Animal evidence for the transgenerational development of diabetes mellitus

Aerts, L.; Assche, F.A. Van

doi:10.1016/j.biocel.2005.07.006

Cited by 194 publications

(149 citation statements)

References 46 publications

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“…Moreover, normalization of the maternal glycaemia by islet transplantation prevents deleterious effects for the fetus and offspring [3] . It seems clear that (over-) stimulation of the fetal B cell reduces the function of this cell in the offspring [4] . However, it may be possible that fetal hyperinsulinism itself may induce malprogramming [41] .…”

Section: Animal Datamentioning

confidence: 99%

“…A population subjected to poor nutrition in the perinatal period can keep a normal glucose tolerance as long as they remain on a low caloric diet. A change to a higher caloric intake and low physical activity increases the incidence of impaired glucose tolerance and type 2 diabetes increases [4] . In this respect, a high caloric intake in the postnatal period inducing catch up growth will aggravate the consequences in later life [25,26] .…”

Section: Fetal Environment and Intra-uterine Growth Restriction Humanmentioning

confidence: 99%

“…Certainly the environment in utero and in early neonatal life may induce a permanent response in the fetus and the newborn, leading to enhanced susceptibility to later diseases. These effects can be transgenerational and are probably due to an epigenetic transmission mediated by the mother [4,44] .…”

Section: Introductionmentioning

confidence: 99%

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Fetal growth and developmental programming

Galjaard

Devlieger²,

Assche³

2012

Journal of Perinatal Medicine

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The environment in utero and in early neonatal life may induce a permanent response in the fetus and the newborn, leading to enhanced susceptibility to later diseases. This review concentrates on the role and mechanisms of events during the antenatal and immediate postnatal period resulting in later life diseases, concentrating on abnormal growth patterns of the fetus. Fetal overgrowth is related to exposure to a diabetic intra uterine environment, increasing the vulnerability to transgenerational obesity and hence an increased sensitivity to more diabetic mothers. This effect has been supported by animal data. Fetal growth restriction is complex due to malnutrition in utero , catch up growth due to a high caloric intake and low physical activity in later life. Metabolic changes and a transgenerational effect of intra uterine malnutrition has been supported by animal data. In recent years the discovery of alterations of the genome due to different infl uences during embryonic life, called epigenetics, has led to the phenomenon of fetal programming resulting in changing transgenerational metabolic effects.

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Section: Animal Datamentioning

confidence: 99%

Section: Fetal Environment and Intra-uterine Growth Restriction Humanmentioning

confidence: 99%

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Fetal growth and developmental programming

Galjaard

Devlieger²,

Assche³

2012

Journal of Perinatal Medicine

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“…A recent review study suggested that inadequate maternal nutrition might disturb the development of the fetus, which must adopt strategies to ensure survival that will programme its future health [3]. In experimental animal models, alteration of the intrauterine environment induced, for example, by gestational diabetes [4], placental insufficiency [5,6] or poor maternal nutrition [7][8][9][10][11] compromise the development of endocrine pancreas in the progeny and impact on its future health even in the subsequent generation [4,6,12]. Reduction of food intake by 50% in rats during gestation reduced the beta cell mass in offspring at birth by 30% [9].…”

Section: Introductionmentioning

confidence: 99%

The intrauterine metabolic environment modulates the gene expression pattern in fetal rat islets: prevention by maternal taurine supplementation

et al. 2008

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Aims/hypothesis Events during fetal life may in critical time windows programme tissue development leading to organ dysfunction with potentially harmful consequences in adulthood such as diabetes. In rats, the beta cell mass of progeny from dams fed with a low-protein (LP) diet during gestation is decreased at birth and metabolic perturbation lasts through adulthood even though a normal diet is given after birth or after weaning. Maternal and fetal plasma taurine levels are suboptimal. Maternal taurine supplementation prevents these induced abnormalities. In this study, we aimed to reveal changes in gene expression in fetal islets affected by the LP diet and how taurine may prevent these changes. Methods Pregnant Wistar rats were fed an LP diet (8% [wt/wt] protein) supplemented or not with taurine in the drinking water or a control diet (20% [wt/wt] protein). At 21.5 days of gestation, fetal pancreases were removed, digested and cultured for 7 days. Neoformed islets were collected and transcriptome analysis was performed. Results Maternal LP diet significantly changed the expression of more than 10% of the genes. Tricarboxylic acid cycle and ATP production were highly targeted, but so too were cell proliferation and defence. Maternal taurine supplementation normalised the expression of all altered genes. Conclusions/interpretation Development of the beta cells and particularly their respiration is modulated by the intrauterine environment, which may epigenetically modify expression of the genome and programme the beta cell towards a pre-diabetic phenotype. This mis-programming by maternal LP diet was prevented by early taurine intervention.Keywords Diabetes . Early programming . Fetal islets . Maternal low-protein diet . Rats . Taurine . Transcriptome Abbreviations EST expressed sequence tag LP low protein LPT low-protein diet supplemented with taurine SAM significance analysis of microarrays TCA tricarboxylic acid Diabetologia (2008) 51:836-845

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“…We do not know what range of phenotypes to expect when epigenetic systems that evolved over millions of years respond to new environmental variables such as refined foods, drugs, and xenobiotics. Glucose (15)(16)(17) and endocrine disrupters (18) are examples of factors leading to apparent epigenetic transgenerational effects in mammals; however, the genes responsible for the effects are not known. Now Cropley et al (5) show that methyl donors have transgenerational effects attributed to a known allele, A vy .…”

mentioning

confidence: 99%

Germ cells carry the epigenetic benefits of grandmother's diet

Cooney

2006

Proc. Natl. Acad. Sci. U.S.A.

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Animal evidence for the transgenerational development of diabetes mellitus

Cited by 194 publications

References 46 publications

Fetal growth and developmental programming

Fetal growth and developmental programming

The intrauterine metabolic environment modulates the gene expression pattern in fetal rat islets: prevention by maternal taurine supplementation

Germ cells carry the epigenetic benefits of grandmother's diet

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