Elaine de Oliveira

Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil

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Publications (30)100.41 Total impact

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    ABSTRACT: Early weaning (EW) is associated with an impairment of offspring development and leads to overweight and higher 25-hydroxyvitamin D (25(OH)D) levels in adulthood, which can be corrected by calcium supplementation, potentially via vitamin D regulation of adipogenesis. We examined vitamin D status in adipose tissue in EW obese rats, treated with calcium. Dams were separated into: EW- dams were wrapped with a bandage to interrupt lactation (last 3 days), and C- pups with free access to milk. At PN120, EW pups were divided in: EW- standard diet, and EWCa- calcium supplementation (10g of calcium carbonate/kg of chow). On PN21, EW group has hypocalcemia. On PN180, EW group showed lower intestinal calbidin, higher adiposity and 25(OH)D. In adipose tissue, Cyp27b1/1alpha-Hydroxylase, C/EBPB, PPARγ, IL6, TNF-A and MCP1 were increased, while VDR and IL10 were decreased. Calcium increased calbidin, VDR and prevented adipose tissue dysfunction. EW group has a long-term effect of vitamin D on adipocyte, contributing to pro-inflammatory status and obesity. Thus we propose that in obese rat adipocytes, 1,25(OH)2D down-regulates VDR, resulting in vitamin D resistance, characterized by higher Cyp27b1/1α-Hydroxylase and adipogenesis. Calcium therapy appears to be an outstanding strategy for weight loss and improving endocrine metabolic disorders that are obesity-associated. This article is protected by copyright. All rights reserved
    No preview · Article · Jan 2016 · Molecular Nutrition & Food Research
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    ABSTRACT: Astrocytes and microglia, the immune competent cells of CNS, can be activated in response to metabolic signals such as obesity and hyperleptinemia. In rats, maternal exposure to nicotine during lactation leads to central obesity, hyperleptinemia, leptin resistance, and alterations in hypothalamic neuropeptides in the offspring, during adulthood. Here, we studied the activation of astrocytes and microglia, as well as the pattern of inflammatory mediators in adult offspring of this experimental model. On the 2(nd) postnatal day (P2), osmotic minipumps releasing nicotine (NIC - 6mg/Kg/day) or saline for 14 days were subcutaneously implanted in dams. Male offspring were killed on P180 and hypothalamic immunohistochemistry, retroperitoneal white adipose tissue (WAT) PCR analysis and multiplex analysis for plasma inflammatory mediators were carried out. At P180, NIC astrocyte cell number was higher in the arcuate nucleus (ARC: medial: +82%; lateral: +110%), in the paraventricular nucleus (PVN: +144%) and in the lateral hypothalamus (LH: +121%). NIC glial fibrillary acidic protein fibre density (GFAP) was higher in the lateral ARC (+178%) and in the PVN (+183%). Interleukin-6 was not affected in the hypothalamus. NIC monocyte chemotactic protein 1 was only higher in the periventricular nucleus (+287%). NIC microglia (iba-1-positive) cell number was higher (+68%) only in the PVN, as was the chemokine (C-X3-C motif) receptor 1 (CX3CR1) density (+93%). NIC interleukin-10 was lower in the WAT (-58%) and plasma (-50%). Thus, offspring of mothers exposed to nicotine during lactation present hypothalamic astrogliosis at adulthood and microgliosis in the PVN. This article is protected by copyright. All rights reserved.
