Adolescência como janela de programação metabólica : efeito de curto e longo prazo da desnutrição em ambos os sexos

• Ano de defesa: 2024
• Autor(a) principal: Saint Paul, Joskame
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Mato Grosso; Brasil; Instituto de Ciências da Saúde (ICS) - Sinop; UFMT CUS - Sinop; Programa de Pós-Graduação em Ciências em Saúde
• Palavras-chave em Português: Desnutrição; Programação metabólica; Estado redox; CNPQ::CIENCIAS DA SAUDE::MEDICINA; Malnutrition; Metabolic programming; Redox state
• Link de acesso: http://ri.ufmt.br/handle/1/6415

Malnutrition is still a serious problem in the world, which has not only social but also health implications. Among the consequences associated to hunger immunological vulnerability are one that triggers many parasitic and infectious diseases, in addition there are the effects associated with the programming of energy metabolism, especially when physiological insult occurs in critical stages of life development, which promotes the onset of many chronic noncommunicable diseases throughout. Herein we aimed to assess the short- and long-term effects of caloric malnutrition during adolescence in male and female rats on metabolic parameters, body composition, glucose homeostasis and redox status. At 30 and 120 days of age, Wistar rats underwent food restriction (RA50 group) until 60 days-old by reducing food supply in 50% of the daily offered to control group (CONT) that eat ad libitum. Body weight, food and water intake were measured every two days. Even at 60 and 120 days-old, rats were submitted to intraperitoneally the glucose tolerance test (ipGTT), insulin (ipITT). After euthanasia the liver and brown adipose tissue (interscapular area) were dissected to assess oxidative stress (catalase, CAT; superoxide dismutase, SOD; glutathione S-transferase, GST; reduced glutathione, GSH; lipid peroxidation, TBARS; vitamin C and carbonyl) as well as white adipose tissue (retroperitoenal, mesenteric and perigonadal fat) and skeletal muscle soleus and extensor digitorum longus (EDL) to assess body composition. All the procedures were approved by the ethics committee for animal studies. There was 36% reduction in body weight gain in RA50- M, 45% reduction in body weight, 30% reduction in food intake versus CONT-M and 22% reduction in body weight gain, 22% reduction in food intake, in RA50-F versus CONT-F during treatment (P<0.001). At the end of the malnutrition there was 45% reduction in body weight in the RA50-M group versus CONT-M and 28% reduction in body weight in RA50-F versus CONT-F (P<0.001). During the post-nutrition period, there was 15% reduction in weight, an increase in food intake of 27% in the RA50-M versus CONT-M (P<0.001) and 33% in the RA50-F rats versus CONT-F (P<0.001). During ipGTT, the RA50-M rats showed glycemia reduced by 22% versus CONT-M (P<0.05), 23% in the RA50-F females versus CONT-F (P<0.05) and increased Kitt by 316% in the RA50-M males versus CONT-M (P<0.05), as well as 29% increase in the adiposity index and 19% decrease in lean mass index in RA50-M versus CONT-M males (P<0.05) and 37% increase in adiposity index in RA50-F versus CONT-F rats (P<0.01). The liver of the RA50-M rats increased by 10% compared to the liver of the CONTM rats (P<0.05) and by 13% in the liver of the RA50-F rats compared to the CONT-F group (P<0.05). In the RA50-M rats, there was a reduction in SOD (41%; P<0.001), CAT (31%; P<0.01), GST (27%; P<0.01) and GSH (28%; P<0.01). In terms of biochemical dosages, there was a 22.51% increase in total cholesterol in the RA50-F versus CONT-F rats (P<0.01), a 48.31% increase in LDL cholesterol in the RA50-M versus CONT-M males (P<0.001) and a 26.73% increase in the RA50-F versus CONT-F rats (P<0.01). There was a 36.12% reduction in HDL cholesterol in the RA50-M group versus CONT-M (P<0.05) and an 84.17% reduction in the RA50-F females versus CONT-F (P<0.01). Adult rats that suffered malnutrition during adolescence have greater visceral adiposity associated with lower redox protection, peripheral insulin hypersensitivity and greater risk factors for cardiovascular disease.