Lactation in mice fed endophyte-infected tall fescue seed

This study was conducted to assess the effects of endophyte-infected Acremonium coenophialum tall fescue (KY-31) seed (80% infected) on lactation in CD-1 dams and suckling performance of pups as measured by pup survival and growth rates. Twenty-four pairs of mature CD-1 mice were randomly allocated to four dietary treatments: 1) 100% mouse chow ad libitum; 2) 40% endophyte-infected tall fescue seed and 60% mouse chow (w/w); 3) reduced intake (100% chow), adjusted daily to the intake level of Treatment 2; and 4) 60% infected tall fescue seed and 40% chow. The mice were preconditioned on their respective diets for 100 d prior to 96 h of cohabitation between pairs of males and females. At parturition the litters were removed, and each dam was given a litter of six pups of equal weight, size and sex ratio to suckle for 15 days. All pups given to all the dams were born to other mice that were not part of the study and had not been exposed to endophyte-containing diets. Dams and litter weights were measured daily for 15 consecutive days. The combined body weight measurements of litters from dams fed the tall fescue containing diets (Treatments 2 and 4) were significantly lower (2.07 +/- 0.41 g/d) than that of litters from dams fed the chow containing diets (Treatments 1 and 3) during the suckling trial (P<0.05). Similarly, nine of ten (90%) dams fed the chow containing diets maintained five or more pups (5.5 +/- 0.2) throughout the study as compared to five of nine (55.6%) dams fed the tall fescue containing diets that maintained less than five pups (4.5 +/- 0.2).     

Leptin levels in rat offspring are modified by the ratio of linoleic to alpha-linolenic acid in the maternal diet

The supply of polyunsaturated fatty acids (PUFA) is important for optimal fetal and postnatal development. We have previously shown that leptin levels in suckling rats are reduced by maternal PUFA deficiency. In the present study, we evaluated the effect of maternal dietary intake of (n-3) and (n-6) PUFA on the leptin content in rat milk and serum leptin levels in suckling pups. For the last 10 days of gestation and throughout lactation, the rats were fed an isocaloric diet containing 7% linseed oil (n-3 diet), sunflower oil (n-6 diet), or soybean oil (n-6/n-3 diet). Body weight, body length, inguinal fat pad weight, and adipocyte size of the pups receiving the n-3 diet were significantly lower during the whole suckling period compared with n-6/n-3 fed pups. Body and fat pad weights of the n-6 fed pups were in between the other two groups at week one, but not different from the n-6/n-3 group at week 3. Feeding dams the n-3 diet resulted in decreased serum leptin levels in the suckling pups compared with pups in the n-6/n-3 group. The mean serum leptin levels of the n-6 pups were between the other two groups but not different from either group. There were no differences in the milk leptin content between the groups. These results show that the balance between the n-6 and n-3 PUFA in the maternal diet rather than amount of n-6 or n-3 PUFA per se could be important for adipose tissue growth and for maintaining adequate serum leptin levels in the offspring.     

Maternal essential fatty acid deficiency depresses serum leptin levels in suckling rat pups

Dietary lipid quantity and quality have recently been shown to affect serum leptin levels in adult rats. Moreover, suckling pups from dams fed a high fat diet had increased serum leptin levels. The aim of the present study was to analyze the influence of essential fatty acid (EFA) deficiency on serum leptin levels in dams and their pups during the suckling period. For the last 10 days of gestation and throughout lactation, pregnant rats were fed a control or an EFA-deficient (EFAD) diet. The levels of leptin and EFA in the serum of the dams and pups were analyzed 1, 2, and 3 weeks after delivery. In parallel, serum levels of glucose and corticosterone were analyzed in the pups. Low serum leptin levels were found in the control lactating dams during the entire lactation period compared with the age-matched nonlactating animals. The leptin concentrations in the lactating dams fed the EFAD diet were lower compared with those fed the control diet. The serum leptin levels of suckling pups from dams on the EFAD diet were markedly decreased compared with controls (P < 0.05). The reduced serum leptin levels could not be explained by nutritional restriction as evaluated by serum levels of glucose and corticosterone. These results indicate the importance of the EFA composition of the maternal diet for serum leptin levels in both dams and pups. EFA deficiency in lactating dams may cause long-term effects on the pups through dysregulation of leptin and leptin-dependent functions. -- Korotkova, M., B. Gabrielsson, L. A. Hanson, and B. Strandvik. Maternal essential fatty acid deficiency depresses serum leptin levels in suckling rat pups. J. Lipid Res. 2001. 42: 359--365.     