    No preview · Article · Oct 2015 · Journal of Neuroendocrinology
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    ABSTRACT: Flaxseed ( Linum usitatissimum L.) has been a focus of interest in the field of functional foods because of its potential health benefits. However, we hypothesised that maternal flaxseed intake during lactation could induce several metabolic dysfunctions in adult offspring. In the present study, we aimed to characterise the adrenal function of adult offspring whose dams were supplemented with whole flaxseed during lactation. At birth, lactating Wistar rats were divided into two groups: rats from dams fed the flaxseed diet (FLAX) with 25 % of flaxseed and controls dams. Pups received standard diet after weaning and male offspring were killed at age 180 days old to collect blood and tissues. We evaluated body weight and food intake during development, corticosteronaemia, adrenal catecholamine content, hepatic cholesterol, TAG and glycogen contents, and the protein expression of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), 11-β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and adrenaline β2 receptor at postnatal day 180 (PN180). After weaning, pups from the FLAX group had a higher body weight (+10 %) and food intake (+10 %). At PN180, the FLAX offspring exhibited higher serum corticosterone (+48 %) and lower adrenal catecholamine ( − 23 %) contents, lower glycogen ( − 30 %), higher cholesterol (4-fold increase) and TAG (3-fold-increase) contents in the liver, and higher 11β-HSD1 (+62 %) protein expression. Although the protein expression of hypothalamic CRH was unaffected, the FLAX offspring had lower protein expression of pituitary ACTH ( − 34 %). Therefore, induction of hypercorticosteronaemia by dietary flaxseed during lactation may be due to an increased hepatic activation of 11β-HSD1 and suppression of ACTH. The changes in the liver fat content of the FLAX group are suggestive of steatosis, in which hypercorticosteronaemia may play an important role. Thus, it is recommended that lactating women restrict the intake of flaxseed during lactation.
    No preview · Article · Sep 2015 · The British journal of nutrition
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    ABSTRACT: Early overnutrition (EO) during lactation leads to obesity, leptin resistance and lower thyroid hormones (TH) levels during adulthood. To better understand the biological significance of this thyroid hypofunction, we studied the long-term effects of postnatal EO on both the function of hypothalamic-pituitary-thyroid (HPT) axis and the metabolism and action of TH. To induce EO, the litter size was reduced to 3 pups per litter (SL group) on the third day of lactation. In the controls (NL group), litter size was adjusted to 10 pups per litter. Rats were killed at PN180. Thyrotropin release hormone (TRH) content and in vitro thyrotropin (TSH) were evaluated. Iodothyronine deiodinase (D1 and D2) activities were measured in different tissues. Mitochondrial alpha-glycerol-3-phosphate dehydrogenase (mGPD), uncoupling protein 1 (UCP1) and TH receptor (TRβ1) were evaluated to assess TH action. The SL group presented lower TRH, intrapituitary and released TSH levels, despite unchanged plasma TSH. They presented lower D1 activity in thyroid, muscle and white adipose tissue (WAT) and higher D2 activity in the hypothalamus, pituitary, brown adipose tissue (BAT) and WAT, which confirmed the hypothyroidism. UCP1 in BAT and TRβ1 in WAT were decreased, which can contribute to a lower catabolic status. Despite the lower TH, the D2 activity in thyroid, heart and testis was unchanged. Hepatic D1, mGPD and TRβ1 were also unchanged in SL rats suggesting that the TH conversion and action were preserved in liver, even with lower TH. Thus, this model indicates that postnatal EO changes thyroid function in adult life in a tissue-specific way, which can help in the understanding of obesogenesis.
