may be the most threatening aspect with regard to the global diabetes epidemics. Finally, some suggestions for intervention are presented.
AB - The global epidemic of diabetes is a serious threat against health and healthcare expenses. Although genetics is important it does not explain the dramatic increase in incidence, which must involve environmental factors. Two decades ago the concept of the thrifty phenotype was introduced, stating that the intrauterine environment during pregnancy has an impact on the gene expression that may persist until adulthood and cause metabolic diseases like obesity and type 2 diabetes. As the pancreatic beta cells are crucial in the regulation of metabolism this article will describe the influence of normal pregnancy on the beta cells in both the mother and the fetus and how various conditions like diabetes, obesity, overnutrition and undernutrition during and after pregnancy may influence the ability of the offspring to adapt to changes in insulin demand later in life. The influence of environmental factors including nutrients and gut microbiota on appetite regulation, mitochondrial activity and the immune system that may affect beta cell growth and function directly and indirectly is discussed. The possible role of epigenetic changes in the transgenerational transmission of the adverse programming may be the most threatening aspect with regard to the global diabetes epidemics. Finally, some suggestions for intervention are presented.
KW - Diabetes, Gestational
KW - Epigenesis, Genetic
KW - Female
KW - Fetal Development
KW - Humans
KW - Insulin-Secreting Cells
KW - Maternal Nutritional Physiological Phenomena
KW - Obesity
KW - Phenotype
KW - Pregnancy
KW - Prenatal Exposure Delayed Effects
KW - Prenatal Nutritional Physiological Phenomena
KW - Risk Factors
U2 - 10.1111/aogs.12504
DO - 10.1111/aogs.12504
M3 - Journal article
C2 - 25225114
VL - 93
SP - 1109
EP - 1122
JO - Acta Obstetricia et Gynecologica Scandinavica
JF - Acta Obstetricia et Gynecologica Scandinavica
SN - 0001-6349
IS - 11
ER -
ID: 132899492