Effect of dietary caffeine and zinc on the activity of antioxidant enzymes,zinc, and copper concentration of the heart and liver in fast-growing rats

The purpose of this study was to determine the relationship between concentrations of Zn and Cu and the activities of superoxide dismutase and glutathione peroxidase in the heart and liver of young rat pups whose dams were fed a diet supplemented with caffeine and/or Zn. Four groups of dams with their newborn pups were fed one of the following diets for 22 d: 20% protein basal diet; the basal diet supplemented with caffeine (2 mg/100 body wt); the basal diet supplemented with Zn (300 mg/kg diet); or the basal diet supplemented with caffeine plus Zn. The Cu levels in the livers of the pups were decreased by maternal intake of the caffeine and Zn diet. The maternal intake of the caffeine diet increased Mn-superoxide dismutase (MnSOD) activity and Cu, Zn-superoxide dismutase (CUZnSOD) in the heart of the pups. On the other hand, the activity of Cu,ZnSOD was significantly reduced in the liver of pups whose dams consumed a caffeine, Zn, or caffeine plus Zn diet. Cu, ZnSOD activity in the liver of the pups seems to be correlated with Cu levels in the tissue. Selenium-dependent glutathione peroxidase (GSH-Px) activities in the heart and liver showed no difference among the groups. The effect of dietary caffeine and/or Zn on the activity of antioxidant enzymes in the heart and liver were different in young rats. The activities of these enzymes in the heart were lower than in the liver of 22-d-old rats. Our experiments indicate that the heart has limited defenses against the toxic effects of peroxides when compared to the liver.     

Brain TRH and Cyclo (His-Pro) and brain protein in the newborn rat are altered by maternal liquid protein feeding

Liquid protein diet (LPD) has been shown previously to produce maternal and fetal weight loss and fetal congenital anomalies, including cataracts and craniofacial malformations. Therefore, to examine the effects of LPD in pregnancy upon the central nervous system of pups, pregnant dams were fed either a 20% casein diet ad libitum, a 20% LPD, or pair-fed with a 20% casein diet. LPD was associated with significant maternal weight loss, and pups had significantly lower birth weights (5.14 +/- 0.64) than pups from the pair-fed controls (5.70 +/- 0.46, p less than 0.05). Total brain protein content was reduced significantly in pups of both sexes from pregnant fed LPD. Moreover, the concentrations of two brain peptides neurotransmitters, thyrotropin-releasing hormone (TRH), and its biologically active metabolite, histidyl-proline diketopiperazine Cyclo (His-Pro), were elevated in the pups from LPD-fed mothers. In contrast, there was no significant difference in brain protein or brain peptides in pups from pair-fed mothers vs. pups from mothers fed ad libitum. These data suggest that qualitative alterations of the protein component in maternal dietary composition have deleterious effects upon the ontogeny of the rat fetal CNS, as reflected by reduced total protein and elevated concentrations of TRH and Cyclo (His-Pro).     

Bile salt sulfotransferase: alterations during maturation and non-inducibility during substrate ingestion

Development of the capacity for hepatic biotransformation of potentially toxic, endogenous compounds such as lithocholate may be dependent on induction by substrate or hormonal modulation. Our aim was to observe the ontogeny of hepatic sulfotransferase (ST) activity, a presumed detoxification pathway, and to determine the effect of substrate ingestion and cortisone administration on ST activity. Pregnant rats were fed a standard chow diet containing lithocholate; the maternal diet was continued during the suckling and weaning phase of the pups. Liver cytosol and serum were obtained from dams and from pups at weekly intervals from fetal life through 4 weeks of age. In controls, there was a progressive increase in hepatic ST activity from 6.2 +/- 2.9 pmol/mg protein per min, (mean +/- SEM) in fetal liver, 18.1 +/- 3.9 at 1 week, an 33.6 +/- 7.2 at 2 weeks to a peak of 56.4 +/- 11.8 at 3 weeks of age. In female rats older than 4 weeks of age, ST activity in hepatic cytosol was threefold higher than in males. There was a decline to adult levels (9.2 +/- 2.4 in males and 39.4 +/- 4.3 in females) at 56 days of life. Cortisone acetate administration had no effect on enzyme activity in pups except those 3 weeks old or older in which there was a precocious decrease in enzyme activity to adult levels. The administration of lithocholate caused a dose-related postnatal alteration of intrahepatic bile ducts manifest as cholangitis with ductular proliferation; hepatocytes were spared.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of late prenatal and/or early postnatal zinc deficiency on the development and some biochemical aspects of the cerebellum and hippocampus in rats

