Maternal fish oil supplementation ameliorates maternal high-fructose diet-induced dyslipidemia in neonatal mice with suppression of lipogenic gene expression in livers of postpartum mice

Maternal fructose consumption during pregnancy and lactation is associated with metabolic dysregulation in offspring. We tested the hypothesis that fish oil (FO) supplementation during pregnancy and lactation improves fructose-induced metabolic dysregulation in postpartum dams and offspring mice. We therefore aimed to determine the effects of FO supplementation on metabolic disruption in neonatal mice and dams induced by a maternal high-fructose diet (HFrD). The weight of the offspring of dams fed with HFrD on postnatal day 5 was significantly low, but this was reversed by adding FO to the maternal diet. Feeding dams with HFrD significantly increased plasma concentrations of triglycerides, uric acid, and total cholesterol, and decreased free fatty acid concentrations in offspring. Maternal supplementation with FO significantly suppressed HFrD-induced hypertriglyceridemia and hyperuricemia in the offspring. Maternal HFrD induced remarkable mRNA expression of the lipogenic genes Srebf1, Fasn, Acc1, Scd1, and Acly in the postpartum mouse liver without affecting hepatic and plasma lipid levels. Although expression levels of lipogenic genes were higher in the livers of postpartum dams than in those of nonmated mice, HFrD feeding increased the hepatic lipid accumulation in nonmated mice but not in postpartum dams. These findings suggest that although hepatic lipogenic activity is higher in postpartum dams than nonmated mice, the lipid consumption is enhanced in postpartum dams during pregnancy and lactation. Maternal FO supplementation obviously suppressed the expression of these lipogenic genes. These findings coincide with reduced plasma triglyceride concentrations in the offspring. Therefore, dietary FO apparently ameliorated maternal HFrD-induced dyslipidemia in offspring by suppressing maternal lipogenic gene expression and/or neonatal plasma levels of uric acid.     

Influence of maternal cholestyramine treatment on cholesterol and bile acid metabolism in adult offspring

To reduce ileal reabsorption of bile acids and to deplete hepatic cholesterol pools, female rats were fed a diet containing 5% (wt/wt) cholestyramine from 4 days prior to mating. Control rats were fed the same diet without cholestyramine. In one group on day 20 of gestation diet-fed dams and their fetuses were investigated. Additional pups were raised in litters of eight and nursed by their mothers for 30 days at which time they were weaned to the control diet. All dams were given the control diet from day 14 of lactation; at no time did neonates have access to cholestyramine. Offspring were raised until 3 months of age then fed the control, cholestyramine or a high fat, high cholesterol diet for 5 days. Maternal cholestyramine produced significant elevation of fetal hepatic 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase; fetal 7 alpha-hydroxylase (7 alpha-OH) activity, plasma cholesterol and triglyceride levels, however, were not significantly altered. The elevated HMG-CoA reductase activity persisted in liver and in addition was present in jejunum of 3-month-old male offspring challenged with the control or cholestyramine diet for 5 days. When challenged with the high fat, high cholesterol diet, male offspring from cholestyramine-treated dams had significantly higher plasma cholesterol levels but HMG-CoA reductase and 7 alpha-OH activity similar to controls. Maternal treatment had no apparent effect on plasma triglyceride or hepatic 7 alpha-OH in 3-month-old male offspring.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gestational and lactational lead intoxication produces alterations in the hepatic system of rat pups.

The effects of lead (Pb) intoxication during pregnancy and lactation were studied in the hepatic system of pups and young Wistar rats to test the hypothesis that gestational and lactational lead exposure alters the normal function of the liver in neonates. Lead acetate (300 mg/L) dissolved in distilled water was administered ad libitum to mothers during gestation and lactation. At days 12 and 21 postnatal (PN), pups were sacrificed, blood was collected, and livers were removed. Blood lead (PbB) levels were also measured. Although, histological evaluation revealed neither abnormalities in the liver structure nor depositions of lead, the toxicant produced biochemical alterations. Lead-intoxicated pups exhibited a decrease in hemoglobin, iron, and alkaline and acid phosphatase levels and an increase in PbB content. Protein, DNA, and lipid total amounts were reduced, and hepatic glycogen content was diminished at days 12 and 21 PN, with a higher level of glucose in the blood. Lead administration also resulted in a decrease in alkaline phosphatase in the liver of pups at day 21 PN, but acid phosphatase was unaltered. The findings of this study support the hypothesis that lead intoxication of mothers in gestation and lactation results in alterations in the hepatic system in neonates and pups.     

