Gestation Lactation Research Articles

Sucrose exposure during gestation lactation and postweaning periods increases the pubococcygeus muscle reflex activity in adult male rats.

Erectile dysfunction is related to metabolic alterations produced by a high carbohydrate diet, which may affect muscle activity during penile reflex in adulthood. We determined whether sucrose water consumption during gestation lactation and postweaning affects pubococcygeus muscle (Pcm) activity during urethrogenital reflex in adult male rat offspring. Twelve female rats were mated and grouped in control mothers consumed tap water and sucrose mothers consumed sucrose water during gestation lactation. Male pups were weaned and assigned into four groups (n = 6 each): those from control mothers who continued drinking tap water (CM-CO group) or sucrose water (CM-SO group) until adult life, and those from sucrose mothers who drank tap water (SM-CO group) or continued drinking sucrose water (SM-SO group) until adult life. Body weight, Pcm activity during penile stimulation by bipolar electrodes and urethrogenital reflex were analyzed. A catheter was placed into the urethra to record variations in urethral pressure after mechanical stimulation. Two-way ANOVA followed by post hoc tests were used considering P ≤ 0.05 as a significant difference. Males from the SM-SO group showed weight gain compared to the control group (P < 0.001). Also, sucrose intake promoted high Pcm activity (P < 0.0001) but reduced urethrogenital reflex duration CM-CO vs CM-SO (P = 0.02); CM-CO vs SM-CO (P = 0.01); CM-SO vs SM-SO (P < 0.003); and SM-CO vs SM-SO (P < 0.002). Our results suggest that a combination of a sucrose-rich diet during gestation lactation and postweaning modifies Pcm activation during penile reflex. The urethrogenital reflex is a spinal ejaculatory-like reflex, these rats could have penile dysfunction equivalent to premature ejaculation in men.

Sex‐Dependent Metabolic Syndrome Phenotype Produced By Developmental Exposure to Indoor Flame Retardants

Chronic low level exposure to endocrine disrupting chemicals such as polybrominated diphenyl ethers (PBDEs) have been associated with diabetogenic and obesogenic phenotypes but mechanistic studies are sparse.1–2 In this study, we examined effects of developmental exposure to DE‐71, an industrial mixture of mostly penta‐brominated PBDE congeners3, on cellular, organ and systems level processes associated with metabolic syndrome after adult and developmental exposure to DE‐71 in C57Bl/6 mice. In an effort to link chemical exposure to health effects via key events (KE), we designed experiments using an adverse outcome pathway framework. Toxicant Exposure: C57BI/6 dams were exposed daily to DE‐71 at low dose (LD, 0.1mg/kg/d), or high dose (HD, 0.4mg/kg/d) and compared to corn oil vehicle control (OD) via ingestion of infused corn flakes for 10wk (mating, gestation lactation). GC/ECNI‐MS showed that livers of female offspring at sacrifice (PND 100) contained only BDE‐25 and 153, whereas, other congeners were detected in dams: BDE 99&gt;47=85=100=154=183. Adverse Outcomes: Glucose tolerance test indicated pronounced glucose intolerance in LD females and dams but not male offspring. Insulin tolerance test showed insensitivity in LD and HD female offspring (p&lt;.05; n=5–10). Compared to LD female offspring, DE‐71 exposed male offspring and dams showed less pronounced glucose intolerance and insulin insensitivity. KE – Systems (Metabolic): Fasting hyperglycemia was observed in HD female offspring (p&lt;.001; n=5–12); Only the LD female offspring showed elevated plasma cholesterol and liver lipids although but dams showed greatest fatty liver (p&lt;.05, n=5–8). KE – Systems (Endocrine): Plasma insulin was significantly decreased in LD (p&lt;.05, n=8–19) and HD female (p&lt;.01, n=8–19) but not male offspring or dams. KEs – Molecular: Adult and developmental PBDE exposure at LD and HD produced liver oxidative stress as indicated by elevated glutathione S‐transferase (GST) and reduced glutathione reductase (GR) activity in male offspring, female offspring and dams when compared with OD (n=12–20/group; p&lt;.01). PBDEs may alter hepatic glycogenesis and glyceroneogenesis and glucose oxidation since they reduce phosphenolpyruvate carboxykinase (PEPCK) and glutamate dehydrogenase (GDH) activity, respectively; both were decreased in LD and HD male offspring, female offspring and dams (n=8–11/group, p&lt;.01). Exposed female offspring values were similar except that only HD showed reduced GR and PEPCK. Summary: The following sequence of KEs is proposed downstream of a yet unknown molecular initiating event: (1) Reduced GR and elevated GST (KE1); (2) Reduced GDH and PEPCK (KE2); (3) Liver lipids, Fatty liver; (4) Fasting hyperglycemia, glucose intolerance, insulin insensitivity and hyperlipidemia. Our results indicate that PBDEs promote a metabolic syndrome phenotype in parallel with hepatic oxidative stress injury. Support: UC MEXUS (MC), Sigma Xi Research Society Grant in Aid (EK), MARC fellowship (GG)Support or Funding InformationSupport: UC MEXUS (MC), Sigma Xi Research Society Grant in Aid (EK), MARC fellowship (GG)

