Nutrient restriction during pregnancy and lactation impairs growth and development. Recent studies demonstrate long-term programming of function of specific organ systems resulting from suboptimal environments during fetal life and development up to weaning. We determined effects of maternal protein restriction (50% control protein intake) during fetal development and/or lactation in rats on the reproductive system of male progeny. Rats were fed either a control 20% casein diet (C) or a restricted diet (R) of 10% casein during pregnancy. After delivery mothers received either C or R diet until weaning to provide four groups: CC, RR, CR and RC. We report findings in male offspring only. Maternal protein restriction increased maternal serum corticosterone, oestradiol and testosterone (T) concentrations at 19 days gestation. Pup birth weight was unchanged but ano-genital distance was increased by maternal protein restriction (P < 0.05). Testicular descent was delayed 4.4 days in RR, 2.1 days in CR and 2.2 days in RC and was not related to body weight. Body weight and testis weight were reduced in RR and CR groups at all ages with the exception of CR testis weight at 270 days postnatal age (PN). At 70 days PN luteinizing hormone and T concentrations were reduced in RR, CR and RC. mRNA for P450 side chain cleavage (P450scc) was reduced in RR and CR at 21 days PN but was unchanged at 70 days PN. Fertility rate was reduced at 270 days PN in RC and sperm count in RR and RC. We conclude that maternal protein delays sexual maturation in male rats and that some effects only emerge in later life.
Suboptimal developmental environments program offspring to lifelong metabolic problems. We evaluated effects of maternal isocaloric low protein diet during pregnancy and/or lactation on milk quantity and leptin concentration at postnatal day 7, 14, and 21. Control mothers ate 20% casein (C) and restricted mothers (R) 10% casein to provide four groups: CC, RR, CR, and RC (first letter pregnancy and second lactation diet) to enable evaluation of effects influenced by maternal diet during pregnancy and lactation. Milk leptin was not a determinant of pup serum leptin. Pup serum leptin did not inhibit milk appetite at any postnatal age. Pup serum leptin did not correlate with pup adipose tissue. Finally, the normal postnatal leptin rise in pup serum was delayed by prenatal undernutrition. These data suggest that fetal nutrition modifies timing of neonatal leptin surge and may contribute to the development of altered appetite and metabolic disorders in later life. H uman epidemiologic (1) and experimental animal studies (2) have shown that suboptimal environments in the womb and during early neonatal life alter growth and predispose individuals to lifelong health problems. Effects of maternal nutrient restriction during pregnancy and/or lactation have been studied in many different models. A variety of growth, endocrine and cardiovascular phenotypes result from nutrient restriction in different developmental windows. Perinatal malnutrition predisposes to offspring obesity in adulthood by changes during the development of central neural pathways mediated by regulatory mechanisms including leptin (3). Rapid catch-up growth after early growth restriction increases the risk of developing obesity and cardiovascular disease in later life (4,5).One of the most important neonatal factors involved in developmental programming is the adequacy of nutrition during the lactation period. Breast feeding decreases the risk of obesity in later childhood (6). Many factors including maternal milk composition, energy content, and quantity may influence future appetite control. Breast milk contains leptin (7) a hormone produced and secreted in a variety of tissues, predominantly by adipocytes (8) which regulates food intake and energy expenditure at the hypothalamic level in adult animals (8,9). Circulating levels of leptin correlate positively with the amount of fat stores (10). During the first days of postnatal life, leptin levels are higher than those observed later in development (11). Several studies have demonstrated a surge of leptin around postnatal days (PND) 10 -14 in the rat (11). This surge has been correlated with maturation of the central nervous mechanisms that regulate appetite in later life. Leptin also seems to play a key role in programming the structural and functional development of hypothalamic orixigenic and anorexigenic centers in the early postnatal period.We have demonstrated that maternal protein restriction in the rat during either pregnancy or lactation alters postnatal growth, appetitive behavior, ...
We conclude that MO during pregnancy and lactation increases F(1) testicular and sperm OS leading to premature aging of reproductive capacity.
Maternal protein restriction (MPR) in pregnancy causes life course organ dysfunction, but few studies link the developmental origins of disease hypothesis to early aging. Suboptimal developmental nutrition increases oxidative stress (OS) and male infertility, damaging sperm function. We hypothesized that MPR in pregnancy accelerates age-related changes in testicular and sperm function related to both maternal diet and increased testicular OS in rat offspring. We studied male rats whose pregnant mothers ate either control (C, 20 % casein) or restricted (R, 10 % casein) isocaloric diet. After birth, mothers and offspring ate C diet. Testes were retrieved at 19 days gestation and across the life course (postnatal day (PND) 21, 36, 110, and 850) to measure OS markers, antioxidant enzymes, serum FSH, LH, and testosterone, and PND 110 sperm OS and quality. Fertility rate was evaluated at PND 110, 450, and 850. Offspring showed age-and MPRrelated changes in testosterone, testicular OS markers and antioxidant enzymes and fertility, and maternal diet-related OS and sperm antioxidant enzyme changes. Developmental programming is considered a key factor in predisposing to chronic disease. Our data show that programming also plays an important role in aging trajectory. This interaction is a little studied area in aging biology that merits more investigation. Keywords
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