A maternal high-fat diet represses the expression of antioxidant defense genes and induces the cellular senescence pathway in the liver of male offspring rats

Maternal high-fat (HF) diet feeding is associated with increased risk of developing metabolism-related diseases in adult offspring, including chronic liver disease. The present study tested the hypothesis that maternal HF diet leads to a decreased antioxidant defense capacity and causes cellular senescence in liver of adult offspring rats, which might increase risk of developing chronic liver disease. Timed-pregnant Sprague Dawley rats were fed a HF diet (45% of energy from fat) or a control (C) diet (16% of energy from fat) during gestation and lactation. The resulting offspring were fed a C diet after weaning to generate 2 offspring groups: C diet-fed offspring of dams fed C diet (C/C) and C diet-fed offspring of dams fed a HF diet (HF/C). At 12 wk of age, male rats were killed and samples were collected for analysis. Maternal HF diet significantly increased plasma TG and hepatic TBARS concentrations and the size of hepatic lipid droplets in offspring rats. The expression of antioxidant defense genes, such as glutathione peroxidase-1, Cu/Zn superoxide dismutase (Sod1), paraoxonase enzymes (Pon1, Pon2, and Pon3), were significantly lower in the liver of HF/C pups than in C/C pups. The expression of Inhibitor of cyclin dependent Kinase 4a (p16INK4a), a marker of cellular senescence, and cyclooxygenase-2 (Cox2), a proinflammatory marker, was significantly higher in the HF/C offspring group than in the C/C offspring group. Western-blot analysis shows that cyclin D1 and phosphorylated retinoblastoma protein were significantly lower in HF/C offspring than in C/C offspring. The results provide the first evidence to our knowledge that maternal HF diet might alter antioxidant defense capacity and program the p16INK4a-dependent cellular senescence in the liver of adult offspring.     

Maternal DHA Supplementation during Pregnancy and Lactation in the Rat Protects the Offspring against High-Calorie Diet-Induced Hepatic Steatosis

Maternal supplementation during pregnancy with docosahexaenoic acid (DHA) is internationally recommended to avoid postpartum maternal depression in the mother and improve cognitive and neurological outcomes in the offspring. This study was aimed at determining whether this nutritional intervention, in the rat, protects the offspring against the development of obesity and its associated metabolic disorders. Pregnant Wistar rats received an extract of fish oil enriched in DHA or saline (SAL) as placebo by mouth from the beginning of gestation to the end of lactation. At weaning, pups were fed standard chow or a free-choice, high-fat, high-sugar (fc-HFHS) diet. Compared to animals fed standard chow, rats exposed to the fc-HFHS diet exhibited increased body weight, liver weight, body fat and leptin in serum independently of saline or DHA maternal supplementation. Nevertheless, maternal DHA supplementation prevented both the glucose intolerance and the rise in serum insulin resulting from consumption of the fc-HFHS diet. In addition, animals from the DHA-fc-HFHS diet group showed decreased hepatic triglyceride accumulation compared to SAL-fc-HFHS rats. The beneficial effects on glucose homeostasis declined with age in male rats. Yet, the preventive action against hepatic steatosis was still present in 6-month-old animals of both sexes and was associated with decreased hepatic expression of lipogenic genes. The results of the present work show that maternal DHA supplementation during pregnancy programs a healthy phenotype into the offspring that was protective against the deleterious effects of an obesogenic diet.     