    No preview · Article · Jul 2015 · Journal of Endocrinology
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    ABSTRACT: Postnatal nicotine exposure leads to obesity and hypothyroidism at adulthood. Then, we studied the effects of maternal nicotine exposure during lactation on thyroid hormone metabolism and function in adult offspring. Lactating rats were implanted with osmotic minipumps releasing nicotine (NIC, 6 mg/kg/day s.c.) or saline (control) from postnatal day 2 to 16. Offspring were killed at 180 days-old. We measured type 1 and 2 deiodinase activity and mRNA, mitochondrial α-glycerol-3-phosphate dehydrogenase (mGPD) activity, thyroid hormone receptor (TR) and uncoupling protein 1 (UCP1), hypothalamic TRH and pituitary TSH, and "in vitro" TRH-stimulated TSH secretion. Expression of deiodinase mRNAs followed the same profile of the enzymatic activity. NIC exposure caused lower 5'-D1 and mGPD activities, and TRβ1 content in liver as well as lower 5'-D1 activity in muscle, higher 5'-D2 activity in brown adipose tissue (BAT), heart and testis, which are in accordance with hypothyroidism. Although deiodinase activities were not changed in hypothalamus, pituitary and thyroid of NIC offspring, UCP1 was lower in BAT. Both TRH and TSH were lower in NIC offspring, which presented higher basal "in vitro" TSH secretion, which was not increased after TRH. Thus, the hypothyroidism in NIC offspring at adulthood was caused, in part, by TRH-TSH "in vivo" suppression and lower sensitivity to TRH. Despite the hypothyroid status of peripheral tissues, these animals seem to develop an adaptive mechanism to preserve T4 to T3 conversion at central level.
    Full-text · Article · Feb 2015 · Journal of Endocrinology
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    ABSTRACT: The suppression of prolactin production with bromocriptine (BRO) in the last 3 d of lactation reduces milk yield (early weaning) and increases the transfer of leptin through the milk, causing hyperleptinaemia in pups. In adulthood, several changes occur in the offspring as a result of metabolic programming, including overweight, higher visceral fat mass, hypothyroidism, hyperglycaemia, insulin resistance, hyperleptinaemia and central leptin resistance. In the present study, we investigated whether overweight rats programmed by early weaning with maternal BRO treatment have hypothalamic alterations in adulthood. We analysed the expression of neuropeptide Y (NPY), cocaine- and amphetamine-regulated transcript (CART), pro-opiomelanocortin (POMC) and α-melanocyte-stimulating hormone (α-MSH) by immunohistochemistry in the following hypothalamic nuclei: medial and lateral arcuate nucleus (ARC); paraventricular nucleus (PVN); lateral hypothalamus (LH). Additionally, we sought to determine whether these programmed rats exhibited hypothalamic inflammation as indicated by astrogliosis. NPY immunostaining showed a denser NPY-positive fibre network in the ARC and PVN (+82 % in both nuclei) of BRO offspring. Regarding the anorexigenic neuropeptides, no difference was found for CART, POMC and α-MSH. The number of astrocytes was higher in all the nuclei of BRO rats. The fibre density of glial fibrillary acidic protein was also increased in both medial and lateral ARC (6·06-fold increase and 9·13-fold increase, respectively), PVN (5·75-fold increase) and LH (2·68-fold increase) of BRO rats. We suggest that early weaning has a long-term effect on the expression of NPY as a consequence of developmental plasticity, and the presence of astrogliosis indicates hypothalamic inflammation that is closely related to overweight and hyperleptinaemia observed in our model.
    Full-text · Article · Jan 2015 · British Journal Of Nutrition
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    ABSTRACT: Gut peptides regulate appetite and adipogenesis. Early weaning (EW) leads to later development of obesity, which can be prevented by calcium supplementation. We evaluated gut peptides that may have a role in the establishment of this dysfunction. At birth, lactating Wistar rats were separated in: EW, lactating rats involved with a bandage interrupting the lactation during the last 4 days of standard lactation, and C (control), dams whose pups had free access to milk during throughout lactation. At 120 days-old, half of EW group received calcium supplementation (EWCa); EW and C received standard diet. At 21 days-old, EW presented higher GLP-1 in plasma and GLP1-R in adipose tissue and hypothalamus, but lower GLP-1 and GLP1-R in the gut. At 180 days-old, GLP-1 response to food intake was blunted in EW and restored by calcium. GLP-1 in the gut was lower in EW and its receptor was lower in adipose tissue, and GLP1-R was higher in the gut of EWCa. Thus, EW had short and long-term effects upon GLP-1 profile, which may have contributed to obesity development, hyperphagia and insulin resistance, due to its adipogenic and appetite control roles. Calcium supplementation was able to prevent most of the changes in GLP-1 caused by EW. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2015 · Molecular Nutrition & Food Research