Efecto de la suplementación con metionina de zinc en el desempeño productivo y morfología del epitelio intestinal en cerdos criados en ambiente caluroso o fresco

ABSTRACT To determine the effect of zinc-methionine supplementation during the gestation-lactation (GL) and growing-finishing (DF) period in the performance and during DF on the epithelium intestinal morphology of fattening pigs under hot and cool condition, two experiments were carried out. The experiment (Exp.) 1 was carried out during the hot season and Exp. 2 during the cool season of the year. 192 pigs were used (96 per Exp.) with an average age of 79 days and 26.39±SD4.97 kg of body weight, piglets of sows that received or not feed added with 100 mg of Zn/kg, from 80 to 114 days of gestation and during 21 d of lactation (GL). In each experiment, the pigs were assigned to one of four treatments in a completely random design with a 2 x 2 factorial arrangement. The treatments were T1 (control, n = 24), non-supplemented mothers-non-supplemented pigs; T2 (Zn FD; n = 24), non-supplemented mothers, pigs supplemented with 100 mg of Zn/kg feed; T3 (Zn GL; n = 24), supplemented mothers – non-supplemented pigs and, T4 (Zn GL + Zn DF; n = 24), supplemented mothers + supplemented pigs. Supplementation with 100 mg of Zn / kg of feed during GL and DF did not modify the productive performance of the pigs during the study period. However, the villus height: crypt depth ratio was higher (p <0.01) in pigs supplemented with Zn (3.36 vs. 2.77) during the hot season. An interaction (p <0.02) between climate and zinc, methionine supplementation was observed in the depth of the crypt and the V:C ratio. Supplementation during GL tended (P = 0.06) to lower the mortality of developing-finishing pigs in the cool season. According to results, it is concluded that the addition of zinc methionine to the diet improves the integrity of the intestinal epithelium in developing-finishing pigs reared under a hot environment, and supplementation during the gestation and lactation period reduces mortality during fattening.

The influence of a diet based on flaxseed, an omega-3 source, during different developmental periods, on the blood pressure of rats submitted to stress

Objective: This study aimed to investigate a flaxseed diet during different developmental periods, and its effect on the blood pressure of rats submitted to stress.Methods: Fifty-six male rats (F1), born from 14 rats (F0), were divided into seven groups (n = 8): flaxseed group (FG); flaxseed group gestation and lactation (FG-GL); flaxseed group weaning (FG-W); flaxseed group weaning and stress (FG-WS); flaxseed group stress (FG-S); flaxseed group gestation lactation and weaning (FG-GLW), and control Group (CG). Stress protocol was undertaken for 1 month. Blood pressure was analysed before and after the stress protocol. The left adrenal glands and serum corticosterone levels were analysed.Results: Systolic blood pressure before stress was lower in all groups with flaxseed diet compared with the CG (p = .00001). After stress, CG showed higher blood pressure compared with FG, FG-GL, and FG-GLW (p = .004). The levels of corticosterone were lower in the FG between all groups (p < .000001) and the CG showed higher compared with FG-W, FG-WS, FG-GL, and FG-GLW (p < .0001). The adrenal gland did not show differences.Conclusions: Results suggest a possible factor from a flaxseed diet against the effects of stress on a blood pressure in all periods of life but especially in the gestation and lactation periods.

Maternal protein restriction during lactation induces early and lasting plasma metabolomic and hepatic lipidomic signatures of the offspring in a rodent programming model