Azuki bean polyphenols intake during lactation upregulate AMPK in male rat offspring exposed to fetal malnutrition

ObjectiveFetal malnutrition is an early-life inducer of dyslipidemia and glucose intolerance. The aim of this study was to examine whether maternal azuki bean (Vigna angularis) polyphenol (AP) intake during lactation affects the adenosine monophosphate–activated protein kinase (AMPK) pathway and lipid metabolism in offspring exposed to fetal malnutrition.MethodsPregnant Wistar rats were divided into three groups: a control diet offered during gestation and lactation (CC), a low-protein diet during gestation and a control diet during lactation (LPC); and a low-protein diet during gestation and a 1.0% AP-containing control diet during lactation (LPAP). Male pups were randomly selected for the study; half the pups were sacrificed at 3 wk of age and the other half were fed a standard diet and sacrificed at 23 wk. Hepatic triacylglycerol levels, phosphorylation levels of AMPK and acetyl-coenzyme A carboxylase (ACC), and mRNA levels of sterol regulatory element-binding protein-1c (SREBP-1c) were evaluated.ResultsSignificant decreases in body weights and hepatic triacylglycerol levels were found in the LPAP compared with the LPC group. Plasma adiponectin levels in the LPAP group were higher than those in the LPC group. AMPK phosphorylation was upregulated in the livers and skeletal muscles in young and adult LPAP compared with LPC rats. ACC phosphorylation was upregulated in skeletal muscles of LPAP rats. SREBP-1c mRNA expression was decreased in the livers of LPAP rats.ConclusionOur results suggest that maternal AP intake during lactation upregulates AMPK phosphorylation not only in young but also in adult offspring exposed to fetal malnutrition and may lead to decreased hepatic lipid accumulation by ACC phosphorylation and downregulation of SREBP-1c expression.     

Ethanol intake during lactation impairs milk production in rats and affects growth and metabolism of suckling pups.

From parturition, lactating Wistar rats were given 20% alcohol in drinking water and fed a solid diet ad lib (group AL). Pair-fed (PF) and control (C) rats were fed solid diet and given water ad lib (C). All animals were sacrificed on the 12th day of lactation. Ethanol treatment decreased food intake and milk production in lactating rats to a greater level than in PF rats, and a greater reduction in body weight of the AL pups was noted. Brain weight, protein concentration, and DNA content were also lower in pups of AL dams than of PF dams, whereas liver glycogen concentration was higher in the former. Pups from AL dams had higher circulating levels of beta-OH-butyrate, triglyceride, and free fatty acids than those from either C or PF dams. Plasma glucose concentration was lower in both PF and AL than in C pups, whereas the AL group had lower plasma protein concentration than any of the other groups. We conclude that maternal alcohol intake during lactation greatly impairs milk production, and although the known increase of lipid content in milk in rats studied under similar conditions allows an enhanced lipidic components in the pups, this adaptation does not allow normal growth and brain development.     

孕哺期PM2.5和高脂饮食联合暴露对大鼠仔鼠血压、血脂、血糖的影响

目的 探讨孕哺期细颗粒物（fine particulate matter,PM2.5）和高脂饮食（high fat diet,HFD）联合暴露对大鼠仔鼠血压、血脂、空腹血糖的影响,观察生命早期同时暴露PM2.5和HFD对子代发育的影响。方法 成年SD大鼠按照雌雄2[DK]∶1进行交配,孕鼠随机分为对照组（CC组）、高脂饮食组（HFD组）、PM2.5低暴露组（L-PM2.5组）、PM2.5高暴露组（H-PM2.5组）、高脂饮食+PM2.5低暴露组（HFD+L-PM2.5组）和高脂饮食+PM2.5高暴露组（HFD+H-PM2.5组）。对照组和PM2.5低、高暴露组给予普通饲料,其余给予高脂饲料。PM2.5染毒采用细颗粒物在线浓缩和动物染毒系统,低、高暴露剂量分别设为室外大气PM2.5浓度的2倍和4倍。母鼠从孕0日开始染毒,每天5h,每周5d,直至仔鼠出生后第21d（Postnatal day,PND21）,记录仔鼠体长和尾长,测量仔鼠的血压、心率,检测空腹血糖、血清甘油三酯、胆固醇水平。结果 PND21雄鼠HFD组、HFD+L-PM2.5组、HFD+H-PM2.5组体长较CC组增加,PND21雌鼠HFD+L-PM2.5组尾长较L-PM2.5组增加（P<0.05）。析因分析显示,PM2.5（F=3.492,P<0.05）和HFD（F=4.346,P<0.05）均使雌鼠收缩压升高,二者不存在交互作用（P>0.05）;HFD使雄鼠收缩压（F=9.259）、舒张压（F=5.981）、平均动脉压（F=7.754）升高（P均<0.05）,HFD+H-PM2.5组雄鼠收缩压、舒张压、平均动脉压均高于CC组（P<0.05）,PM2.5和HFD不存在交互作用（P>0.05）。PM2.5、HFD使雌鼠（F值分别为13.346,32.277,P均<0.05）、雄鼠血清甘油三酯（F值分别为5.723,10.360,P均<0.05）均升高,HFD+H-PM2.5组雌雄仔鼠甘油三酯含量均高于CC组,两者对雌鼠的血清甘油三酯含量存在协同作用（F=8.651,P<0.05）,对雄鼠不存在交互作用（P>0.05）。各组仔鼠空腹血糖水平差异无统计学意义（P>0.05）。结论 PM2.5和HFD联合暴露能引起PND21仔鼠血压、血脂升高,二者对血压的影响不存在交互作用,对雌性仔鼠血脂的影响存在协同作用。PM2.5和HFD对血压的影响存在性别差异。     

