O treinamento físico na prevenção de danos renais causados pela dieta hiperlipídica e o papel do estresse de retículo endoplasmático
Data
2022-09-29
Autores
Pereira, Renata Oliveira 
Orientadores
Farah, Vera de Moura Azevedo
Tipo
Tese de doutorado
Título da Revista
ISSN da Revista
Título de Volume
Resumo
Objetivos: Avaliar o potencial do treinamento físico aeróbio (TFA) moderado na prevenção de alterações morfofisiológicas renais em ratos Wistar submetidos à dieta hiperlipídica desde o desmame, e investigar o envolvimento da via da resposta à proteína não dobrada (UPR) mediada pela PERK. Métodos: Ratos Wistar machos recém-desmamados foram separados em 4 grupos: Normolipídico Sedentário (NS), Normolipídico Treinado (NT), Hiperlipídico Sedentário (HS) e Hiperlipídico Treinado (HT). A dieta hiperlipídica foi administrada a partir do desmame durante 12 semanas. O TFA foi realizado em esteira rolante, 5x por semana, nas últimas 8 semanas de protocolo. Foram avaliados parâmetros corporais, bioquímicos, metabólicos e realizadas análises histológicas dos tecidos renal e adiposo, estimativa do número de adipócitos, marcadores de estresse oxidativo e expressão de proteínas da via da PERK de estresse de retículo endoplasmático renais. Resultados: Os animais treinados atingiram tempos máximos significativamente maiores no último teste de esforço. O grupo HS apresentou intolerância a glicose, aumento do peso dos tecidos adiposos, aumento da deposição lipídica renal, aumento da deposição de fibras de colágeno e fibronectina nos rins e o TFA preveniu completamente tais alterações. O grupo HS também apresentou aumento dos triglicérides, retração glomerular, aumento significativo da área e do diâmetro dos adipócitos e o treinamento preveniu parcialmente tais alterações. O TFA não foi capaz de prevenir a redução da taxa de filtração glomerular, diminuição do HDL e da uréia, aumento do VLDL e redução no peso dos rins. A dieta não alterou os marcadores de estresse oxidativo, mas o TFA promoveu redução dos níveis de TBARS e aumento na atividade da SOD nos rins. Não houve diferença no peso corporal, níveis de glicemia basal, colesterol total, proteínas totais, número de adipócitos e na expressão das proteínas envolvidas na via da PERK. Conclusão: O consumo de dieta hiperlipídica desde o desmame é capaz de provocar importantes danos morfológicos e funcionais aos rins de ratos Wistar adultos. O TFA atenuou ou preveniu a maior parte dos prejuízos morfofisiológicos, mas não foi capaz de evitar todos. Os dados sugerem que a via da PERK da UPR não está envolvida nas alterações renais provocadas pela dieta hiperlipídica, neste modelo.
Objectives: To investigate the potential of moderate aerobic exercise training (AET) in the prevention of renal morphophysiological alterations in adult Wistar rats, submitted to the consumption of a high-fat diet since weaning, and to investigate the involvement of the PERK-mediated unfolded protein response (UPR) pathway. Methods: Post-weaned male Wistar rats were divided into four groups: Sedentary Normolipidic (NS), Trained Normolipidic (NT), Sedentary High-fat (HS) and Trained High-fat (HT). The high-fat diet was provided since post-weaning during 12 weeks. AET was performed on a treadmill, 5 times a week. Evaluations: Biochemical, metabolic and body parameters, histological analysis of renal and adipose tissues, estimation of adipocytes number, oxidative stress markers and expression of proteins from the PERK pathway. Results: NT and HT groups reached significantly higher maximum time in the last maximum effort test. HS group presented glucose intolerance, increased adipose tissue weight, increased renal lipid deposition, increased collagen and fibronectin fiber deposition in the kidneys, and AET completely prevented such changes. HS group also showed an increase in triglycerides, glomerular retraction, a significant increase in the area and diameter of adipocytes, and AET partially prevented such changes. AET was not able to prevent a reduction in glomerular filtration rate, a decrease in HDL and urea, an increase in VLDL and a reduction in kidney weight. The diet did not change oxidative stress markers, but AET promoted a reduction in TBARS levels and an increase in SOD activity in the kidneys. There was no difference in body weight, basal blood glucose levels, total cholesterol, total proteins, number of adipocytes and in the expression of proteins involved in the PERK pathway. Conclusion: The consumption of a high-fat diet since weaning causes significant morphological and functional damage to the kidneys of adult Wistar rats. AET attenuated or prevented most of the morphophysiological damage, but it was not able to avoid all of them. The data suggest that the PERK pathway of the UPR is not involved in the renal changes caused by the high-fat diet in this model.
Objectives: To investigate the potential of moderate aerobic exercise training (AET) in the prevention of renal morphophysiological alterations in adult Wistar rats, submitted to the consumption of a high-fat diet since weaning, and to investigate the involvement of the PERK-mediated unfolded protein response (UPR) pathway. Methods: Post-weaned male Wistar rats were divided into four groups: Sedentary Normolipidic (NS), Trained Normolipidic (NT), Sedentary High-fat (HS) and Trained High-fat (HT). The high-fat diet was provided since post-weaning during 12 weeks. AET was performed on a treadmill, 5 times a week. Evaluations: Biochemical, metabolic and body parameters, histological analysis of renal and adipose tissues, estimation of adipocytes number, oxidative stress markers and expression of proteins from the PERK pathway. Results: NT and HT groups reached significantly higher maximum time in the last maximum effort test. HS group presented glucose intolerance, increased adipose tissue weight, increased renal lipid deposition, increased collagen and fibronectin fiber deposition in the kidneys, and AET completely prevented such changes. HS group also showed an increase in triglycerides, glomerular retraction, a significant increase in the area and diameter of adipocytes, and AET partially prevented such changes. AET was not able to prevent a reduction in glomerular filtration rate, a decrease in HDL and urea, an increase in VLDL and a reduction in kidney weight. The diet did not change oxidative stress markers, but AET promoted a reduction in TBARS levels and an increase in SOD activity in the kidneys. There was no difference in body weight, basal blood glucose levels, total cholesterol, total proteins, number of adipocytes and in the expression of proteins involved in the PERK pathway. Conclusion: The consumption of a high-fat diet since weaning causes significant morphological and functional damage to the kidneys of adult Wistar rats. AET attenuated or prevented most of the morphophysiological damage, but it was not able to avoid all of them. The data suggest that the PERK pathway of the UPR is not involved in the renal changes caused by the high-fat diet in this model.