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    ABSTRACT: Aims: We evaluated the effects of yerba mate treatment over 30 days on body weight, food intake, hypothalamic leptin action and inflammatory profile in adult rats that were weaned early. Main methods: To induce early weaning, the teats of lactating rats were blocked with a bandage to interrupt milk access for the last 3 days of lactation (EW group). Control offspring had free access to milk throughout lactation. On postnatal day (PN) 150, EW offspring were subdivided into: EW and M groups were treated with water and mate aqueous solution (1g/kg BW/day, gavage), respectively, for 30 days. Control offspring received water by gavage. On PN180, offspring were killed. Key findings: EW group presented hyperphagia; higher adiposity; higher NPY and TNF-α expression in the ARC nucleus; higher TNF-α and IL-1β levels in the adipose tissue; and lower IL-10 levels in the adipose tissue. These characteristics were normal in M group. As expected, the leptin injection in control offspring caused lower food intake. However, EW group exhibited no change in food intake after the leptin injection, indicating leptin resistance. In contrast, M group had a normal response to the leptin injection. Significance: Thirty days of mate treatment prevented the development of hyperphagia, overweight, visceral obesity and central leptin resistance. This beneficial effect on the satiety of M offspring most likely occurred after the improvement of inflammatory markers in the hypothalamus and adipocytes, which suggests that Ilex paraguariensis plays an important role in the management of obesity by acting on the inflammatory profile.
    Full-text · Article · Sep 2014 · Life Sciences
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    ABSTRACT: We have reported several changes in neonate or adult offspring after the maternal use of whole flaxseed or its components. However, it is unknown the use of higher oil intake in the neonatal period. Here we evaluated the effects of high maternal intake of flaxseed oil during lactation upon milk and body composition in male and female offspring. Lactating rats were divided into: control (C, n=10), 7% soybean oil; (2) hyper 19% soybean oil (HS, n=10); and (3) hyper 17% flaxseed oil + 2% soybean oil (HF, n=10). Dams and offspring were killed at weaning. HS and HF dams, male and female offspring presented lower body weight during lactation. HF mothers presented lower body and visceral fat masses. HF male offspring presented lower body and subcutaneous fat masses. HS and HF milk presented lower triglycerides (TG) and cholesterol. HF male and female offspring showed lower triglyceridemia and insulinemia, but no changes in glycemia and leptinemia. The higher intake of flaxseed oil during lactation reduced the body weight of mothers and offspring, decreases milk lipids and apparently increases insulin sensitivity in this critical period of life. Those changes may explain the previously reported programming effect of maternal flaxseed intake during lactation.
    Full-text · Article · Apr 2014 · Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association
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    ABSTRACT: Studies have demonstrated that early weaning can promote metabolic syndrome during adulthood and that obesity increases oxidative stress. Thus, we aimed to evaluate redox status in a pharmacological early weaning rodent model programmed for metabolic syndrome at adulthood. Lactating dams were randomly assigned into 2 groups: the early weaning group (BRO), which was treated intraperitoneally with bromocriptine (1mg/day) to inhibit prolactin secretion for the last 3days of lactation, and the control group (C), which received the BRO diluent for the same time period. The offspring were killed at 90 (PN90) and 180 (PN180) days after birth. Early weaning induced greater visceral adiposity and dyslipidemia. At PN90, the BRO offspring showed glucose intolerance with normoinsulinemia and increased plasma and liver superoxide dismutase, and liver glutathione peroxidase activities, which reduced the liver malondialdehyde but not the increased plasma malondialdehyde levels. However, the BRO offspring showed insulin resistance at PN180 and increased plasma glutathione peroxidase, liver superoxide dismutase, and catalase activities. These changes reduced the plasma and liver malondialdehyde levels, which aided in hepatocyte architecture preservation. Additionally, we observed that sirtuin 1 was overexpressed in the BRO group at PN90, but the increased expression was not maintained through PN180, which suggests unfavorable metabolic conditions in the older offspring. Significance Despite the observed obesity and glucose homeostasis dysfunction, our data suggest that the early weaning programming induced by bromocriptine can improve the offspring's redox status and may prevent liver damage during adulthood.