Effects of peroxidation products in thermoxidised dietary oil in female rats during rearing, pregnancy and lactation on their reproductive performance and the antioxidative status of their offspring

The present study was performed to investigate whether lipid peroxidation products in thermoxidised dietary oil fed during rearing, pregnancy and lactation influences the reproductive performance of female rats and the antioxidant status of their offspring. Twenty-four female rats were divided into two groups at 4 weeks of age. They were fed diets containing fresh or oxidised oil (the latter prepared by heating at a temperature of 50 degrees C for 16 d) for 14 weeks. At the age of 12 weeks female rats were mated. The number of total pups and pups born alive was not different between both groups. However, individual pups and litters of dams fed oxidised oil were lighter at birth and gained less weight during the suckling period than those of dams fed fresh oil (P < 0.05). Pups of dams fed oxidised oil contained less protein and more fat in their carcasses than those of dams fed fresh oil (P < 0.05). The milk of dams fed oxidised oil had a lower concentration of triacylglycerols and a lower energy content than that of dams fed the fresh oil (P < 0.05). The pups of dams fed oxidised oil had higher concentrations of lipid peroxidation products in the liver at birth and day 19 of lactation than those of dams fed fresh oil (P < 0.05). In conclusion, the present study shows that feeding oxidised oil with a high concentration of lipid peroxidation products to female rats during rearing, pregnancy and lactation influences the development and antioxidant status of fetus and suckling pups.     

Protein malnutrition during pregnancy alters maternal behavior and anxiety-like behavior in offspring

Objective: The aim of this study was to evaluate the effects of protein malnutrition during pregnancy on maternal behavior, on the early behavior in pups by ultrasonic vocalizations (USVs) emission, and on the behavior of offspring in adulthood in an elevated T-maze.

Methods: Pregnant female rats were fed a normal protein-powdered diet (22% casein; control) or a low-protein (hypoproteic) diet (6% casein; protein restriction) during the first 2 weeks of pregnancy. On the fifth postpartum day (PND5), the number of USV was rated. On PND7, maternal behavior was assessed. Male offspring in adulthood were evaluated for behavioral performance in an elevated T-maze.

Results: Our results demonstrated that a hypoproteic diet during early pregnancy increased the maternal behavior, increased the number of USV by pups, and reduced the inhibitory avoidance responses in an elevated T-maze during adulthood. In addition, there was a reduction in weight gain of rats during pregnancy and of offspring during lactation.

Conclusion: In conclusion, the data found in our study suggest that the increase in USV emitted by pups due to hypoproteic diet during pregnancy accentuated maternal behavior. In addition, an increase in maternal care promoted the reduction in anxiety-like behavior in adult male offspring.     

