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Made available in DSpace on 2021-06-25T10:36:25Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-02-01 Background: Exercise is commonly recommended to control hyperglycemia, including during pregnancy. We conducted this study to understand the potential benefits and risks of exercise during pregnancy of women with diabetes. Specifically, we evaluated the effects of swimming on a diabetic rat during pregnancy and assayed maternal-fetal parameters. Methods: Diabetes was induced in the female newborn from Wistar rats by the streptozotocin administration on first postnatal day. At 110 days of life, after confirm mild symptoms of diabetes, the rats were mated and randomly distributed into four experimental groups (minimum of 13 animals/group): Control (C)—nondiabetic animals without swimming; Control and Exercise (CEx)—nondiabetic animals submitted to swimming; Mild Diabetic (MD)—diabetic animals without swimming; Mild Diabetic and Exercise (MDEx)—diabetic animals submitted to swimming. The swimming program was performed from day 7 to 21 of pregnancy. Maternal parameters were evaluated during the pregnancy period. On day 21 of pregnancy, the rats were sacrificed and maternal and fetal parameters analyzed. Results: There are no alterations in body weight, food consumption, water intake, and reproductive outcomes among the groups. The swimming program did not normalize maternal glycemia and other biochemical biomarkers. The diabetes and exercise combination increased organ weight. The fetuses born to these exercising diabetic rats had reduced fetal weight and increased skeletal anomalies (mainly incomplete ossification of sternebra). Conclusion: The intense swimming exercise imposed on female rats during pregnancy impaired maternal metabolic repercussions, contributing to intrauterine growth restriction and fetal skeletal anomalies. Laboratory of General Physiology and Reproductive Toxicology Institute of Biological and Health Sciences University Center of Araguaia Federal University of Mato Grosso (UFMT) Laboratory of Experimental Research on Gynecology and Obstetrics Postgraduate Course on Tocogynecology Botucatu Medical School Univ Estadual Paulista_Unesp Laboratory of Experimental Research on Gynecology and Obstetrics Postgraduate Course on Tocogynecology Botucatu Medical School Univ Estadual Paulista_Unesp

Calcitonin Gene-Related Peptide (CGRP) is a potent vasodilator peptide widely distributed in the central nervous system and various peripheral tissues, including cardiac muscle. However, its role in heart protein metabolism remains unknown. We examined the acute effects of CGRP on autophagy and the related signaling pathways in the heart mice and cultured neonatal cardiomyocytes. CGRP (100 μg kg-1; s.c.) or 0.9% saline was injected in awake male C57B16 mice, and the metabolic profile was determined up to 60 min. In fed mice, CGRP drastically increased glycemia and reduced insulinemia, an effect that was accompanied by reduced cardiac phosphorylation levels of Akt at Ser473 without affecting FoxO. Despite these catabolic effects, CGRP acutely inhibited autophagy as estimated by the decrease in LC3II:LC3I and autophagic flux. In addition, the fasting-induced autophagic flux in mice hearts was entirely abrogated by one single injection of CGRP. In parallel, CGRP stimulated PKA/CREB and mTORC1 signaling and increased the phosphorylation of Unc51-like kinase-1 (ULK1), an essential protein in autophagy initiation. Similar effects were observed in cardiomyocytes, in which CGRP also inhibited autophagic flux and stimulated Akt and FoxO phosphorylation. These findings suggest that CGRP in vivo acutely suppresses autophagy in the heart of fed and fasted mice, most likely through the activation of PKA/mTORC1 signaling but independent of Akt.

