A Low-Protein Isocaloric Diet During Gestation Affects Brain Development and Alters Permanently Cerebral Cortex Blood Vessels in Rat Offspring

BennisTaleb, N; Remacle, Claude; Hoet, J. J.; Reusens, Brigitte

doi:10.1093/jn/129.8.1613

Cited by 100 publications

(51 citation statements)

References 26 publications

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“…Brain growth is spared and as a proportion of body weight it is greater in the low-protein offspring. This factor may not reflect brain function, as vascularisation of the developing brain is permanently reduced in these animals (Bennis-Taleb et al 1999). By contrast, the pancreas shows reduced b-cell proliferation, islet size, vascularisation (Snoeck et al 1990) and a reduction in islet cell function (Cherif et al 1998).…”

Section: Experimental Models Of Early Growth Restrictionmentioning

confidence: 99%

Fetal origins of insulin resistance and obesity

2005

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A number of epidemiological studies worldwide have demonstrated a relationship between poor early growth and an increased susceptibility to insulin resistance, visceral obesity, type 2 diabetes and other features of the metabolic syndrome in adulthood. However, the mechanistic basis of this relationship and the relative roles of genes and the environment remain a subject of debate. The ‘thrifty phenotype’ hypothesis proposes that poor fetal nutrition leads to programming of metabolism and an adult phenotype that is adapted to poor but not plentiful nutrition. The maternal reduced-protein rat model has been used to examine the importance of the maternal environment in determining susceptibility to adult disease. Pregnant and lactating rat dams are fed a diet containing 80 g protein/kg as compared with 200 g protein/kg, which leads to growth restriction in utero. Offspring of low-protein dams have increased susceptibility to diabetes, insulin resistance and hypertension when fed a palatable high-fat diet that promotes obesity. Administration of leptin during pregnancy and lactation to these protein-restricted dams produces offspring that have increased metabolic rate and do not become obese or insulin resistant when fed on a high-fat diet. Increased glucocorticoid exposure, particularly during late gestation, has been linked with insulin resistance in adulthood. High levels of fetal glucocorticoids may result from a decreased activity of placental 11β-hydroxysteroid dehydrogenase (11β-HSD) type 2, which normally protects the fetus from high maternal glucocorticoid levels. Leptin administration to protein-restricted dams inhibits the suppression of 11β-HSD-2 and may be one mechanism by which the metabolic syndrome is prevented.

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Section: Experimental Models Of Early Growth Restrictionmentioning

confidence: 99%

Fetal origins of insulin resistance and obesity

2005

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“…Malnutrition during gestation and lactation in rats resulted in metabolic programming of the hypothalamus, muscle, liver and pancreatic islets in the offspring, accompanied by adult-onset diseases in these offspring. [1][2][3][4] Paternal programming also influences offspring metabolism. High-fat programming is induced by maternal high saturated fat intake during defined periods of gestation and/or lactation and programs the physiology and metabolism of the offspring 18 but can be extended to include the influence of paternal high-fat feeding on offspring development and health.…”

Section: Introductionmentioning

confidence: 99%

Parental high-fat programming of offspring development, health and β-cells

Cerf¹

2011

Islets

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“…Even a low protein diet during the last week of pregnancy only led to an impaired pancreatic beta cell mass (Bertin et al, 1999). In adult offspring increased hepatic glucose output, age-related loss of glucose tolerance, hyperinsulinaemia, insulin resistance, altered brain development and hypertension was observed (Ozanne et al, 1996(Ozanne et al, , 2001(Ozanne et al, , 2003Gardner et al, 1997;Bennis-Taleb, 1999;Fernandez-Twinn et al, 2005). demonstrated that low protein intake during pregnancy compromises the immune system in the young adult offspring.…”

Section: Protein Undernutrition and Protein Excessmentioning

confidence: 99%

Nutritional programming: prenatal nutritional effects on the regulation of growth and metabolism

Metges¹,

Hammon²

2005

J. Anim. Feed Sci.

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Research on the foetal nutritional origins of adult onset disease in rodents have uncovered a plethora of programming effects on adult metabolic and cardiovascular health. This relationship is a consequence of disordered foetal growth and alteration of the programmed development of various homeostatic control points. Until recently, applicability of early nutritional programming to livestock species has received little attention. An overview is given on the evidence of foetal programming effects brought about by global and protein under-and overnutrition in rodents and sheep. Maternal and foetal endocrine alterations of glucocorticoids, insulin and the insulin-like growth factor system related to maternal malnutrition during pregnancy are discussed.

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A Low-Protein Isocaloric Diet During Gestation Affects Brain Development and Alters Permanently Cerebral Cortex Blood Vessels in Rat Offspring

Cited by 100 publications

References 26 publications

Fetal origins of insulin resistance and obesity

Fetal origins of insulin resistance and obesity

Parental high-fat programming of offspring development, health and β-cells

Nutritional programming: prenatal nutritional effects on the regulation of growth and metabolism

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