同型半胱氨酸与宫内生长受限大鼠胰岛素敏感性关系及可能机制探讨

目的 分析同型半胱氨酸(Hcy)与宫内生长受限(IUGR)大鼠胰岛素抵抗关系,探讨改变早期膳食是否可影响Hcy水平进而影响胰岛素敏感性及可能的分子机制。方法 1)采用孕中晚期低蛋白及限制饮食的方法建立宫内发育迟缓(IUGR)大鼠模型,将新生IUGR仔鼠随机分为饮食干预组和未干预组,其中饮食干预组的哺乳期母鼠饲以高叶酸和维生素B₁₂的饲料,未干预组和对照组饲以普通饲料。三组仔鼠(饮食干预组、未干预组和对照组)均于生后21 d断奶,饲以普通饲料至生后120 d。2)测定三组仔鼠(每组各8只,雌雄各半)生后120 d空腹血浆血糖(FPG)、空腹血清胰岛素(FINS)和Hcy,计算胰岛素抵抗指数(IRI),探讨Hcy与IRI的关系。3)在生后120 d分别留取三组仔鼠的骨骼肌组织,采用Western Blotting法检测三组仔鼠骨骼肌组织骨骼肌磷脂酰肌醇3激酶的蛋白激酶B(PI3K/AKT)胰岛素信号通路中关键分子磷脂酰肌醇3激酶(PI3K)、人第10号染色体缺失的磷酸酶及张力蛋白同源基因(PTEN)蛋白表达情况,探讨Hcy与关键分子蛋白表达的关系。结果 1)生后120 d,饮食干预组仔鼠的FPG、FINS、IRI和Hcy均显著低于未干预组,但均高于对照组,差异均有统计学意义(P＜0.05)。2)三组仔鼠的Hcy水平与IRI呈高度正相关(r=0.937,P<0.05)。3)生后120 d,Hcy与PI3K蛋白表达呈负相关(r=-0.88),与PTEN蛋白表达呈正相关(r=0.85),均具有统计学意义(P<0.05)。结论 母鼠哺乳期可作为生后早期营养干预的一个窗口期,通过补充叶酸和维生素B₁₂,可降低IUGR仔鼠成年后Hcy水平,Hcy水平与胰岛素抵抗高度正相关。PI3K/AKT胰岛素信号通路中关键分子PI3K、PTEN蛋白表达与Hcy的变化也密切相关,提示Hcy可能影响了胰岛素受体后信号传导,进而影响了胰岛素的敏感性。     

Age-related changes in fatty acids in obese offspring of streptozotocin-induced diabetic rats

OBJECTIVE: The long-term effects of fetal hyperinsulinemia, time course of changes in liver and very-low-density lipoprotein (VLDL) lipid levels and fatty acid compositions were investigated in obese offspring of streptozotocin-induced mildly diabetic rats. RESEARCH METHODS AND PROCEDURES: Mild hyperglycemia in pregnant rats was induced by intraperitoneal injection of streptozotocin on day 5 of gestation. Control pregnant rats were injected with citrate buffer. Liver and VLDL lipids and fatty acids were analyzed in offspring at different ages. RESULTS: At birth, obese pups had higher VLDL triglyceride levels, saturated fatty acids, and C20:4n-6. They also had lower C18:2n-6 proportions in VLDL triglycerides, phospholipids, and cholesteryl esters than controls pups. In 1-month-old male and female obese rats, VLDL and liver lipid amounts were similar to those in their respective controls; however, high levels of C18:2n-6 and C20:4n-6 were noted in liver and VLDL lipids. At the age of 2 months, liver and VLDL triglyceride levels were higher in obese females than in control females. Fatty acid abnormalities seen in obese rats included low C18:3n-3 and high C22:6n-3 proportions in liver triglycerides and phospholipids. At the age of 3 months, obese rats, both males and females, compared with control animals, had higher VLDL and hepatic lipids with reduced C20:4n-6 levels and polyunsaturated/saturated fatty acids ratios in hepatic and VLDL triglycerides and phospholipids. DISCUSSION: Fetal obesity, associated with alterations in VLDL lipid fatty acid composition, represents an important risk factor for adult obesity and diabetes.     

