The Effect of Maternal Malnutrition During Lactation on the Endometrial ERα Expression, Collagen Type, and Blood Vessels in the Rats Offspring at Puberty

Brasil, Flávia Bittencourt; Faria, T.; Sampaio, Francisco J.B.; Ramos, Cristiane da Fonte

doi:10.1002/ar.21028

Cited by 6 publications

(4 citation statements)

References 45 publications

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“…Female mammals are expected to be more likely to suppress reproduction when food is limited [7]. While constrained food intake can alter hypothalamic [1; 6; 35] and uterine [4] sensitivity to estrogens, food restriction and photoperiod had no effect on estradiol levels in female California mice [40]. Several studies have suggested that glial cells may play an important role in regulation of the female reproductive axis.…”

Section: Introductionmentioning

confidence: 99%

Effects of photoperiod and food restriction on the reproductive physiology of female California mice

Steinman

Knight

Trainor

2012

General and Comparative Endocrinology

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Many temperate-zone animals use changes in photoperiod to time breeding. Shorter term cues, like food availability, are integrated with photoperiod to adjust reproductive timing under unexpected conditions. Many mice of the genus Peromyscus breed in the summer. California mice (Peromyscus californicus), however, can breed year round, but tend to begin breeding in the winter. Glial cells may be involved in transduction of environmental signals that regulate gonadotrophin releasing hormone (GnRH) activity. We examined the effects of diet and photoperiod on reproduction in female California mice. Mice placed on either short days (8L:16D) or long days (16L:8D) were food restricted (80% of normal intake) or fed ad libitum. Short day-food restricted mice showed significant regression of the reproductive system. GnRH-immunoreactivity was increased in the tuberal hypothalamus of long day-food restricted mice. This may be associated with the sparing effect long days have when mice are food restricted. The number of GFAP-immunoreactive fibers in proximity to GnRH nerve terminals correlated negatively with uterine size in ad libitum but not food restricted mice, suggesting diet may alter glial regulation of the reproductive axis. There was a trend towards food restriction increasing uterine expression of c-fos mRNA, an estrogen dependent gene. Similar to other seasonally breeding rodents, short days render the reproductive system of female California mice more susceptible to effects of food restriction. This may be vestigial, or it may have evolved to mitigate consequences of unexpectedly poor winter food supplies.

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Section: Introductionmentioning

confidence: 99%

Effects of photoperiod and food restriction on the reproductive physiology of female California mice

Steinman

Knight

Trainor

2012

General and Comparative Endocrinology

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“…For example, protein malnourishment in the mother during lactation resulted in reproductive defects in the offspring due to disturbances in the follicular development and alterations in the endometrial angiogenesis [51] . Protein deprivation only during the early lactation period produced alterations in the innate immune response [52] as well as in the insulin sensitivity in peripheral tissues in adulthood [53] .…”

Section: Malnourished Mothermentioning

confidence: 99%

Metabolic Programming in the Immediate Postnatal Life

Patel

Srinivasan²

2011

Ann Nutr Metab

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nourishment during the suckling period induced several adaptations in the energy circuitry in the hypothalamus of the offspring predisposing them for the onset of obesity later in life. Another approach for a nutritional modification in the immediate postnatal period is the artificial rearing of newborn rat pups on a high-carbohydrate (HC) milk formula without changes in the total calorie availability. Hyperinsulinemia, immediately evident in the HC pups, persisted in the post-weaning period even after withdrawal of the HC milk. Significant alterations in pancreatic islets supported chronic hyperinsulinemia in the HC rats. Alterations in the gene expression of hypothalamic neuropeptides predisposing to hyperphagia were evident during the period of the HC dietary modification. The persistence of these hypothalamic adaptations supported the obese phenotype in adult HC rats. A transgenerational effect gave rise to the development of chronic hyperinsulinemia and adult-onset obesity in the offspring of the HC female rats. Other studies have shown that lactation by a diabetic, obese or malnourished mother resulted in predisposition for the onset of metabolic disorders in the offspring. These observations from animal studies on the metabolic programming effects due to altered nutritional experiences in the immediate postnatal life strongly suggest that altered feeding practices for infants (formula feeding and early introduction of infant foods) could contribute to the rising incidence of overweight/obesity in children and adults. • Overnourishment and increased carbohydrate intake during the suckling period predisposes to adult-onset obesity and related metabolic diseases.• Is there a link between altered feeding practices for infants and adult-onset obesity? Key WordsHyperinsulinemia ؒ Hyperphagia ؒ Hypothalamic energy homeostasis ؒ Increased carbohydrate intake ؒ Nutritional experiences ؒ Obesity ؒ Overnourishment ؒ Suckling period AbstractThe metabolic programming effects of nutritional modifications in the immediate postnatal life are increasingly recognized to independently contribute to the development of metabolic syndrome in later life. Adjustment of litter size in rodents has been used to induce either under-or overnourishment in the immediate postnatal life of the offspring. While undernourishment led to growth retardation in the offspring, overnourishment produced increased body weight gains, hyperinsulinemia and hyperleptinemia. Over-

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“…Offspring of pregnant rats given a LP diet during gestation exhibit a reduction in capillary density in a variety of tissues, including skeletal muscle, endometrium, ovaries and pancreatic islets [5,[72][73][74] . Endothelial dilatation was similarly impaired [75] .…”

Section: Evidence That Early Nutritional Insults Impair β-Cell Regenementioning

confidence: 99%

Nutritional programming of pancreatic β-cell plasticity

Hill

2011

WJD

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Nutritional insufficiency during pregnancy has been shown to alter the metabolism of the offspring and can increase the risk of type 2 diabetes. The phenotype in the offspring involves changes to the morphology and functional capacity of the endocrine pancreas, and in the supporting islet microvasculature. �ancreatic β-cells possess a plastic potential and can partially recover from catastrophic loss. This is partly due to the existence of progenitors within the islets and the ability to generate new islets by neogenesis from the pancreatic ducts. This regenerative capacity is induced by bone marrow-derived stem cells, including endothelial cell progenitors and is associated with increased angiogenesis within the islets. Nutritional insults in early life, such as feeding a low protein diet to the mother, impair the regenerative capacity of the β-cells. The mechanisms underlying this include a reduced ability of β-cells to differentiate from the progenitor population, changes in the inductive signals from the microvasculature and an altered presence of endothelial progenitors. Statin treatment within animal models was associated with angiogenesis in the islet microvasculature, improved vascular function and an increase in β-cell mass. This demonstrates that reversal of the impaired β-cell phenotype observed following nutritional insult in early life is potentially possible.

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The Effect of Maternal Malnutrition During Lactation on the Endometrial ERα Expression, Collagen Type, and Blood Vessels in the Rats Offspring at Puberty

Cited by 6 publications

References 45 publications

Effects of photoperiod and food restriction on the reproductive physiology of female California mice

Effects of photoperiod and food restriction on the reproductive physiology of female California mice

Metabolic Programming in the Immediate Postnatal Life

Nutritional programming of pancreatic β-cell plasticity

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