Evidence that a maternal “junk food” diet during pregnancy and lactation can reduce muscle force in offspring

Background  Obesity is a multi-factorial condition generally attributed to an unbalanced diet and lack of exercise. Recent evidence suggests that maternal malnutrition during pregnancy and lactation can also contribute to the development of obesity in offspring. We have developed an animal model in rats to examine the effects of maternal overeating on a westernised “junk food” diet using palatable processed foods rich in fat, sugar and salt designed for human consumption. Using this model, we have shown that such a maternal diet can promote overeating and a greater preference for junk food in offspring at the end of adolescence. The maternal junk food diet also promoted adiposity and muscle atrophy at weaning. Impaired muscle development may permanently affect the function of this tissue including its ability to generate force. Aims  The aim of this study is to determine whether a maternal junk food diet can impair muscle force generation in offspring. Methods  Twitch and tetanic tensions were measured in offspring fed either chow alone (C) or with a junk food diet (J) during gestation, lactation and/or post-weaning up to the end of adolescence such that three groups of offspring were used, namely the CCC, JJC and JJJ groups. Results  We show that adult offspring from mothers fed the junk food diet in pregnancy and lactation display reduced muscle force (both specific twitch and tetanic tensions) regardless of the post-weaning diet compared with offspring from mothers fed a balanced diet. Conclusions  Maternal malnutrition can influence muscle force production in offspring which may affect an individual’s ability to exercise and thereby combat obesity.     

Maternal low-protein diet during lactation programmes body composition and glucose homeostasis in the adult rat offspring

Previously we have reported that maternal malnutrition during lactation programmes body weight and thyroid function in the adult offspring. In the present study we evaluated the effect of maternal protein restriction during lactation upon body composition and hormones related to glucose homeostasis in adult rats. During lactation, Wistar lactating rats and their pups were divided into two experimental groups: control (fed a normal diet; 23% protein) and protein-restricted (PR; fed a diet containing 8% protein). At weaning, offspring received a normal diet until they were 180 d old. Body weight (BW) and food intake were monitored. Serum, adrenal glands, visceral fat mass (VFM) and carcasses were collected. PR rats showed lower BW (-13%; P < 0.05), VFM (-33%; P < 0.05), total body fat (-33%; P < 0.05), serum glucose (-7%; P < 0.05), serum insulin (-26%, P < 0.05), homeostasis model assessment index (-20%), but higher total adrenal catecholamine content (+90%; P < 0.05) and serum corticosterone concentration (+51%; P < 0.05). No change was observed in food intake, protein mass or total body water. The lower BW of PR rats is due to a reduction of white fat tissue, probably caused by an increase in lipolysis or impairment of lipogenesis; both effects could be related to higher catecholaminergic status, as well as to hypoinsulinaemia. To conclude, changes in key hormones which control intermediary metabolism are programmed by maternal protein restriction during lactation, resulting in BW alterations in adult rats.     

Mild maternal iron deficiency anemia during pregnancy and lactation in guinea pigs causes abnormal auditory function in the offspring

Iron deficiency (ID) anemia (IDA) adversely affects different aspects of the nervous system such as myelinogenesis, neurotransmitters synthesis, brain myelin composition, and brain fatty acid and eicosanoid metabolism. Infant neurophysiological outcome in response to maternal IDA is underexplored, especially mild to moderate maternal IDA. Furthermore, most human research has focused on childhood ID rather than prenatal or neonatal ID. Thus, our study evaluated the consequences of mild maternal IDA during pregnancy and lactation on the offsprings' auditory function using the auditory brainstem response (ABR). This technique provides objective measures of auditory acuity, neural transmission times along the peripheral and brainstem portions of the auditory pathway, and postnatal brain maturation. Female guinea pigs (n = 10/group) were fed an iron sufficient diet (ISD) or an iron deficient diet (IDD) (144 and 11.7 mg iron/kg) during their acclimation, gestation, and lactation periods. From postnatal d (PNd) 9 onward, the ISD was given to all weaned offspring. ABR were collected from the offspring on PNd24 using a broad range of stimulus intensities in response to 2, 4, 8, 16, and 32 kHz tone pips. IDA siblings (n = 4), [corrected] compared with the IS siblings (n = 5), had significantly elevated ABR thresholds (hearing loss) in response to all tone pips. These physiological disturbances were primarily due to a sensorineural hearing loss, as revealed by the ABR's latency-intensity curves. These results indicate that mild maternal IDA during gestation and lactation altered the hearing and nervous system development of the young offspring.     