Metabolic MRI of myocardial and hepatic triglyceride content in response to nutritional interventions

PURPOSE OF REVIEW: To discuss the technique and clinical applications of myocardial and hepatic H magnetic resonance spectroscopy to study myocardial and hepatic triglyceride content, in relation to changes in plasma nonesterified fatty acids induced by nutritional interventions. RECENT FINDINGS: Progressive caloric restriction induces a dose-dependent increase in myocardial triglyceride content and a dose-dependent decrease in diastolic function in lean healthy men. Hepatic triglyceride content shows a differential response to progressive caloric restriction, indicating that redistribution of endogenous triglyceride stores is tissue specific, at least in lean healthy men. A short-term high-fat high-energy diet in healthy men results in major increases in hepatic fat content, whereas it does not influence myocardial triglyceride content or myocardial function. Apparently, there is a differential, tissue-specific partitioning of either triglyceride or fatty acids or both between nonadipose organs such as the human heart and liver during different physiological conditions. SUMMARY: Metabolic MRI of myocardial and hepatic triglyceride content is a promising new tool to study the effects of nutritional interventions on myocardial and hepatic lipid metabolism in relation to heart function. Future studies should aim to apply these magnetic resonance techniques to obesity and type 2 diabetes mellitus.     

Organ growth and cellular development in ethanol-exposed rats

Effects of perinatal exposure to ethanol on growth and cellular development were investigated. Alcohol was administered in liquid diets designed to provide optimal nutrition during pregnancy. Pair-fed and ad lib control groups were included. The 3 groups of females were similar in body weight during gestation and lactation, and offspring weights were similar on gestation Day 21 and at birth. By Day 9 of lactation control pups weighted more than both alcohol and pair-fed pups which were similar in body weight. Weights of brain, heart, liver and kidney were reduced in alcohol pups compared to pair-feds and controls. Decreased liver weight reflected both decreased cell size and decreased protein content, but was primarily due to decreased caloric intake. Decreased heart weight appeared to result from a direct effect of ethanol on heart protein content. Even more marked were the adverse effects of ethanol on kidney protein content and kidney DNA (reflecting a decrease in cell number). In contrast, although both absolute brain weight and DNA content were decreased in ethanol-exposed offspring, relative brain weight was increased. Finally, maternal ethanol consumption significantly increased relative placenta weights as well as placental DNA and protein content.     

Mitochondrial dysfunction: maternal protein restriction as a trigger of reactive species overproduction and brainstem energy failure in male offspring brainstem

Mitochondria are important organelles in eukaryotic organisms, wherein their capacity to produce energy vary among the tissues depending upon the amounts of oxygen consumed. Part of the oxygen consumed during ATP generation produces reactive oxygen species, which if not efficiently removed can trigger a systemic damage to molecular compounds characterized as oxidative stress. Several studies have demonstrated that mitochondrial dysfunction and oxidative stress in the central nervous system (CNS) are related to a plethora of neural disorders. Herein, we hypothesize that a late autonomic imbalance-induced hypertension might be related to long-lasting effects of protein restriction during the critical period of the CNS development on the mitochondrial function and oxidative stress in the brainstem of adult (i.e. 150 days of age) male Wistar rats. Maternal protein restriction was induced by offering a diet based on 8% of casein from first day of pregnancy until weaning, when the male pups started to receive laboratory chow up to 150 days of life. The protein restriction induced an extended detrimental modulation in mitochondria function, decreasing the phosphorylation capacity with concomitant decrease in the mitochondrial membrane potential, wherein the reactive species overproduction triggered a disruption in proton conductance, which may gradually compromise mitochondria energy conservation. Interestingly, the elevated activity of glutathione-S-transferase and the augmented expression of uncoupling protein 2 are likely protective mechanisms induced by lipid peroxidation products, being feasible molecular changes attempting to deal with oxidative stress-induced ageing.     

Emergence of ageing-related changes in insulin secretion by pancreatic islets of male rat offspring of mothers fed a low-protein diet