In rats, late prenatal and/or early postnatal zinc deficiency results in behavioural anomalies in adult animals, but not in overt dysmorphogenesis of the central nervous system. Cerebellar and hippocampal development occurs mainly in the first three weeks postnatally and zinc accumulates specifically in the mossy fibres of the hippocampus during this period.In the present investigation, rat pups were suckled by dams fed a zinc-deficient (<0.5 mg/kg) diet either from day 19 of pregnancy or from parturition. Control animals were restricted-fed the same diet supplemented with 100 mg zinc/kg. Studies were performed on pups either on day 18 postpartum in the case of animals fed the experimental diets from parturition, or on day 20 for pups which received treatment from day 19 of gestation.Cerebellar and hippocampal weights were lower in pups suckling from zinc-deficient dams but zinc levels were not affected in either organ, although histological evidence suggested less zinc in the hippocampal mossy fibres. Incorporation of H-thymidine into cerebellar and hippocampal DNA was not affected by maternal zinc status, nor was the activity of the zinc metalloenzyme alkaline phosphatase.The activity of the myelin-marker enzyme 2′, 3′-cyclic nucleotide 3′-phosphohydrolase was substantially lower in both regions of the brain in zinc deprived pups, especially in the hippocampus. Activity of the zinc metalloenzyme L-glutamic acid dehydrogenase was also diminished in both tissues from 20-day-old pups and in the hippocampi of 18-day-old animals.The data suggest that cerebellar and hippocampal DNA synthesis is not seriously affected by late prenatal and/or early postnatal zinc depletion, but that the activities of two enzymes associated with neural function are. The possibility is raised that these defects may be associated with the behavioural changes observed in rats subjected to zinc impoverishment during the period of maximal cerebellar and the hippocampal development.     

Dietary low linolenic acid compared with docosahexaenoic acid alter synaptic plasma membrane phospholipid fatty acid composition and sodium-potassium ATPase kinetics in developing rats

The objective of this study was to investigate if maternal dietary 20:4n-6 arachidonic acid (AA) and 22:6n-3 compared with adequate or low levels of 18:3n-3 linolenic acid (LNA) increases synaptic plasma membrane (SPM) cholesterol and phospholipid content, phospholipid 20:4n-6 and 22:6n-3 content, and Na,K-ATPase kinetics in rat pups at two and five weeks of age. At parturition, Sprague-Dawley rats were fed semi-purified diets containing either AA + docosahexaenoic acid (DHA), adequate LNA (control; 18:2n-6 : 18:3n-3 ratio of 7.1 : 1) or low LNA (18:2n-6 : 18:3n-39 ratio of 835 : 1). During the first two weeks of life, the rat pups received only their dams' milk. After weaning, pups received the same diet as their respective dams to five weeks of age. No significant difference was observed among rat pups fed the diet treatments for SPM cholesterol or total and individual phospholipid content at two and five weeks of age. Fatty acid analysis revealed that maternal dietary AA + DHA, compared with feeding the dams the control diet or the low LNA diet, increased 20:4n-6 in phosphatidylserine and 22:6n-3 content of SPM phospholipids. Rats fed dietary AA + DHA or the control diet exhibited a significantly increased Vmax for SPM Na,K-ATPase. Diet treatment did not alter the Km (affinity) of SPM Na,K-ATPase in rat pups at two and five weeks of age. It is concluded that dietary AA + DHA does not alter SPM cholesterol and phospholipid content but increases the 22:6n-3 content of SPM phospholipids modulating activity of Na,K-ATPase.     