    Full-text · Article · Dec 2013 · Life sciences
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    ABSTRACT: The most frequently used animal models of early weaning (EW) in rodents, maternal deprivation and pharmacological inhibition of lactation, present confounding factors, such as high stress or drug side effects, that can mask or interact with the effects of milk deprivation per se. Given these limitations, the development of new models of EW may provide useful information regarding the impact of a shortened period of breastfeeding on the endocrine and nervous systems, both during development and at adulthood. Using a model of EW in which lactating Wistar rat dams are wrapped with a bandage to block access to milk during the last three days of lactation, we have recently shown that the adult offspring presented higher body mass, hyperphagia, hyperleptinemia, leptin as well as insulin resistance, and higher adrenal catecholamine contend at adulthood. Here, we used this EW model, which involves no pharmacological treatment or maternal separation, to analyze anxiety-like, novelty-seeking and memory/learning behavioral traits in the adult male offspring. To that end, animals were tested in the elevated plus maze, in the hole board arena and in the radial arm water maze. Except for an increased number of rearing events (a measure of vertical activity), no other behavioral differences were observed between EW and control animals. The contrasting behavioral results between the three EW models may be associated with differences in HPA axis function in the offspring at weaning, since it has been observed that bandaging does not affect corticosteronemia while maternal separation and pharmacological EW increases it.
    Full-text · Article · Nov 2013 · Physiology & Behavior
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    ABSTRACT: The inhibition of maternal prolactin production in late-lactation leads to metabolic syndrome and hypothyroidism in adult offspring. Physical training is a therapeutic strategy that could prevent or reverse this condition. We evaluated the effects of a short-duration low-intensity running wheel training program on the metabolic and hormonal alterations in rats. Lactating Wistar rats were treated with bromocriptine (Bro, 1 mg twice a day) or saline on days 19, 20 and 21 of lactation, and the training of offspring began at 35 days of age. Offspring were divided into: sedentary and trained controls (C-Sed, C-Ex) and sedentary and trained Bro-treated rats (Bro-Sed, Bro-Ex). Chronic exercise delayed the onset of weight gain in Bro-Ex offspring, and the food intake did not change during the experimental period. At 180 days, visceral fat mass was higher (+46%) in the Bro-Sed offspring than in C-Sed and Bro-Ex rats. As expected, running capacity was higher in trained animals. Most parameters observed in the Bro-Sed offspring were consistent with hypothyroidism and metabolic syndrome, and were reversed in Bro-Ex group. Chronic exercise did not influence the muscle glycogen in the C-Ex group; however, the liver glycogen was higher (+30%) in C-Ex group and was unchanged in both Bro offspring groups. Bro-Ex animals had higher plasma LDH (lactate dehydrogenase) levels, indicating skeletal muscle damage and intolerance of the training program. Low-intensity chronic training is able to normalize many clinical aspects in Bro animals; however, these animals might have had a lower threshold for exercise adaptation than the control rats.
