RESUMO
NEW FINDINGS: What is the central question of this study? 3,5-Diiodothyronine (3,5-T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models, and ameliorates insulin resistance: what are its effects on cardiac electrical and contractile properties and autonomic regulation? What is the main finding and its importance? Chronic 3,5-T2 administration has no adverse effects on cardiac function. Remarkably, 3,5-T2 improves the autonomous control of the rat heart and protects against ischaemia-reperfusion injury. ABSTRACT: The use of 3,5,3'-triiodothyronine (T3) and thyroxine (T4) to treat metabolic diseases has been hindered by potential adverse effects on liver, lipid metabolism and cardiac electrical properties. It is recognized that 3,5-diiodothyronine (3,5-T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models and ameliorates insulin resistance, suggesting 3,5-T2 as a potential therapeutic tool. However, a comprehensive assessment of cardiac electrical and contractile properties has not been made so far. Three-month-old Wistar rats were daily administered vehicle, 3,5-T2 or 3,5-T2+T4 and no signs of atrial or ventricular arrhythmia were detected in non-anaesthetized rats during 90 days. Cardiac function was preserved as heart rate, left ventricle diameter and shortening fraction in 3,5-T2-treated rats compared to vehicle and 3,5-T2+T4 groups. Power spectral analysis indicated an amelioration of the heart rate variability only in 3,5-T2-treated rats. An increased baroreflex sensitivity at rest was observed in both 3,5-T2-treated groups. Finally, 3,5-T2 Langendorff-perfused hearts presented a significant recovery of left ventricular function and remarkably smaller infarction area after ischaemia-reperfusion injury. In conclusion, chronic 3,5-T2 administration ameliorates tonic cardiac autonomic control and confers cardioprotection against ischaemia-reperfusion injury in healthy male rats.
Assuntos
Traumatismo por Reperfusão Miocárdica , Animais , Di-Iodotironinas/farmacologia , Di-Iodotironinas/uso terapêutico , Coração , Masculino , Traumatismo por Reperfusão Miocárdica/metabolismo , Ratos , Ratos WistarRESUMO
NEW FINDINGS: What is the central question of this study? How does an acute session of exercise affect food intake of male Wistar rats? What is the main finding and its importance? Food intake in male Wistar rats is decreased in the first hour after physical exercise independent of the intensity. Moreover, high-intensity exercise potentiates the anorexic effect of peripheral glucose administration. This work raises new feeding-related targets that would explain how exercise drives body weight loss. ABSTRACT: Obesity has emerged as a critical metabolic disorder in modern society. An adequate lifestyle with a well-oriented programme of diet and physical exercise (PE) can prevent or potentially even cure obesity. Additionally, PE might lead to weight loss by increasing energy expenditure and decreasing hunger perception. In this article, we hypothesize that an acute exercise session would potentiate the glucose inhibitory effects on food intake in male Wistar rats. Our data show that moderate- or high-intensity PE significantly decreased food intake, although no changes in the expression of feeding-related neuropeptide in the arcuate nucleus of the hypothalamus were found. Exercised animals demonstrated a reduced glucose tolerance and increased blood insulin concentration. Intraperitoneal administration of glucose decreased food intake in control animals. In the animals submitted to moderate-intensity PE, the decrease in food intake promoted by glucose was similar to controls; however, an interaction was observed when glucose was injected in the high-intensity PE group, in which food intake was significantly lower than the effect produced by glucose alone. A different pattern of expression was observed for the monocarboxylate transporter isoforms (MCT1, 2 and 4) and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFBP3) in the hypothalamus, which was dependent on the exercise intensity. In conclusion, PE decreases food intake independently of the intensity. However, an interaction between PE and the anorexic effect of glucose is only observed when a high-intensity exercise is performed. These data show an essential role of exercise intensity in the modulation of the glucose inhibitory effect on food intake.
Assuntos
Ingestão de Alimentos/fisiologia , Glucose/farmacologia , Condicionamento Físico Animal/fisiologia , Animais , Núcleo Arqueado do Hipotálamo/metabolismo , Ingestão de Alimentos/efeitos dos fármacos , Ingestão de Energia/fisiologia , Metabolismo Energético/efeitos dos fármacos , Metabolismo Energético/fisiologia , Masculino , Transportadores de Ácidos Monocarboxílicos/metabolismo , Fosfofrutoquinase-2/metabolismo , Ratos , Ratos WistarRESUMO
Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiodinase (D1) activation on exercise-induced GH secretion. Ten days after bilateral ovariectomy, animals were submitted to 20 min of treadmill exercise at 75% of maximum aerobic capacity and tissues were harvested immediately or 30 min after exercise. Non-exercised animals were used as controls. A significant increase in D1 activity occurred immediately after exercise (~60%) in sham-operated animals and GH was higher (~6-fold) 30 min after exercise. Estrogen deficient rats exhibited basal levels of GH and D1 activity comparable to those found in control rats. However, after exercise both D1 activity and serum GH levels were blunted compared to sedentary rats. To understand the potential cause-effect of D1 activation in exercise-induced GH release, we pharmacologically blocked D1 activity by propylthiouracil (PTU) injection into intact rats and submitted them to the acute exercise session. D1 inhibition blocked exercise-induced GH secretion, although basal levels were unaltered. In conclusion, estrogen deficiency impairs the induction of thyroid hormone activating enzyme D1 in the pituitary, and GH release by acute exercise. Also, acute D1 activation is essential for exercise-induced GH response.