A high-fat diet during rat pregnancy or suckling induces cardiovascular dysfunction in adult offspring

Epidemiological and animal studies suggest that diet-induced epigenetic modifications in early life can contribute to development of the metabolic syndrome in adulthood. We previously reported features of the metabolic syndrome in adult offspring of rats fed a diet rich in animal fat during pregnancy and suckling. We now report a study to compare the relative effects of high-fat feeding during 1) pregnancy and 2) the suckling period in the development of these disorders. As observed previously, 6-mo-old female offspring of fat-fed dams suckled by the same fat-fed dams (OHF) demonstrated raised blood pressure, despite being fed a balanced diet from weaning. Female offspring of fat-fed dams "cross fostered" to dams consuming a control diet during suckling (OHF/C) demonstrated raised blood pressure compared with controls (OC) [systolic blood pressure (SBP; mmHg) means +/- SE: OHF/C, 132.5 +/- 3.0, n = 6 vs. OC, 119.0 +/- 3.8, n = 7, P < 0.05]. Female offspring of controls cross fostered to dams consuming the fat diet (OC/HF) were also hypertensive [SBP (mmHg) 131.0 +/- 2.5 mmHg, n = 6 vs. OC, P < 0.05]. Endothelium-dependent relaxation (EDR) of male and female OHF and OHF/C mesenteric small arteries was similar and blunted compared with OC (P < 0.001). OC/HF arteries showed profoundly impaired EDR (OC/HF vs. OHF, P < 0.001). OHF/C and OC/HF demonstrated hyperinsulinemia and increased adiposity. Features of the metabolic syndrome in adult offspring of fat-fed rats can be acquired both antenatally and during suckling. However, exposure during pregnancy confers adaptive protection against endothelial dysfunction induced by maternal fat feeding during suckling.     

Behavioural responses of rats to early housing conditions and to protein-energy malnutrition

Lactating rats were fed either the commercial diet (CO) or the low protein diet which induced symptoms of protein - energy deprivation (PD). They were housed in cages either individually (IH) together with eight offspring or in a large community cage (COM) shared by six dams and 48 youngs. After weaning all rats lived in cages by 4-5 animals. The PD terminated at the age of 49 days. Behaviour was tested on the 10th, 42nd and 150 th days of life. Body weight was recorded during nursing period both in dams and pups, after weaning in male rats. The low protein diet affected both body weight and maternal behaviour of the dams. In PD + IH pups growth as well as behavioural development was retarded. Behavioural alterations persisted even after the PD had been treated. The COM housing improved the body weight in the PD + COM dams, behaviour of both the PD + COM dams ond the pups was less affected than of the PD + IH group. The effect of the early housing was long lasting, manifested itself in elevated exploratory activity and in the decreased emotional responses in both the PD + COM and the CO + COM groups at the age of 42 and 150 days.     

Differential Responses of Orexigenic Neuropeptides to Fasting in Offspring of Obese Mothers

Maternal obesity due to long‐term high‐fat diet (HFD) consumption leads to faster growth in offspring during suckling, and increased adiposity at 20 days of age. Decreased expression of the orexigenic neuropeptide Y (NPY) and increased anorexigenic proopiomelanocortin (POMC) mRNA expression were observed in the fed state. However, hunger is the major drive to eat and hypothalamic appetite regulators change in response to meals. Therefore, it is important to compare both satiated and fasting states. Female Sprague–Dawley rats (8 weeks old) were fed a cafeteria‐style HFD (15.33 kJ/g) or chow for 5 weeks before mating, with the same diet continuing throughout gestation and lactation. At postnatal day 20, male pups were killed either after overnight fasting or in the fed state. Pups from obese dams were hyperphagic during both pre‐ and postweaning periods. Pups from obese dams had higher hypothalamic mRNA expression of POMC and NPY Y1 receptor, but lower hypothalamic melanocortin‐4 receptor (MC4R) and its downstream target single‐minded gene 1 (Sim1), in the fed state. Overnight fasting reduced circulating glucose, insulin, and leptin and increased hypothalamic NPY Y1 receptor mRNA in pups from both lean and obese dams. Hypothalamic NPY and agouti‐related protein (AgRP) were only increased by fasting in pups from obese dams; reductions in MC4R and Sim1 were only seen in pups from lean dams. At weaning, the suppressed orexigenic signals in offspring from obese dams were normalized after overnight fasting, although anorexigenic signaling appeared impaired in these animals. This may contribute to their hyperphagia and faster growth.     