Maternal low-protein (LP) diets programme β-cell secretion, potentially altering the emergence of ageing of offspring pancreatic function. We hypothesised that isolated pancreatic islet β-cell secretory responses are blunted in offspring exposed to LP during development and age-related reduction is influenced by the developmental stage of exposure to decreased nutrition. We studied male offspring of rats fed control (C) or LP protein (R) diets in pregnancy, first letter and/or lactation second letter of CC, RR, CR or RC groups. Serum glucose, insulin and homeostatic model assessment (HOMA) were measured. Pancreatic islets were isolated and in vitro insulin secretion quantified in low (LG - 5 mM) or high glucose (HG - 11 mM). Body weight and serum values between groups were similar at all ages. Insulin and HOMA rose with age and were highest at postnatal day (PND) 450 in all groups. At PND 36, insulin secretion was greatest in RR and RC. Only CC increased insulin secretion to HG. By PND 110, restricted groups responded less to LG but increased secretion to HG. By PND 450, CC offspring alone increased secretion to HG. Despite minimal differences in circulating insulin and glucose, reduced maternal protein intake affected insulin secretion at all ages. In addition, ageing reduced function in all R groups compared with CC by PND 110 and further by PND 450 most markedly in RC. We conclude that maternal LP diet during pregnancy and/or lactation impairs offspring insulin secretory response to a glucose challenge and alters the trajectory of ageing of pancreatic insulin secretion.     

Long-chain fatty acid composition of maternal liver lipids during pregnancy and lactation in the rat: comparison of triglyceride to phospholipid

The change in long-chain fatty acid composition in maternal liver was studied during pregnancy and lactation in the rat. Maternal liver triglycerides and phospholipids transiently accumulated and were depleted of long-chain fatty acids during pregnancy and lactation. During pregnancy, maternal liver accumulated triglyceride, but triglyceride fatty acid composition changed little. However, maternal liver total phospholipid fatty acid composition changed significantly without a change in the total pool size throughout pregnancy or lactation. The change in composition of (n-3) and (n-6) essential fatty acids in maternal liver triglyceride and total phospholipid occurred in an apparently dyssynchronous manner throughout pregnancy and lactation.     

Copper metabolism in iron-deficient maternal and neonatal rats

Groups of rats were fed diets providing 8 ppm iron (-Fe) and 250 ppm iron (+Fe) throughout pregnancy and lactation. In spite of the increase in apparent absorption of iron in pregnant -Fe dams, iron deficiency anemia developed, resulting in decreased iron levels in placenta, amniotic fluid and fetal liver. Copper concentration of amniotic fluid was elevated in -Fe dams. On day 17 of lactation, -Fe dams and their suckling pups had hematologic evidence of iron deficiency. While liver and spleen iron decreased in 17-day-old pups, levels of copper increased. Subcellularly, the greatest increase in hepatic copper in -Fe pups was found in the cytosol, thus the increased copper deposition is not similar to copper loading. Serum ceruloplasmin activity was significantly elevated in -Fe lactating dams and was slightly, but not significantly, increased in -Fe pregnant dams and suckling pups.     

Vitamin A during lactation: relationship of maternal diet to milk vitamin A content and to the vitamin A status of lactating rats and their pups

We have investigated the effects of maternal vitamin A intake during pregnancy and lactation or during lactation alone on the concentration of vitamin A in rat's milk and on vitamin A levels in plasma and liver of dams and their pups. Groups of Sprague-Dawley rats were fed diets having either a high vitamin A content [15 retinol equivalents (R.E.)/g diet] or a low vitamin A content (0.6 R.E./g) for 42 d, including 7-8 d prior to pregnancy, pregnancy, and for 14 d of lactation. The concentration of vitamin A in milk on d 14 of lactation was significantly greater on the high vitamin A diets [114 +/- 16 micrograms/dl (mean +/- SEM; n = 8) versus 52 +/- 7.3 micrograms/dl (n = 11), P less than 0.005]. However, milk vitamin A concentration on d 1 of lactation did not vary with maternal vitamin A intake during pregnancy. In a second study in which supplementation with vitamin A (30 R.E./g diet) was begun on d 1 postpartum, the milk vitamin A content increased progressively with duration of lactation. Maternal plasma vitamin A concentrations did not differ between rats fed the higher or lower vitamin A diets. However, liver vitamin A concentrations both of dams and of their 14-d-old pups were significantly higher when dams were fed the higher vitamin A diets during pregnancy and/or lactation. The results of these studies indicate that the transfer of vitamin A from mother to offspring by milk and the vitamin A status of dams and their suckling neonates is influenced by maternal vitamin A intake during lactation.(ABSTRACT TRUNCATED AT 250 WORDS)