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- ItemSomente MetadadadosAvaliação reprodutiva tardia da prole exposta à nicotina durante as fases de prenhez e lactação(Universidade Federal de São Paulo (UNIFESP), 2014-07-30) Silva, Mayra Miranda Rodrigues da [UNIFESP]; Valdeolivas, Sandra Maria Miraglia Valdeolivas [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Introduction: About 1/3 of the population smokes. The nicotine found in cigarettes, reaches breast milk and crosses the placental membrane. Previously, it was observed that nicotine administered to female rats during pregnancy and lactation, causes morphofunctional alterations Leydig cells and overt damage of the seminiferous epithelium of the offspring. Objective: To evaluate the spermatogenic damage, previously observed in offspring at 90 days of age, from pregnant rats and exposed infants to nicotine, are held or aggravated after up to two full terms of spermatogenesis (53 + 53 days). Methods: Rats were exposed to nicotine (2 mg / kg / day) throughout pregnancy and lactation, using a subcutaneous osmotic minipump implantation (C) performed in each of these periods. Control groups "sham" (CS, with subcutaneously implanted minipumps, but containing 0.9% saline) and absolute (CA without implants) were established. The offspring were euthanized at 90, 143 and 196 days postpartum (subgroups). Testicular parameters, reviews and sperm and testosterone plasma levels and cholesterol intratesticular were investigated. Results: The progenies showed significant changes of biometric parameters, morphometric and stereological testicular, in all subgroups. Histopathology showed in rats of all subgroups nicotine, normal characteristics of the seminiferous epithelium, except for the more exacerbated peeling germ cells into the lumen, observed in these animals. Quantitative evaluation and sperm plasma levels and cholesterol and testosterone intratesticular no significant changes. However, the offspring of the subgroups nicotine exhibited high frequency of morphologically abnormal sperm and reduced sperm motility of these gametes. A significant loss of mitochondrial activity and an increase in sperm DNA fragmentation (comet assay) were observed in these animals. Conclusions: The results indicate reproductive harm late in the offspring, concerning the quality of the epididymal sperm tail, due to exposure of rats to nicotine in pregnancy and lactation.
- ItemSomente MetadadadosEthanol intake during lactation impairs milk production in rats and affects growth and metabolism of suckling pups(Elsevier B.V., 1999-05-01) Do Carmo, MGT; Do Nascimento, CMO; Martin, A.; Herrera, E.; Universidade Federal do Rio de Janeiro (UFRJ); Universidade Federal de São Paulo (UNIFESP); Hosp Ramon y Cajal; Univ San PabloFrom 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. (C) 1999 Elsevier Science Inc. All rights reserved.
- ItemAcesso aberto (Open Access)Influência da ingestão de sardinha nos níveis de ácidos graxos poliinsaturados da série ômega3 no leite materno(Sociedade Brasileira de Pediatria, 2006-02-01) Patin, Rose Vega [UNIFESP]; Vítolo, Márcia R. [UNIFESP]; Valverde, Mara A. [UNIFESP]; Carvalho, Patrícia O.; Pastore, Gláucia M.; Lopez, Fábio Ancona [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Estadual de Campinas (UNICAMP); Universidade Estadual Paulista (UNESP)OBJECTIVES: The purpose of this study was to investigate what effect the intake of sardines, rich in omega-3 series polyunsaturated fatty acids, has on the composition of breastmilk. METHODS: This was a prospective study of 31 nursing mothers under observation at the Hospital Guilherme Álvaro. Each was given 2 kg of fresh sardines twice with a 15-day interval. Milk was sampled and a 24-hour dietary recall questionnaire was applied on days 0, 15 and 30. Milk was assayed for fatty acid content by gas chromatography. Statistical analysis of the results was performed using nonparametric tests with significance set at p < 0.05. RESULTS: The results demonstrate that the nutritional intake of the nursing mothers was adequate at all three sample points. With regard to the omega-3 series fatty acid content of the breastmilk, it was observed that regular consumption and shorter intervals between intake and milk collection resulted in higher concentrations of docosapentaenoic acid and docosahexaenoic acid at 15 and 30 days into the study. Fatty acids from the omega-3 and omega-6 series exhibited a significant correlation, r² was 0.58 and 0.59 at 15 and 30 days, respectively. CONCLUSION: These results suggest that incorporating fish into the diets of nursing mother during lactation, in the form of 100 g of sardines two or three times a week, contributes to an increase in omega-3 series fatty acids.