Influence of pregnancy and lactation on maternal deposition and perinatal uptake of 241Am in the rat

To investigate the metabolism of 241Am as affected by pregnancy and lactation, female rats were injected with 5 muCi of 241Am intravenously while nulliparous, pregnant or lactating. The females and subsequent litters were killed at various times after injection to determine 241Am distribution and retention. The temporal relationship between injection and pregnancy influenced the tissue retention of 241Am in both dams and progeny. The half-time of 241Am in livers of pregnant or lactating rats was more than twice that of nulliparous rats, although the initial uptake was approximately 50% of the activity in all groups. Both spleen and femur accumulated more 241Am at 7-10 weeks after injection than at earlier times, but this increase could not be related to pregnancy. Approximately 10 times more 241Am was transferred to offspring from dams that were lactating when exposed than was transferred via the placenta when exposure occurred late in gestation. Furthermore, more 241Am was transmitted to the progeny via milk if exposure of the dam occurred during lactation rather than during pregnancy.     

Effect of maternal iron restriction during pregnancy on renal morphology in the adult rat offspring

In rats, maternal anaemia during pregnancy causes hypertension in the adult offspring, although the mechanism is unknown. The present study investigated the renal morphology of adult rats born to mothers who were Fe-deficient during pregnancy. Rats were fed either a control (153 mg Fe/kg diet, n 7) or low-Fe (3 mg/kg diet, n 6) diet from 1 week before mating and throughout gestation. At delivery, the Fe-restricted (IR) mothers were anaemic; the IR pups were also anaemic and growth-retarded at 2 d of age. At 3 and 16 months, systolic blood pressure in the IR offspring (163 (sem 4) and 151 (sem 4) mmHg respectively, n 13) was greater than in control animals (145 (sem 3) and 119 (sem 4) mmHg respectively, n 15, P<0.05). At post mortem at 18 months, there was no difference in kidney weight between treatment groups, although relative kidney weight as a fraction of body weight in the IR offspring was greater than in control animals (P<0.05). Glomerular number was lower in the IR offspring (11.4 (sem 1.1) per 4 mm(2), n 13) compared with control rats (14.8 (sem 0.7), n 15, P<0.05). Maternal treatment had no effect on glomerular size, but overall, female rats had smaller and more numerous glomeruli per unit area than male rats. When all animals were considered, inverse relationships were observed between glomerular number and glomerular size (r-0.73, n 28, P<0.05), and glomerular number and systolic blood pressure at both 3 months (r-0.42, n 28, P<0.05) and 16 months of age (r-0.64, n 28, P<0.05). Therefore, in rats, maternal Fe restriction causes hypertension in the adult offspring that may be due, in part, to a deficit in nephron number.     

Enhanced sensitivity of skeletal muscle growth in offspring of mice long-term selected for high body mass in response to a maternal high-protein/low-carbohydrate diet during lactation

Aim

To investigate the effects of a high-protein/low-carbohydrate diet fed to mice of different genotypes during pregnancy and/or lactation on offspring skeletal muscle growth and metabolism.