    Full-text · Article · Jul 2013 · Journal of Endocrinology
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    ABSTRACT: Maternal exposure to nicotine during lactation causes hyperleptinemia in the pups and, at adulthood, these animals are overweight and hyperleptinemic, while, in their hypothalamus, the leptin signalling pathway is reduced, evidencing a central leptin resistance. Then, we evaluated the expression of pro-opiomelanocortin (POMC), alpha-melanocyte stimulating hormone (α-MSH), cocaine and amphetamine-regulated transcript (CART), neuropeptide Y (NPY), agouti-related peptide (AgRP) and others in different hypothalamic nuclei in order to better understand the mechanisms underlying the obese phenotype observed in these animals at adulthood. On the 2(nd) postnatal day (P2), dams were subcutaneously implanted with osmotic minipumps releasing nicotine (NIC-6mg/Kg/day) or saline for 14 days. Offspring were killed in P180 and immunohistochemistry and Western blot analysis were carried out. Significance data had P<0.05. Adult NIC offspring showed more intense NPY staining in the paraventricular nucleus (PVN) (+21%) and increased number of POMC-positive cells in the: arcuate nucleus (+33%), as an increase in fibre density of α-MSH in PVN (+85%). However, the number of CART-positive cells was reduced in the PVN (-25%). CRH staining was more intense in NIC offspring (+136%). Orexins and AgRP were not altered. Thus, maternal nicotine exposure changes hypothalamic neuropeptides in the adult progeny that is partially compatible with leptin resistance.
    Full-text · Article · Apr 2013 · Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association
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    ABSTRACT: Children from pregnant smokers show more susceptibility to develop obesity in adult life. Previously, we failed to demonstrate in rats offspring a programming for obesity when only the mothers were tobacco smoke-exposed during lactation. Here, we studied the short- and long-term effects of smoke exposure to both dams and their pups during lactation upon endocrine and metabolic parameters. For this, we designed an experimental model where nursing rats and their pups were divided into: SE group, smoke-exposed in a cigarette smoking machine (4 times/day, from the 3rd to the 21th day of lactation) and C group, exposed to filtered air. Pups were killed at 21 and 180 days old. At weaning, SE pups showed lower body weight (7%), length (5%), retroperitoneal fat mass (59%), visceral adipocyte area (60%) and higher subcutaneous adipocyte area (95%) with hypoinsulinemia (-29%), hyperthyroxinemia (59%), hypercorticosteronemia (60%) and higher adrenal catecholamine content (+58%). In adulthood, SE offspring showed higher food intake (+10%), body total fat mass (+50%), visceral fat mass (retroperitoneal: 55%; mesenteric: 67%; epididymal: 55%), and lower subcutaneous adipocyte area (24%) with higher serum glucose (11%), leptin (85%), adiponectin (1.4 fold-increase), TT3 (71%), FT4 (57%), TSH (36%), triglycerides (65%), VLDL-c (+66%), HDL-c (91%) levels, lower corticosteronemia (41%) and adrenal cathecolamine content (57%). Our present findings suggest that tobacco smoke exposure to both dams and their pups during lactation causes a malnutrition in early life that programs for obesity and hormonal and metabolic disturbances in adulthood, only if the pups are submitted to the same smoke environment than the mother.
    Full-text · Article · Apr 2013 · Journal of Endocrinology
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    ABSTRACT: Effects of maternal malnutrition during lactation on the kidneys in mice infected with Schistosoma mansoni. Kidneys from programmed infected mice and their respective controls fed a normal diet (23% protein), a protein-restricted group (PR) (8% protein) and a caloric-restricted group (CR) (according to the PR group intake) evaluated by biometry, morphometry and histopathology. Both PR and CR groups showed a reduction in the number of glomeruli when compared with the control group (CR:-29% vs C; PR:-41% vs C; p < 0.05) as well as infected mice (ICR:-32% vs IC; IPR:-47% vs IC; p < 0.05). Among infected mice, ICR group showed higher kidney weights (+18% vs IC and +12% vs IPR; p < 0.01). The ICR and IPR groups showed largest perimeter and area when compared to the corresponding uninfected group (ICR vs CR:+26%; IPR vs PR:+21%, p < 0.05) and area (ICR vs CR:+95%; IPR vs PR:+50%, p < 0.05). The ICR group showed an increase of within Bowman (CR vs ICR + 56%, p < 0.05), whereas Bowman's space was reduced (PR vs IPR, -61%; p < 0.05). Conclude that malnutrition during lactation programmed the metabolic state of the host, resulting in the evolution of the histology of the renal parenchyma.