Fructose feeding in the suckling-weaning transition in rats: effects on hyperlipidemia in adulthood

The sucking-weaning transition is characterized by high rates of growth and development and may be a sensitive period during which dietary intake could program metabolism to increase the risk of cardiovascular disease and diabetes in adulthood. Intake of a high fructose (FR) diet is known to induce hypertriglyceridemia and insulin resistance in rats when they are consuming this diet. We examined whether a FR diet fed early in life produces detrimental changes in lipid and glucose metabolism that persist to adulthood. Weanling rats were fed 65% FR (wt/wt), a purified control diet (CNTL) or standard chow (CHOW) for 5 weeks. Beyond 9 weeks of age, all rats were fed CHOW. During FR feeding, plasma triglycerides (TG) were significantly elevated in the FR group (FR = 217 +/- 20; CNTL = 163 +/- 17; chow = 156 +/- 10). At 21 wks of age, TG's were similar in rats fed FR or CNTL versus CHOW at weaning (p > 0.87). Hepatic fatty acid synthase (FAS) activity was elevated in FR and CNTL groups vs. CHOW (65 +/- 7, 72 +/- 6 vs. 48 +/- 4 nmol NADPH/mg protein/min, p < 0.01). There were no differences in indices of glucose homeostasis at 21 weeks of age. Early exposure to a diet high in simple sugars (FR or CNTL) and/or low in fiber during the suckling-weaning transition may contribute to modest dyslipidemia later in life. Together, changes observed in this study may increase the risk of cardiovascular disease in adulthood.     

Puberty onset in the female offspring of rats submitted to protein or energy restricted diet during lactation

This study aims to determine the effects of maternal protein and energy malnutrition during lactation on the linear growth, body weight and onset of puberty of the female offspring. At parturition, dams were randomly assigned to the following groups: (C) control group, with free access to a standard laboratory diet containing 23% protein; (PR) protein-restricted group, with free access to an isoenergy and protein-restricted diet containing 8% protein; and (ER) energy-restricted group, receiving standard laboratory diet in restricted quantities. After weaning, the female pups had free access to standard laboratory diet. From day 30 onwards, the pups were inspected daily for vaginal opening. Cyclic stages of the ovaries were studied by daily vaginal smears after vaginal opening until day 40 when all animals were sacrificed with pentobarbital. From day 4 after birth until day 40, body weight and linear growth in the PR and ER rats were significantly lower than in controls (p < 0.001). In spite of the significant (p<0.05) delayed in the vaginal opening in PR and ER rats, the first estrous cycle occurred at the same time of vaginal opening in all groups. The PR and ER rats exhibited a lower uterine (PR = 42%, ER = 40%, p < 0.001) and ovarian (PR = 26%, ER=19%, p < 0.05) absolute weight and uterus relative weight (PR = 27%, ER = 22%, p < 0.05). Our data showed that maternal protein and energy malnutrition during lactation leads to growth retardation and delayed on the onset of puberty in female pups, with vaginal opening and estrous cycle occurring at the same time.     

SUPPLEMENTATION OF A WHEAT BREAD DIET WITH LYSINE AND THREONINE: EFFECTS UPON INTRAUTERINE GROWTH AND BRAIN BIOCHEMISTRY

Abstract— During pregnancy, rats were fed either a standard chow diet, a wheat bread diet or a wheat bread diet supplemented with lysine and threonine. At birth, the offspring of the dams fed the supplemented diet differed from the chow fed animals only in having a smaller amount of protein in the combined cerebellum and brain stem area while the pups whose dams were fed the bread diet showed lower brain weights, deficits in protein in all brain parts and deficits in DNA in the cerebrum.     

Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring

Epidemiological and animal studies suggest that the alteration of hormonal and metabolic environment during fetal and neonatal development can contribute to development of metabolic syndrome in adulthood. In this paper, we investigated the impact of maternal high-fat (HF) diet on hypothalamic leptin sensitivity and body weight gain of offspring. Adult Wistar female rats received a HF or a control normal-fat (C) diet for 6 wk before gestation until the end of the suckling period. After weaning, pups received either C or HF diet during 6 wk. Body weight gain and metabolic and endocrine parameters were measured in the eight groups of rats formed according to a postweaning diet, maternal diet, and gender. To evaluate hypothalamic leptin sensitivity in each group, STAT-3 phosphorylation was measured in response to leptin or saline intraperitoneal bolus. Pups exhibited similar body weights at birth, but at weaning, those born to HF dams weighed significantly less (-12%) than those born to C dams. When given the HF diet, males and females born to HF dams exhibited smaller body weight and feed efficiency than those born to C dams, suggesting increased energy expenditure programmed by the maternal HF diet. Thus, maternal HF feeding could be protective against adverse effects of the HF diet as observed in male offspring of control dams: overweight (+17%) with hyperleptinemia and hyperinsulinemia. Furthermore, offspring of HF dams fed either C or HF diet exhibited an alteration in hypothalamic leptin-dependent STAT-3 phosphorylation. We conclude that maternal high-fat diet programs a hypothalamic leptin resistance in offspring, which, however, fails to increase the body weight gain until adulthood.     

