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Menopause induces osteoporosis, sarcopenia, insulin resistance, and dyslipidemia. Ovariectomized (OVX) rat is an animal model, which mimetics postmenopausal conditions. The present study aimed to test the effects of strength training protocol on bone mineral density and metabolic parameters in OVX rats. Female Wistar rats were randomly separated in four groups: non-ovariectomized rats (Sham); ovariectomized rats (OVX); OVX treated with 17β-estradiol (HR); and OVX trained group (TR). At 70-days-old OVX groups were submitted to a bilateral ovariectomy. Hormonal replacement and strength training were performed three times per week, for 60 days. 17β-estradiol was administered by intramuscular injection (50 μg/kg of BW) and strength training protocol was composed by four series of 12 repetitions with 65-75% of 1RM. As expected, OVX impaired glucose homeostasis, promoted weight and adiposity gain, dyslipidemia, sarcopenia and osteoporosis, but hormonal replacement and strength training improved most of these parameters. Both HR and TR normalize glucose homeostasis; however, only TR restores blood insulin. OXV also reduced the maximum force in 42%, but TR improved this parameter in 110%, in addition TR prevents sarcopenia and fat mass gain. Interestingly, strength training was able to improve significantly BMD. Taken together, these data suggest that strength training can be effective in the treatment of damage caused by OVX, which in a translational context, becomes an effective non-pharmacological strategy to improve the health of postmenopausal women, reducing costs with secondary symptoms, mainly caused by weight gain, sarcopenia and osteoporosis., (Copyright © 2018 Elsevier Inc. All rights reserved.)

During the early post-natal period, offspring are vulnerable to environmental insults, such as nutritional and hormonal changes, which increase risk to develop metabolic diseases later in life. Our aim was to understand whether maternal obesity during lactation programs offspring to metabolic syndrome and obese phenotype, in addition we aimed to assess the peripheral glucose metabolism and hypothalamic leptin/insulin signaling pathways. At delivery, female Wistar rats were randomly divided in two groups: Control group (CO), mothers fed a standard rodent chow (Nuvilab); and Diet-induced obesity group (DIO), mothers who had free access to a diet performed with 33% ground standard rodent chow, 33% sweetened condensed milk (Nestlé), 7% sucrose and 27% water. Maternal treatment was performed throughout suckling period. All offspring received standard rodent chow from weaning until 91-day-old. DIO dams presented increased total body fat and insulin resistance. Consequently, the breast milk from obese dams had altered composition. At 91-day-old, DIO offspring had overweight, hyperphagia and higher adiposity. Furthermore, DIO animals had hyperinsulinemia and insulin resistance, they also showed pancreatic islet hypertrophy and increased pancreatic β-cell proliferation. Finally, DIO offspring showed low ObRb, JAK2, STAT-3, IRβ, PI3K and Akt levels, suggesting leptin and insulin hypothalamic resistance, associated with increased of hypothalamic NPY level and decreased of POMC. Maternal obesity during lactation malprograms rat offspring to develop obesity that is associated with impairment of melanocortin system. Indeed, rat offspring displayed glucose dyshomeostasis and both peripheral and central insulin resistance., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Gluconeogenesis overstimulation due to hepatic insulin resistance is the best-known mechanism behind elevated glycemia in obese subjects with hepatic steatosis. This suggests that glucose production in fatty livers may differ from that of healthy livers, also in response to other gluconeogenic determinant factors, such as the type of substrate and modulators. Thus, the aim of this study was to investigate the effects of these factors on hepatic gluconeogenesis in cafeteria diet-induced obese adult rats submitted to a cafeteria diet at a young age. The livers of the cafeteria group exhibited higher gluconeogenesis rates when glycerol was the substrate, but lower rates were found when lactate and pyruvate were the substrates. Stearate or glucagon caused higher stimulations in gluconeogenesis in cafeteria group livers, irrespective of the gluconeogenic substrates. An increased mitochondrial NADH/NAD⁺ ratio and a reduced rate of 14 CO₂ production from [ 14 C] fatty acids suggested restriction of the citric acid cycle. The higher glycogen and lipid levels were possibly the cause for the reduced cellular and vascular spaces found in cafeteria group livers, likely contributing to oxygen consumption restriction. In conclusion, specific substrates and gluconeogenic modulators contribute to a higher stimulation of gluconeogenesis in livers from the cafeteria group.