    Full-text · Article · Apr 2013 · Experimental Parasitology
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    ABSTRACT: Purpose: We showed that early weaned rats developed obesity, hyperleptinemia, leptin and insulin resistance at adulthood. Here, we studied the potential beneficial effects of Ilex paraguariensis aqueous solution upon body composition, glycemia, lipid and hormonal profiles, leptin signaling and NPY content. Methods: To induce early weaning, lactating rats' teats were blocked with a bandage to interrupt lactation during the last 3 days (EW group), while control offspring had free access to milk throughout lactation (C group). In postnatal day (PN) 150, EW offspring were subdivided into: EW and EW+ mate groups treated, respectively, with water or yerba mate aqueous solution (1 g/kg BW/day, gavage) during 30 days. C offspring received water for gavage. In PN180, offspring were killed. Results: EW+ mate group presented lower body weight (-10 %), adipose mass (retroperitoneal:-40 % and epididymal:-44 %), total body fat (-43 %), subcutaneous fat (-46 %), visceral adipocyte area (-21 %), triglyceridemia (-31 %) and hypothalamic NPY content (-37 %) compared to EW group. However, hyperglycemia and lower HDL-c levels observed in EW group were not reverted with mate treatment. Although the hyperleptinemia, lower hypothalamic JAK2 and pSTAT3 content of EW group were not corrected by mate treatment, the hyperphagia and higher hypothalamic SOCS-3 content were normalized in EW+ mate group, indicating that the central leptin resistance could be restored. Conclusion: Thus, the therapy with yerba mate solution was capable to reverse abdominal obesity, leptin resistance and hypertriglyceridemia, suggesting an important role of this bioactive component in the management of obesity in this programming model.
    Full-text · Article · Feb 2013 · European Journal of Nutrition
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    ABSTRACT: Objective Obesity and osteoporosis seems to have a common pathogenesis, especially because bone and adipose tissue have common origins. Since early weaning (EW) decreases adipogenesis and osteogenesis in neonate, further programming for obesity and hyperleptinemia, we hypothesized that these changes in adipogenesis could affect bone metabolism. Materials/Methods Lactating rats were separated into 3 groups: control - dams whose pups ate milk throughout lactation; mechanical EW (MEW) - dams were involved with a bandage interrupting suckling in the last 3 days of lactation; pharmacological EW (PEW) - dams were bromocriptine-treated (0.5 mg/twice a day via intraperitoneal injection) 3 days before weaning. The adult offspring was subjected to dual-energy X-ray absorptiometry and bone tissue was also evaluated by computed tomography, microcomputed tomography and biomechanical tests, beyond serum analyses. Results MEW and PEW presented total bone mineral density (BMD), total bone mineral content, spine BMD and bone area in postnatal day 150 (PN150). In PN180, both groups also presented increase of these parameters and higher femur BMD and fourth lumbar vertebra (LV4) BMD, femoral head radiodensity and LV4 vertebral body radiodensity, trabecular number, stiffness and break load; lower trabecular separation, maximal deformation and break deformation, and also hyperleptinemia and higher visceral fat mass and 25-hydroxivitamin D, whereas parathyroid hormone was unchanged. Serum C-terminal cross-linked telopeptide of type I collagen was lower for both groups. Conclusions Since both models program for obesity and increased bone mass, and leptin increases plasma vitamin D levels, probably leptin is the link between obesity and higher bone mass.