Methods

Pregnant mice from strains selected for high body mass (DU6) or endurance running performance (DUhLB) and from an unselected control strain (DUK) were fed iso-energetic diets containing 20 % (C) or 40 % protein and low carbohydrate (HP) from mating to weaning at day 21 of age. At birth, offspring were cross-fostered resulting in different exposure to maternal prenatal-preweaning diets (C–C, HP–C, C–HP, HP–HP). Rectus femoris muscle of male mice (n = 291) was examined at day 23, 44, 181 and 396 of age for cellular growth and metabolism.

Results

At day 23 of age, body and muscle growth was retarded by 30–40 % (P < 0.0001) in response to the C–HP and HP–HP, but not to the HP–C diet, due to reduced fibre size (P < 0.0001) but not fibre number. DNA was highly reduced in DU6, less in DUhLB, but not in DUK muscle (strain × diet; P < 0.0001). Despite some compensation, muscle growth was still impaired (P < 0.001) in adulthood (day 44; day 181), but at senescence only in DU6 mice (strain × diet; P < 0.05). Only at weaning, isocitrate and lactate dehydrogenase activities were increased or decreased (P < 0.0001), respectively, without influence on fibre type composition.

Conclusion

A high-protein/low-carbohydrate diet fed to dams during lactation, but not during pregnancy, retards skeletal muscle growth in offspring with greater response of a heavy, obese compared with a physically fit and a control genotype and causes a transient shift towards oxidative versus glycolytic muscle metabolism.     

Effect of diet during pregnancy and lactation on the activity of HMG-CoA reductase in the developing rat

Wistar rats were fed a control diet or a diet containing either cholestyramine or high fat and cholesterol throughout gestation and the first 14 d of lactation. New-born litters were cross-fostered from rats fed the control diet to rats fed either cholestyramine or high fat and cholesterol, or from rats fed cholestyramine to rats fed the control diet. Hepatic hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase activity, plasma cholesterol and triglycerides were assayed on gestation d 20 and postnatal d 8, 14, 22 and 30. Cholestyramine had no effect on maternal or fetal plasma lipid levels but increased fetal hepatic HMG-CoA reductase activity by approximately 50%. The increased reductase activity persisted on postnatal d 8 and 14. Control pups suckled by dams fed cholestyramine also had significantly increased HMG-CoA reductase activities on postnatal d 8 and 14. The high fat and cholesterol diet significantly increased maternal plasma cholesterol but had no effect on HMG-CoA reductase activity in the fetus or suckling pups. Neither cholestyramine nor high fat and cholesterol altered the rat milk cholesterol levels. The studies demonstrate that HMG-CoA reductase activity in the developing rat can be altered by factors dependent on maternal diet. They do not support a hypothesis for regulation by maternal dietary or milk cholesterol supply.     

Formulation of a liquid diet for ethanol studies involving gestation and lactation in the rat

This report describes the preparation of a liquid diet for rat studies involving ethanol ingestion during gestation and lactation. The control diet was formulated to contain 30% of energy from casein including methionine at 0.5 mg/kcal, 11.5% of energy from corn oil, 58.5% of energy from dextrose, cellulose, and adequate vitamins and minerals. Calculations for the isocaloric substitution of dextrose with ethanol are described as well as the use of xanthan gum to disperse and emulsify ordinary solid diet components. The use of this liquid diet as the sole source of nutrition for the rat during gestation and lactation produced energy intakes, gestational weight gains, litter sizes, percent survival to weaning and weaning weights similar to those expected of a conventional diet even when ethanol was substituted for dextrose to provide 30% of total energy.     

