The effects of maternal protein deprivation on the fetal rat pancreas: major structural changes and their recuperation

Berney, Daniel M.; Desai, Mintu; Palmer, Dennis; Greenwald, Stephen E.; Brown, A.; Hales, C. N.; Berry, C. L.

doi:10.1002/(sici)1096-9896(199709)183:1<109::aid-path1091>3.3.co;2-2

Cited by 17 publications

(20 citation statements)

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“…A Cochrane systematic review, which uses trials conducted in developing countries and/or in poor communities, demonstrated that balanced protein-energy supplementation can reduce the risk of small for gestational age neonates by approximately 30% (Kramer and Kakuma, 2003). It is important to stress that maternal protein deprivation modifies hepatic lipogenic transcription factors and lipid enzymes such as lipolytic lipoprotein lipase (Berney et al, 1997;Desai et al, 1996). Lipid dysfunction is sex-gender dependent.…”

Section: Pregnancymentioning

confidence: 99%

Nutrition and human health from a sex–gender perspective

Marino

Masella

Bulzomi

et al. 2011

Molecular Aspects of Medicine

127

108

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Section: Pregnancymentioning

confidence: 99%

Nutrition and human health from a sex–gender perspective

Marino

Masella

Bulzomi

et al. 2011

Molecular Aspects of Medicine

127

108

View full text Add to dashboard Cite

“…The most commonly used animal models for IUGR are caloric or protein restriction, glucocorticoid administration, or induction of uteroplacental insufficiency in the pregnant rodent. In the rat, maternal dietary protein restriction (approximately 40-50% of normal intake, termed LP) throughout gestation and lactation has been reported to alter insulin secretory capacity and reduce β-cell mass through a reduction in β-cell proliferation rate and an increase in apoptosis [47][48][49][50][51][52][53][54][55]. Expression of Pdx-1 (pancreatic duodenal homeobox-1), a homeodomain-containing transcription factor that regulates early development of both endocrine and exocrine pancreas, and later differentiation and function of β-cells [56], is also reduced in islets from pups of LP mothers [57].…”

Section: What Animal Models Can Tell Usmentioning

confidence: 99%

Role of metabolic programming in the pathogenesis of β-cell failure in postnatal life

Simmons

2007

Rev Endocr Metab Disord

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Intrauterine growth retardation (IUGR) has been linked to later development of type 2 diabetes in adulthood. Human studies indicate that individuals who were growth retarded at birth have impaired insulin secretion and insulin resistance. Multiple animal models of IUGR demonstrate impaired beta-cell function and development. We have developed a model of IUGR in the rat that leads to diabetes in adulthood with the salient features of most forms of type 2 diabetes in the human: progressive defects in insulin secretion and insulin action prior to the onset of overt hyperglycemia. Decreased beta-cell proliferation leads to a progressive decline in beta-cell mass. Using this model, we have tested the hypothesis that uteroplacental insufficiency disrupts the function of the electron transport chain in the fetal beta-cell and leads to a debilitating cascade of events: increased production of reactive oxygen species, which in turn damage mitochondrial (mt) mtDNA and causes further production of reactive oxygen species (ROS). The net result is progressive loss of beta-cell function and eventual development of type 2 diabetes in the adult. Studies in the IUGR rat also demonstrate that an abnormal intrauterine environment induces epigenetic modifications of key genes regulating beta-cell development; experiments directly link chromatin remodeling with suppression of transcription. Future research will be directed at elucidating the mechanisms underlying epigenetic modifications in offspring.

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“…For instance, it has been demonstrated that maternal malnutrition during pregnancy and lactation may induce the loss of proliferative capacity and decreases pancreatic islets' vascularization in the offspring, reducing insulin secretion and inducing glucose intolerance [7][8][9][10][11]. Insulin secretion depends essentially on glucose uptake by the pancreatic beta cells.…”

Section: Introductionmentioning

confidence: 99%