Made available in DSpace on 2020-12-10T20:01:26Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-01-01 Fundacao de Amparo a Pesquisa do Estado de Mato Grosso (FAPEMAT), Cuiaba, Brazil (2014-2016) Background: Limited studies have been canied out with prednisone (PRED) in treatment by glucose intolerant individuals, even in this model the animals presented low blood glucose levels at adulthood, by the high regenerative capacity of beta-cell. Objective: The aim was to evaluate the effects of the treatment of PRED in mild diabetes on biochemical and immunological biomarkers. Methods: Rats were randomly divided into four groups: control (C), treated control C+PRED (treatment of 1.25 mg/Kg/day PRED); diabetic DM (mild diabetes) and treated diabetic DM PRED (treatment with same dose as C+PRED group). Untreated groups received vehicle, adjusted volume to body weight. The treatment lasted 21 days and measured body weight, food and water intake, and glycemia weekly. In the 3rd week, the Oral Glucose Tolerance Test (OGTT) and the Insulin Tolerance Test (ITT) was performed. On the last day, the rats were killed and the blood was collected for biochemical analyzes, leukogram and imm.unoglobulin G levels. Results: There was a significant decrease in body weight in mild diabetes; however, the treatment in diabetic groups increased food intake, glycemia, and the number of total leukocytes, lymphocytes and neutrophils. On the other hand, it decreased the levels of triglycerides, high -density and very low density lipoproteins. In addition, diabetic groups showed glucose intolerance and mild insulin resistance, confirming that this model induces glucose intolerant in adult life. Conclusion: The results showed that the use of prednisone is not recommended for glucose intolerant individuals and should he replaced in order to not to aggravate this condition. Sao Paulo State Univ UNESP, Inst Biosci, Postgrad Program Pharmacol & Biotechnol, Botucatu, SP, Brazil Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Physiol, Sao Paulo, Brazil Fed Univ Mato Grosso UFMT, Inst Biol Sci & Hlth, Lab Syst Physiol & Reprod Toxicol, Barra Do Garcas, Mato Grosso, Brazil Sao Paulo State Univ UNESP, Inst Biosci, Postgrad Program Pharmacol & Biotechnol, Botucatu, SP, Brazil Fundacao de Amparo a Pesquisa do Estado de Mato Grosso (FAPEMAT), Cuiaba, Brazil (2014-2016): 002 - 004/2015 Fundacao de Amparo a Pesquisa do Estado de Mato Grosso (FAPEMAT), Cuiaba, Brazil (2014-2016): 36016.541.21414.17082016

Objective Although it is well established that a-calcitonin gene-related peptide (CGRP) stabilizes muscle-type cholinergic receptors nicotinic subunits (AChR), the underlying mechanism by which this neuropeptide regulates muscle protein metabolism and neuromuscular junction (NMJ) morphology is unclear. Methods To elucidate the mechanisms how CGRP controls NMJ stability in denervated mice skeletal muscles, we carried out physiological, pharmacological, and molecular analyses of atrophic muscles induced by sciatic nerve transection. Results Here, we report that CGRP treatment in vivo abrogated the deleterious effects on NMJ upon denervation (DEN), an effect that was associated with suppression of skeletal muscle proteolysis, but not stimulation of protein synthesis. CGRP also blocked the DEN-induced increase in endocytic AChR vesicles and the elevation of autophagosomes per NMJ area. The treatment of denervated animals with rapamycin blocked the stimulatory effects of CGRP on mTORC1 and its inhibitory actions on autophagic flux and NMJ degeneration. Furthermore, CGRP inhibited the DEN-induced hyperactivation of Ca2+-dependent proteolysis, a degradative system that has been shown to destabilize NMJ. Consistently, calpain was found to be activated by cholinergic stimulation in myotubes leading to the dispersal of AChR clusters, an effect that was abolished by CGRP. Conclusion Taken together, these data suggest that the inhibitory effect of CGRP on autophagy and calpain may represent an important mechanism for the preservation of synapse morphology when degradative machinery is exacerbated upon denervation conditions., Highlights • CGRP exerts antiproteolytic effects in atrophic denervated muscles and maintains the stability of NMJ. • CGRP blocks the endocytosis of AChRs and decreases the colocalization of autophagosome to NMJ in denervated muscles. • CGRP inhibits the Ca2+-dependent proteolysis, a degradative system that destabilizes NMJ during muscle atrophy. • The inhibition of autophagy and calpain induced by CGRP represents an important mechanism for the preservation of synapse.

Background Obesity is a pathophysiology that influences the metabolism, worsening the lipidic and glycemic profiles, and the population search for alternatives to decrease its side effects. Duguetia furfuracea has been used for obesity and also kidney disease treatment, however a very few studies have been conducted to verify its effectiveness and safety for using as well as to evaluate its influence on metabolic profile.

Background Obesity is a pathophysiology condition that influences the metabolic pathways, and the association with pregnancy can worsen the lipidic and glycemic profiles. Moreover, Duguetia furfuracea has been used for obesity and also kidney disease treatment, however a very few studies have been conducted to verify its effectiveness and safety for using as well as to evaluate its influence on metabolic profile.