- ItemAcesso aberto (Open Access)Maternal high-fat diet during pregnancy or lactation changes the somatic and neurological development of the offspring(Academia Brasileira de Neurologia - ABNEURO, 2014-02-01) Mendes-da-Silva, Cristiano [UNIFESP]; Giriko, Catherine Ássuka; Mennitti, Laís Vales; Hosoume, Lilian Fazion; Souto, Tayane dos Santos; Silva, Alexandre Valotta da [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Hospital Israelita Albert Einstein Instituto do CérebroThe maternal exposure to high fat diet (HFD) during pregnancy and breastfeeding have been considered an important inducer of alterations in offspring normal programming, both in animals and humans, and may disturb brain development. In the present study we investigated the somatic and sensory-motor development of the offspring from rat dams fed a HFD, compared with dams fed a control diet, during pregnancy or lactation. Indicators of the body growth, physical maturation, and reflex ontogeny were evaluated. Offspring of dams fed a HFD showed reduced weight and body growth, delayed physical maturation, and delayed maturation of the physiological reflexes, such as vibrissa placing, auditory startle response, and free-fall righting. Our findings suggest that maternal HFD during pregnancy or lactation modifies somatic and neurological development of the offspring, possibly increasing the risk of neuroendocrine and neuropsychiatric disorders later in life.
- ItemSomente MetadadadosMKP-1 mediates glucocorticoid-induced ERK1/2 dephosphorylation and reduction in pancreatic beta-cell proliferation in islets from early lactating mothers(Amer Physiological Soc, 2010-12-01) Nicoletti-Carvalho, Jose E.; Lellis-Santos, Camilo; Yamanaka, Tatiana S.; Nogueira, Tatiane C.; Caperuto, Luciana C. [UNIFESP]; Leite, Adriana R.; Anhe, Gabriel F.; Bordin, Silvana; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Universidade Estadual de Campinas (UNICAMP)Maternal pancreatic islets undergo a robust increase of mass and proliferation during pregnancy, which allows a compensation of gestational insulin resistance. Studies have described that this adaptation switches to a low proliferative status after the delivery. the mechanisms underlying this reversal are unknown, but the action of glucocorticoids (GCs) is believed to play an important role because GCs counteract the pregnancy-like effects of PRL on isolated pancreatic islets maintained in cell culture. Here, we demonstrate that ERK1/2 phosphorylation (phospho-ERK1/2) is increased in maternal rat islets isolated on the 19th day of pregnancy. Phospho-ERK1/2 status on the 3rd day after delivery (L3) rapidly turns to values lower than that found in virgin control rats (CTL). MKP-1, a protein phosphatase able to dephosphorylate ERK1/2, is increased in islets from L3 rats. Chromatin immunoprecipitation assay revealed that binding of glucocorticoid receptor (GR) to MKP-1 promoter is also increased in islets from L3 rats. in addition, dexamethasone (DEX) reduced phospho-ERK1/2 and increased MKP-1 expression in RINm5F and MIN-6 cells. Inhibition of transduction with cycloheximide and inhibition of phosphatases with orthovanadate efficiently blocked DEX-induced downregulation of phospho-ERK1/2. in addition, specific knockdown of MKP-1 with siRNA suppressed the downregulation of phosphoERK1/2 and the reduction of proliferation induced by DEX. Altogether, our results indicate that downregulation of phospho-ERK1/2 is associated with reduction in proliferation found in islets of early lactating mothers. This mechanism is probably mediated by GC-induced MKP-1 expression.