Perinatal undernutrition affects not only fetal and neonatal growth but also adult health outcome, as suggested by the metabolic imprinting concept. However, the exact mechanisms underlying offspring metabolic adaptations are not yet fully understood. Specifically, it remains unclear whether the gestation or the lactation is the more vulnerable period to modify offspring metabolic flexibility. We investigated in a rodent model of intrauterine growth restriction (IUGR) induced by maternal protein restriction (R) during gestation which time window of maternal undernutrition (gestation, lactation or gestation–lactation) has more impact on the male offspring metabolomics phenotype. Plasma metabolome and hepatic lipidome of offspring were characterized through suckling period and at adulthood using liquid chromatography–high-resolution mass spectrometry. Multivariate analysis of these fingerprints highlighted a persistent metabolomics signature in rats suckled by R dams, with a clear-cut discrimination from offspring fed by control (C) dams. Pups submitted to a nutritional switch at birth presented a metabolomics signature clearly distinct from that of pups nursed by dams maintained on a consistent perinatal diet. Control rats suckled by R dams presented transiently higher branched-chain amino acid (BCAA) oxidation during lactation besides increased fatty acid (FA) β-oxidation, associated with preserved insulin sensitivity and lesser fat accretion that persisted throughout their life. In contrast, IUGR rats displayed permanently impaired β-oxidation, associated to increased glucose or BCAA oxidation at adulthood, depending on the fact that pups experienced slow postnatal or catch-up growth, as suckled by R or C dams, respectively. Taken together, these findings provide evidence for a significant contribution of the lactation period in metabolic programming.

Early and post-weaning malnutrition impairs alpha-MSH expression in the hypothalamus: a possible link to long-term overweight

The present study explored the effects of early and post-weaning malnutrition and nutritional rehabilitation on orexigenic (orexin (ORX) and neuropeptide Y (NPY)) and anorexigenic peptides (alpha-melanocyte stimulating hormone (alpha-MSH)) expressed in hypothalamic nuclei. Male Wistar rats were malnourished during gestation–lactation (MGL) or from weaning to post-natal day 55 (MPW; P55). Two groups of rats were rehabilitated with a balanced diet until P90 (MGL-R and MPW-R, respectively). After a glucose tolerance test (GTT) brains were processed for immunohistochemistry. Malnourished groups were hyperglycemic after GTT. ORX expression did not display any difference. Only MGL rats showed increased NPY immunoreactivity in ARC and PVN nuclei, and both malnourished groups showed low alpha-MSH expression in the PVN and DMH, as compared with their controls. After nutritional rehabilitation rats showed normal GTT, increased rate of body and adipose tissue weights and high proportion of food ingestion. Both rehabilitated groups maintained low alpha-MSH expression in the PVN, indicating a deleterious long-lasting effect.

Altered Fos immunoreactivity in the hypothalamus after glucose administration in pre- and post-weaning malnourished rats

The present study explored the effects of malnutrition and nutritional rehabilitation on the response to glucose in hypothalamic nuclei involved in metabolic homeostasis. Male Wistar rats were malnourished during gestation–lactation (MGL) or at weaning to 55 days (MPW). Two groups of rats were rehabilitated with a balanced diet until 90 days (MGL-R and MPW-R, respectively). After a glucose tolerance test (GTT), brains were processed for Fos immunoreactivity (Fos-IR). Both malnourished groups displayed hyperglycemia after GTT. MGL exhibited an increased number of Fos-IR neurons in the ventromedial hypothalamic nucleus (VMH), while MPW showed increased Fos-IR in the arcuate nucleus (ARC) and VMH and a decrease in the paraventricular nucleus (PVN), as compared with their controls. Nutritional rehabilitation normalized values of glucose after GTT in both groups, while low number of Fos-IR neurons remained in the ARC, PVN and VMH of MPW-R rats, indicating a deleterious, long-lasting effect after post-weaning malnutrition.

Arginine Deficiency during Gestation and Lactation in the Rat

The effects of dietary arginine deprivation during gestation and lactation were studied in the rat. Placental development, as indicated by the total protein and RNA content, of rats fed a diet devoid of arginine was inferior to that of pair-fed controls. Fetal cerebral protein plus body weights were reduced by maternal arginine deprivation. Urinary excretion of orotic acid and citric acid was significantly increased in arginine-deficient rats throughout the gestational period. Pups nursed by arginine-deficient dams during lactational periods had smaller body and organ weights than those nursed by pair-fed control dams regardless of their prenatal nutritional states. Nursing performance of the dam was most affected by feeding arginine-free diet throughout gestation and lactation. Consumption of an arginine-free diet by the dam during gestation resulted in lower birth weight and higher perinatal mortality of the pups nursed. Deletion of arginine from the diet after parturition significantly reduced nursing performance after 18 days of lactation. The reduction in nursing performance caused by arginine deficiency during gestation could be corrected by replenishing arginine after parturition. Mammary gland development, as indicated by nucleic acid content, was reduced by either reducing dietary arginine or food intake during lactation. All these results provided evidence that dietary arginine is required during gestation and lactation for optimal reproductive response and nursing performance in rats.arginine gestation lactation