Genotype and diet effects in lean and obese Zucker rats fed either safflower or coconut oil diets

Previously we reported that suckling lean heterozygous (FA/fa) Zucker rats had a number of adipose tissue measurements intermediate between those of homozygous lean (FA/FA) and obese (fa/fa) rats. However, in young adult male rats maintained on a low-fat diet, these differences were no longer apparent (i.e., values for the two lean genotypes were similar). In the present study we determined whether the heterozygous effect of the "fa" gene was dependent on the consumption of a high-fat diet. Mother rats were fed high-fat diets containing either safflower (SOD) or coconut (COD) oil throughout mating and lactation. Homozygous lean male and female rats were bred, as well as obese male and lean heterozygous female rats. Suckling rats were studied at 17 days of age. Additional male rats were maintained on the same diet as their mothers until 11-12 weeks of age. Obese suckling rats had higher body weights than lean pups. Inguinal fat pad weights and pad-to-body weight ratios followed the pattern of obese greater than lean (FA/fa) pups that were greater than lean (FA/FA) pups. A similar relationship was found for adipose tissue lipogenic enzyme activities. At 11-12 weeks of age, measurements followed the general pattern of obese rats having greater values than lean rats (i.e., FA/fa = FA/FA). SOD-fa/fa rats had higher hepatic lipogenic enzyme activities than COD-fa/fa rats. In addition, SOD rats had higher fat cell numbers than COD rats. These results suggest that specific fatty acids can alter adipocyte proliferation and/or differentiation in vivo. In addition, there appears to be a defect of fatty acid regulation in livers of genetically obese rats. The heterozygous effect of the "fa" gene in suckling Zucker rats was confirmed. However, high-fat feeding did not result in a heterozygous effect in young adult lean male rats. We will next evaluate the role of sex on this effect.     

Effect of modified egg* on developmental defects in neonates of NIDDM induced Wistar rats

Maternal Zn deficiency has been suggested as the contributing factor for all congenital malformations during pregnancy particularly in diabetes. Maternal Zn-supplementation, therefore, was suggested as one possible nutrition intervention during pregnancy to improve its outcome. But a number of trials with Zn-supplementation are not consistent and discourage the use of excessive Zn-supplementation during pregnancy. Instead a multivitamin/ mineral supplement to them has been suggested to reduce its complication. Accordingly, the poultry egg was modified for trace elements, vitamin-E and omega-3 fatty acids so as to use it as a dietary supplement for diabetics to reduce their complications during the pregnancy. The results showed that NIDDM induced rats fed either on 40 or 80 mg Zn/kg diet delivered less number of pups/litter and their body weight was higher at birth as compared to control group fed 20 mg Zn/kg diet. During the weaning period, some abnormalities characterized by restricted movements of the hind legs, curl toes of limbs, eye opening problems, less hair on the body and more head to body ratio were observed. Whereas number of pups delivered per litter were more with higher body weights without abnormalities in the pups in NIDDM groups fed egg mixed diet. Further Zn, Cu and Mg concentrations were significantly less in the liver, hair and abdominal muscles in pups in NIDDM groups but their concentrations were restored approaching closer to control in pups in groups fed egg mixed diet estimated on 18th day of weaning period. The excretion of these trace elements increased in the urine of dams fed Zn supplemented diet but decreased in the dams fed egg mixed diet on 15th day of their suckling period. The data suggest that if these modified eggs are included in the regular diet during pregnancy, they may protect the neonates in womb against the damaging effect of imbalances of physiologically important nutrients due to diabetes or environmental contamination.     