The aim of this study was to verify the maximum number of repetitions, fatigue index, blood lactate concentration ([Lac]), and cardiac autonomic responses after LED irradiation (LEDI) in the ipsilateral and contralateral limb. Twelve male subjects (22.0 ± 3.86 years; weight 82.94 ± 12.58 kg; height 1.77 ± 0.05 m), physically active, took part in this study. The subjects underwent a one repetition maximum (1RM) test and performed four randomly experimental sessions in the horizontal leg press exercise, which consisted in four sets of maximum repetitions at 80% of 1RM. The subjects performed two experimental sessions applying LED active or placebo on ipsilateral limb and two experimental sessions applying LED active or placebo on contralateral limb prior exercise and in the interval of sets on quadriceps and hamstrings muscles. A number of repetitions and fatigue index were verified. [Lac] and heart rate variability (HRV) were collected during post-exercise recovery and analyzed. It was observed that active LEDI promoted an increase in maximal number of repetitions (LEDI = 44.4 ± 9.0 vs placebo = 39.9 ± 11.4; p < 0.05) and decreases the fatigue index (LEDI = 34.3 ± 21.8% vs placebo = 50.0 ± 26.6%; p < 0.05) comparing to placebo situation, only in the ipsilateral application. There were no differences on [Lac] and in HRV parameters comparing LEDI vs placebo on post-exercise recovery in both applications (p > 0.05). The LEDI improves performance only in the ipsilateral application, but there were no differences on [Lac] and cardiac autonomic responses after exercise for both the applications.

Background: Trypanosoma cruzi causes neuronal myenteric depopulation compromising intestinal function., Aim: The purpose of this study was to evaluate the influence of moderate physical exercise on NADH diaphorase (NADH-d)-positive neurons in the myenteric plexus and intestinal wall of the colon in mice infected with T. cruzi., Materials and Methods: Forty 30-day-old male Swiss mice were divided into the following groups: trained infected (TI), sedentary infected (SI), trained control (TC), and sedentary control. The TC and TI groups were subjected to a moderate physical exercise program on a treadmill for 8 weeks. Three days after finishing physical exercise, the TI and SI groups were intraperitoneally inoculated with 1,300 blood trypomastigotes of the Y strain of Trypanosoma cruzi. Parasitemia was evaluated from days 4 to 61 after inoculation. On day 75 of infection, myenteric neurons in the colon were quantified (NADH-d), and inflammatory foci were counted. Tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β) levels were evaluated in plasma. The results were compared using analysis of variance and the Kruskal-Wallis test at a 5 % significance level., Results: Moderate physical exercise reduced the parasite peak on day 8 of infection (p = 0.0132) and total parasitemia (p = 0.0307). It also prevented neuronal depopulation (p < 0.01), caused hypertrophy of these cells (p < 0.05), prevented the formation of inflammatory foci (p < 0.01), and increased the synthesis of TNF-α (p < 0.01) and TGF-β (p > 0.05)., Conclusion: These results reinforce the therapeutic benefits of moderate physical exercise for T. cruzi infection.

Creatine is widely used by athletes as an ergogenic resource. The aim of this study was to evaluate the influence of creatine supplementation on the duodenum of rats submitted to physical training. The number and myenteric neuronal cell bodies as well mucosal and muscular tunic morphometry were evaluated. Control animals received a standard chow for 8 weeks, and the treated ones received the standard chow for 4 weeks and were later fed with the same chow but added with 2% creatine. Animals were divided in groups: sedentary, sedentary supplemented with creatine, trained and trained supplemented with creatine. The training consisted in treadmill running for 8 weeks. Duodenal samples were either processed for whole mount preparations or for paraffin embedding and hematoxylin-eosin staining for histological and morphometric studies of the mucosa, the muscular tunic and myenteric neurons. It was observed that neither creatine nor physical training alone promoted alterations in muscular tunic thickness, villus height or crypts depth, however, a reduction in these parameters was observed when both were associated. The number of myenteric neurons was unchanged, but the neuronal cell body area was reduced in trained animals but not when training and creatine was associated, suggesting a neuroprotector role of this substance.

Objective: The effects of a cafeteria diet on the small intestine were investigated in adult Wistar rats under sedentary conditions and after physical training., Methods: Parameters including morphometry, enzyme activities, and total myenteric populations in the jejunum were evaluated., Results: The cafeteria diet, characterized as hyperlipidic, produced obese rats, corroborated by increases in the Lee index and the weights of the periepididymal and retroperitoneal adipose tissues (P<0.01). Obesity caused increases in the length of the small intestine, villi height, crypt depth, whole-wall thickness (P<0.05), and the enzymatic activities of alkaline phosphatase, lipase, and sucrase (P<0.01), in addition to a reduction in the number of goblet cells (P<0.05). With reference to the jejunal intrinsic innervations, the total number and area of myenteric neurons was unchanged regardless of the group. Physical training promoted 1) a reduction of the weight in the retroperitoneal and periepididymal adipose tissues (P<0.05) and 2) an increase in the thickness of the muscular layer (P<0.05)., Conclusion: The cafeteria diet promoted obesity in rodents, leading to alterations in morphometry and enzymatic intestinal parameters, which were partily attenuated by physical training., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)