Maternal high-fructose intake during pregnancy and lactation induces metabolic syndrome in adult offspring

BACKGROUND/OBJECTIVESNutritional status and food intake during pregnancy and lactation can affect fetal programming. In the current metabolic syndrome epidemic, high-fructose diets have been strongly implicated. This study investigated the effect of maternal high-fructose intake during pregnancy and lactation on the development of metabolic syndrome in adult offspring.SUBJECTS/METHODSDrinking water with or without 20% fructose was administered to female C57BL/6J mice over the course of their pregnancy and lactation periods. After weaning, pups ate regular chow. Accu-Chek Performa was used to measure glucose levels, and a tail-cuff method was used to examine systolic blood pressure. Animals were sacrificed at 7 months, their livers were excised, and sections were stained with Oil Red O and hematoxylin and eosin (H&E) staining. Kidneys were collected for gene expression analysis using quantitative real-time Polymerase chain reaction.RESULTSAdult offspring exposed to maternal high-fructose intake during pregnancy and lactation presented with heavier body weights, fattier livers, and broader areas under the curve in glucose tolerance test values than control offspring. Serum levels of alanine aminotransferase, aspartate aminotransferase, glucose, triglycerides, and total cholesterol and systolic blood pressure in the maternal high-fructose group were higher than that in controls. However, there were no significant differences in mRNA expressions of renin-angiotensin-aldosterone system genes and sodium transporter genes.CONCLUSIONSThese results suggest that maternal high-fructose intake during pregnancy and lactation induces metabolic syndrome with hyperglycemia, hypertension, and dyslipidemia in adult offspring.     

Energy stress during pregnancy and lactation: consequences for maternal nutrition in rural Bangladesh

OBJECTIVE: To assess the relationship of energy stress during pregnancy and lactation to maternal body stores in marginally nourished rural Bangladeshi women. SUBJECTS AND METHODS: Two-hundred and fifty-two women were followed from 5-7 months of pregnancy until 6 months postpartum. Energy intake was estimated during pregnancy and at 1, 3 and 6 month(s) postpartum using 24 h dietary recall. Body weight was measured on enrollment, another once or twice during pregnancy, and at 1, 3 and 6 month(s) postpartum. The weekly rates of pregnancy weight gain and postpartum weight changes were determined. Weight and length of the infants were measured at birth and at approximately 1, 3 and 6 month(s). RESULTS: Maternal energy intake at 5-7 months of gestation was 1464+/-416 kcal/day (mean+/-s.d.). Women gained a mean of 200 g/week or a total of 4 kg during the second half of pregnancy. An analysis of maternal weight showed no indication of accrual of fat stores during pregnancy. Dietary energy during lactation exceeded the intake during pregnancy by 248-354 kcal/day. Mothers lost an estimated average of 1 kg of weight during the first 6 months of lactation. The mean (+/-s.d.) birth weight was 2.55+/-0.38 kg, and the prevalence of low birth weight (<2500 g) was 48%. Infants exhibited some catch-up growth only during the first 3 months but overall growth during the first 6 months did not change from their relative status at birth when compared with NCHS reference. CONCLUSIONS: These rural Bangladeshi women failed to gain sufficient weight during the last half of pregnancy to maintain body weight during lactation when the energy demand is high. Poor growth of their primarily breastfed infants raises concern about the adequacy of lactation in this community.     

运用倾向值匹配法分析孕妇早期呼吸道感染与新生儿出生孕周的关联

目的 探讨孕妇呼吸道感染与活产单胎新生儿出生孕周之间的关联。方法 采用分层随机整群抽样方法,抽取陕西省30个区（县）。面对面问卷调查2010－2013年符合纳入指标的育龄妇女及其生育子女。应用倾向值匹配法,对孕早期呼吸道感染组和无呼吸道感染组进行1∶1匹配。以母亲孕早期呼吸道感染和子女出生孕周分别作为自变量和因变量,通过逐步校正混杂因素共建立3个线性回归模型,其中模型1仅分析匹配前呼吸道感染变量,模型2在模型1的基础上进一步校正母亲及新生儿个体差异因素,模型3仅分析匹配后呼吸道感染变量。结果 共纳入28 848人,孕早期呼吸道感染3 676人（12.74%）。匹配后感染组和非感染组分别为2 762人。模型1显示母亲孕早期出现呼吸道感染,新生儿出生孕周减少0.111周（P<0.001）,模型2减少0.058周（P=0.025）,模型3减少0.076周（P=0.036）。结论 孕妇出现呼吸道感染与子代出生孕周减少有关。     