- ItemSomente MetadadadosSerum leptin and insulin levels in lactating protein-restricted rats: implications for energy balance(Cambridge Univ Press, 2007-01-01) Ferreira, C. L. P.; Macedo, G. M.; Latorraca, M. Q.; Arantes, V. C.; Veloso, R. V.; Carneiro, E. M.; Boschero, A. C.; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Gaiva, M. H.; Univ Fed Mato Grosso; Universidade Estadual de Campinas (UNICAMP); Universidade Federal de São Paulo (UNIFESP)The present study analysed the effect of protein restriction on serum insulin and leptin levels and their relationship with energy balance during lactation. Four groups of rats received isocaloric diets containing 170 g protein/kg or 60 g protein/kg from pregnancy until the 14th day of lactation: control non-lactating, control lactating (both fed a control diet), low-protein non-lactating and low-protein lactating. Energy intake, body composition, energy balance. serum insulin and leptin concentrations and the relationship between these hormones and several factors related to obesity were analysed. Low-protein-intake lactating rats exhibited hypoinsulinaemia, hyperleptinaemia, hypophagia and decreased energy expenditure compared with control lactating rats. the protein level in the carcasses was lower in the low-protein lactating group than in the control lactating group, resulting in a higher fat content in the first group compared with the latter. Body fat correlated inversely with serum insulin and positively with serum leptin level. There was a significant negative correlation between serum leptin and energy intake, and a positive relationship between energy intake and serum insulin level in lactating rats and in the combined data from both groups. Energy expenditure was correlated positively with serum insulin and negatively with serum leptin in lactating rats and when data from control non-lactating and lactating rats were pooled. Lactating rats submitted to protein restriction, compared with lactating control rats, showed that maternal reserves were preserved owing to less severe negative energy balance. This metabolic adaptation was obtained, at least in part, by the hypoinsulinaemia that resulted in increased insulin sensitivity favouring enhanced fat deposition, hyperleptinaemia and hypophagia.
- ItemSomente MetadadadosUPR induces transient burst of apoptosis in islets of early lactating rats through reduced AKT phosphorylation via ATF4/CHOP stimulation of TRB3 expression(Amer Physiological Soc, 2011-01-01) Bromati, Carla R.; Lellis-Santos, Camilo; Yamanaka, Tatiana S.; Nogueira, Tatiane C. A.; Leonelli, Mauro; Caperuto, Luciana C. [UNIFESP]; Gorjao, Renata; Leite, Adriana R.; Anhe, Gabriel F.; Bordin, Silvana; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Cruzeiro do Sul Univ; Universidade Estadual de Campinas (UNICAMP)Bromati CR, Lellis-Santos C, Yamanaka TS, Nogueira TC, Leonelli M, Caperuto LC, Gorjao R, Leite AR, Anhe GF, Bordin S. UPR induces transient burst of apoptosis in islets of early lactating rats through reduced AKT phosphorylation via ATF4/CHOP stimulation of TRB3 expression. Am J Physiol Regul Integr Comp Physiol 300: R92-R100, 2011. First published November 10, 2010; doi:10.1152/ajpregu.00169.2010.-Endocrine pancreas from pregnant rats undergoes several adaptations that comprise increase in beta-cell number, mass and insulin secretion, and reduction of apoptosis. Lactogens are the main hormones that account for these changes. Maternal pancreas, however, returns to a nonpregnant state just after the delivery. the precise mechanism by which this reversal occurs is not settled but, in spite of high lactogen levels, a transient increase in apoptosis was already reported as early as the 3rd day of lactation (L3). Our results revealed that maternal islets displayed a transient increase in DNA fragmentation at L3, in parallel with decreased RAC-alpha serine/threonine-protein kinase (AKT) phosphorylation (pAKT), a known prosurvival kinase. Wortmannin completely abolished the prosurvival action of prolactin (PRL) in cultured islets. Decreased pAKT in L3-islets correlated with increased Tribble 3 (TRB3) expression, a pseudokinase inhibitor of AKT. PERK and eIF2 alpha phosphorylation transiently increased in islets from rats at the first day after delivery, followed by an increase in immunoglobulin heavy chain-binding protein (BiP), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP) in islets from L3 rats. Chromatin immunoprecipitation (ChIP) and Re-ChIP experiments further confirmed increased binding of the heterodimer ATF4/CHOP to the TRB3 promoter in L3 islets. Treatment with PBA, a chemical chaperone that inhibits UPR, restored pAKT levels and inhibited the increase in apoptosis found in L3. Moreover, PBA reduced CHOP and TRB3 levels in beta-cell from L3 rats. Altogether, our study collects compelling evidence that UPR underlies the physiological and transient increase in beta-cell apoptosis after delivery. the UPR is likely to counteract prosurvival actions of PRL by reducing pAKT through ATF4/CHOP-induced TRB3 expression.