The effects of prenatal protein deprivation on thyrotroph development

Maternal dietary protein restriction produced by feeding a diet containing 4% casein throughout gestation adversely affects body size and retards development of various organs in the progeny. For the most part, alterations are present in structural or functional entities which evolve during the last trimester of gestation. Fetal thyroid follicle formation and iodine concentrating capacity, which increase rapidly between the 17th gestational day and birth in pups of dams fed the control (24% casein) ration, are retarded in age-matched pups of protein-deficient females. The first immunoreactive thyrotrophs appear in the fetal pituitary on day 17 in both control and prenatally protein-deprived (PPD) young. The total number of thyrotrophs per pituitary was unaffected by maternal protein deficiency, except on day 21 when there were significantly more thyrotrophs per pituitary in fetal control rats. Although pituitary volume was significantly reduced in 18-, 19- and 21-day old fetal PPD rats, as compared with controls, pituitary volume:body weight ratios differed between young in the two dietary groups only on day 21, when the ratio was significantly higher in PPD as compared to control young. Maternal protein deprivation does not affect the morphological maturation of the thyrotrophs of the anterior pituitary of the fetal rat.     

Body weight deficit in the absence of reduction in cerebrum weight and nucleic acid content in progeny of swine restricted in protein intake during pregnancy

Fifty-six castrated male progeny of crossbred (Chester White x Landrace x Large White x Yorkshire) dams fed an adequate diet (control, C), a control diet fed at one-third of C (restricted, R), or diets severely deficient in protein (PF) or restricted in nonprotein calories (RCal) were killed at age 25 weeks. Dams were fed their respective diets in the following regimens: C, 1.8 kg (6000 kcal daily) throughout pregnancy; R, 0.6 kg of C diet daily for 70 days, then 1.8 kg of C daily to parturition at about 114 days; PF, 1.8 kg of a "protein-free" diet (less than 0.2% protein) throughout pregnancy; RCal, 0.6 kg daily (2000 kcal) of a diet containing three times the concentration of protein, minerals, and vitamins provided by the C diet for 70 days, then 1.8 kg of C daily to parturition. All dams were fed an adequate diet ad libitum through a 28-day lactation. Castrated male progeny were assigned to one of two replicates based on birth date and fed a corn-soybean meal diet ad libitum from weaning to age 25 weeks, supplemented from age 10 to 12 weeks with 0, 110, or 220 mg/kg of thyroprotein (iodinated casein). Cerebrum weight was unaffected by maternal diet, despite a significant (P less than 0.001) reduction in body weight of progeny of PF dams compared with other groups, resulting in a higher relative cerebrum weight in progeny of PF dams than in progeny of C, R, and RCal dams. Absolute and relative weights of RNA, DNA, and total protein in cerebrum were unaffected by maternal diet. Thyroprotein supplementation to the diet of the progeny had no effect on cerebrum weight or its protein or nucleic acid content. It is concluded that maternal protein deprivation but not restriction of feed or nonprotein calorie intake to one-third of recommended allowance during gestation results in stunting of body weight in young adult progeny but does not affect cerebrum weight, cerebrum cell number (DNA), or protein synthetic activity (RNA), or RNA-to-protein ratio.     

Maternal treatment with oleoyl-estrone induces resistance to lipid accrual in their descendants

Objective: To determine whether treatment of rat dams with oleoyl‐estrone (OE) has an effect on the offspring's long‐term response to diet restriction during lactation. Methods and Procedures: Control, OE‐treated, and diet‐restricted dams were treated up to day 15 of lactation. Changes in food intake and body weight were recorded for dams and their pups. After weaning, pups received a 4‐week standard diet followed by a 4‐week period of high‐fat diet. Lipid, protein, and energy content of pups plus energy intake and efficiency. Serum metabolites (glucose, urea, and cholesterol) and serum hormones (adiponectin, leptin, insulin, and sexual hormones). Results: Neither pups from dams in the OE‐treated nor in the diet‐restricted group showed significant changes in weight, though these two groups ingested 79% of food ingested by controls. At weaning, the pups from OE‐treated rats were smaller than those of the control or diet‐restricted groups. These pups maintained the differences in size and lipid content during the 4‐week standard‐diet period, whereas pups from diet‐restricted dams showed a sharp decrease in their lipid content. During the 4 weeks of high‐fat diet, the male offspring from OE‐treated dams increased the difference in lipid content in relation to the pups from control dams whereas in females the differences decreased. Female offspring from diet‐restricted dams showed the most marked changes in metabolite and hormone levels in relation to controls. Discussion: Treatment of lactating dams with OE programs the metabolic response of their offspring to resist the challenge of a high‐fat diet that would lead to obesity in adulthood.