Hydrogenated fat diet intake during pregnancy and lactation modifies the PAI-1 gene expression in white adipose tissue of offspring in adult life

We examine whether feeding pregnant and lactating rats hydrogenated fats rich in trans fatty acids modifies the plasma lipid profiles and the expression of adipokines involved with insulin resistance and cardiovascular disease in their 90-day-old offspring. Pregnant and lactating Wistar rats were fed with either a control diet (C group) or one enriched with hydrogenated vegetable fat (T group). Upon weaning, the male pups were sorted into four groups: CC, mothers were receiving C and pups were kept on C; CT, mothers were receiving C and pups were fed with T; TT, mothers were receiving T and pups were kept on T; TC, mothers were receiving T and pups were fed with C. Pups' food intake and body weight were quantified weekly and the pups were killed at day 90 of life by decapitation. Blood and carcass as well as retroperitoneal, epididymal, and subcutaneous white adipose tissues were collected. Food intake and body weight were lower in TC and TT, and metabolic efficiency was reduced in TT. Offspring of TT and TC rats had increased white adipose tissue PAI-1 gene expression. Insulin receptor was higher in TT than other groups. Ingestion of hydrogenated vegetable fat by the mother during gestation and lactation could promote deleterious consequences, even after the withdrawal of the causal factor.     

A dose-response relationship between maternal smoking during late pregnancy and adult intelligence in male offspring

An association between maternal smoking during pregnancy and cognitive and behavioural development has been observed in several studies, but potential effects of maternal smoking on offspring adult intelligence have not been investigated. The objective of the present study was to investigate a potential association between maternal smoking during pregnancy and offspring intelligence in young adulthood. Adult intelligence was assessed at the mean age of 18.7 years by a military draft board intelligence test (Borge Priens Prove) for 3044 singleton males from the Copenhagen Perinatal Cohort with information regarding maternal smoking during the third trimester coded into five categories (about 50% of the mothers were smokers). The following potential confounders were included as covariates in multivariable analyses: parental social status and education, single mother status, mother's height and age, number of pregnancies, and gestational age. In separate analyses, birthweight and length were also included as covariates. Maternal cigarette smoking during the third trimester, adjusted for the seven covariates, showed a negative association with offspring adult intelligence (P=0.0001). The mean difference between the no-smoking and the heaviest smoking category amounted to 0.41 standard deviation, corresponding to an IQ difference of 6.2 points [95% confidence interval 0.14, 0.68]. The association remained significant when further adjusted for birthweight and length (P=0.007). Both unadjusted and adjusted means suggested a dose-response relationship between maternal smoking during pregnancy and offspring adult intelligence. When subjects with missing data were excluded, essentially the same results were obtained in the reduced sample (n=1829). These results suggest that smoking during pregnancy may have long-term negative consequences on offspring adult intelligence.     