    Full-text · Article · Jan 2013 · Metabolism: clinical and experimental
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    ABSTRACT: Obesity is a global epidemic, and maternal smoking has been shown to be associated with the development of childhood obesity. Overall, approximately 40% of children worldwide are exposed to tobacco smoke at home. It is well known that environmental changes within a critical window of development, such as gestation or lactation, can initiate permanent alterations in metabolism that lead to diseases in adulthood, a phenomenon called programming. It is known that programming is based on epigenetic alterations (changes in DNA methylation, histone acetylation, or small interfering RNA expression) that change the expression pattern of several genes. However, little is known concerning the mechanisms by which smoke exposure in neonatal life programs the adipose tissue and endocrine function. Here, we review several epidemiological and experimental studies that confirm the association between maternal nicotine or tobacco exposure during gestation or lactation and the development of obesity and endocrine dysfunction. For example, a positive correlation was demonstrated in rodents between increased serum leptin in the neonatal period and exposure of the mothers to nicotine during lactation, and the further development of leptin and insulin resistance, and thyroid and adrenal dysfunction, in adulthood in the same offspring. Thus, a smoke-free environment during the lactation period is essential to improving health outcomes in adulthood and reducing the risk for future diseases. An understanding of the pathophysiological mechanisms underlying the effects of smoking on programming can provide new insights into therapeutic strategies for obesity.
    Full-text · Article · Nov 2012 · Frontiers in Physiology
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    ABSTRACT: The interruption of lactation for a short period, without the use of pharmacological substances or maternal separation, causes offspring malnutrition and hypoleptinaemia and programmes for metabolic disorders such as higher body weight and adiposity, hyperphagia, hyperleptinaemia and central leptin resistance in adulthood. Here, in order to clarify the mechanisms underlying the phenotype observed in adult early-weaned (EW) rats, we studied the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) in different hypothalamic nuclei by immunohistochemistry and Western blot. In the EW group, the teats of lactating rats were blocked with a bandage to interrupt lactation during the last 3 d, while control pups had free access to milk throughout the entire lactation period. At age 180 d, EW offspring showed higher NPY staining in the paraventricular nucleus (PVN), as well as NPY protein content (+68 %) in total hypothalamus than control ones. AgRP showed no changes in staining or Western blot. POMC content was not affected; however, its distribution pattern was altered. CART-positive cells of EW offspring had lower immunoreactivity associated with reduced cell number in the PVN and lower protein content ( - 38 %) in total hypothalamus. The present data indicate that precocious weaning can imprint the neuronal circuitry, especially in the PVN, and cause a long-term effect on the expression of specific orexigenic and anorexigenic neuropeptides, such as NPY and CART, that can be caused by leptin resistance and are coherent with the hyperphagia observed in these animals.
    Full-text · Article · Jul 2012 · The British journal of nutrition
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    ABSTRACT: The effects of maternal moderate-low physical training on postnatal development, glucose homeostasis and leptin concentration in adult offspring subjected to a low-protein diet during the perinatal period were investigated. Male Wistar rats (aged 150 d old) were divided into four groups according to maternal group: untrained (NTp, n 8); trained (Tp, n 8); untrained with a low-protein diet (NT+LPp, n 8); trained with a low-protein diet (T+LPp, n 8). The trained mothers were subjected to a protocol of moderate physical training over a period of 4 weeks (treadmill, 5 d/week, 60 min/d, at 65 % VO2max) before mating. At pregnancy, the intensity and duration of exercise was progressively reduced (50-20 min/d, at 65-30 % VO2max). The low-protein diet groups received an 8 % casein diet, and their peers received a 17 % casein diet during gestation and lactation. The pups' birth weight and somatic growth were recorded weekly up to the 150th day. Fasting blood glucose, cholesterol, serum leptin concentration, glucose and insulin tolerance tests were evaluated. The Tp animals showed no changes in somatic and biochemical parameters, while the NT+LPp group showed a greater abdominal circumference, hyperglycaemia, hypercholesterolaemia, glucose intolerance and lower plasma leptin. In the T+LPp animals, all of those alterations were reversed except for plasma leptin concentration. In conclusion, the effects of a perinatal low-protein diet on growth and development, glucose homeostasis and serum leptin concentration in the offspring were attenuated in pups from trained mothers.
    Full-text · Article · May 2012 · The British journal of nutrition