孕期及哺乳期n-6/n-3脂肪酸变化对仔鼠脑源性神经营养因子基因表达的影响

目的 探讨孕期及哺乳期n-3 多不饱和脂肪酸(n-3 polyunsaturated fatty acids,n-3 PUFAs)摄入量及其与n-6 PUFAs比例对仔鼠脑源性神经营养因子(brain-derived neurotrophic factor,bdnf)基因表达的影响。方法 使用6~8周龄清洁级C57BL/6J雌性小鼠,随机分为5 组,分别给予n-3 PUFAs缺乏和4种不同含量n-3 PUFAs(n-6/n-3 PUFAs比值分别为15∶1、5∶1、1∶1及1∶5)饲料喂养。小鼠12~14周龄时雌雄合笼交配繁殖,仔鼠断乳后继续行母鼠相同饲料喂养,分别在生后7 d、21 d和3 月时被处死后取脑。同时,分别从n-3 PUFAs缺乏组和n-6/n-3 PUFAs(5∶1)组中选取等量仔鼠,21 d断乳后相互交换饲料喂养至3个月,处死后取脑。采用实时荧光定量PCR技术测定脑皮质bdnf基因mRNA的表达。结果 与n-3 PUFAs缺乏饲料组相比,对于7 d和21 d幼年仔鼠,只有n-6/n-3 PUFAs(1∶5)饲料组bdnf基因mRNA表达量显著升高;对于3 月龄成年仔鼠,各含n-3 PUFAs饲料组bdnf基因mRNA的表达均升高。对于孕期和哺乳期n-3 PUFAs缺乏饲料组仔鼠,断乳后给予含n-3 PUFAs饲料喂养未能提升脑皮质bdnf基因mRNA表达;而孕期和哺乳期含n-3 PUFAs饲料喂养的仔鼠,断乳后给予n-3 PUFAs缺乏饲料喂养时,脑皮质bdnf基因mRNA表达量见一定程度的升高。结论 孕期及哺乳期可能需要较高的n-3 PUFAs摄入,才能满足幼年期诱导脑bdnf表达之需。保证生命早期n-3 PUFAs的适量摄入,有助于维持成年期bdnf的正常表达。     

Evidence for increased selenium requirement for the rat during pregnancy and lactation

Adequacy of the National Research Council (NRC) selenium (Se) requirement for growth (0.1 ppm Se) was assessed in reproducing Sprague-Dawley rats. Either a casein-based diet with no added Se or the same diet supplemented with selenite to contain 0.05, 0.1, or 0.2 ppm Se was fed during pregnancy and lactation and to nonreproducing controls. Only 0.05 ppm Se was necessary to maintain maximal red blood cell (RBC) and liver Se concentrations and glutathione peroxidase (GSH-Px) activities in controls, whereas 0.2 ppm Se was necessary to maintain comparable RBC Se during pregnancy and tissue Se and GSH-Px activities during lactation. On d 2 of lactation, no differences in pup tissue Se or GSH-Px activities could consistently be related to maternal Se intake. By d 18 of lactation, however, Se status of nursing pups reflected maternal Se intake. Pups of dams fed 0.2 ppm Se had tissue Se and GSH-PX activities significantly greater than those of all other pups. Milk Se content correlated significantly with maternal Se intake and plasma Se and with pup tissue Se and GSH-Px activities. These results indicate that during reproduction 0.1 ppm Se is not adequate to maintain maternal tissue Se or GSH-Px activities comparable to those of normal controls; 0.2 ppm dietary Se is more appropriate, resulting in maternal GSH-PX activities similar to those of controls fed 0.1 ppm Se and milk Se concentrations that result in greater pup tissue GSH-Px activities.     

Relationships among lactation performance, maternal diet, and body protein metabolism in humans

The relationships between lactation performance and maternal diet and body protein metabolism were determined at 1, 5, and 12 months postpartum in lactating women who consumed a controlled diet of measured protein and energy. Milk production was measured by the 24-h test weighing procedure. Maternal body protein metabolism was evaluated by nitrogen balance and a primed, constant infusion of [1-13C]leucine and [alpha-15N]lysine. Milk production was associated positively with lysine flux (P less than 0.05, r = 0.59), leucine incorporation into body protein (P less than 0.05, r = 0.58), nitrogen intakes (P less than 0.05, r = 0.56), and energy intakes (P less than 0.01, r = 0.69). When adjusted for postpartum time, significant associations between total nitrogen concentrations in milk and nitrogen balance also were present (P less than 0.05, r = 0.77). These observations document associations among lactation performance, maternal diet, and the metabolic responses of body protein stores in well-nourished women and suggest strategies for the improvement of milk production in settings where nutrient insufficiency and malnutrition prevail.