Efeito da hipertrigliceridemia, induzida pela superexpressão gênica da apo-CIII, sobre o metabolismo hepático da glicose em camundongos transgênicos submetidos ao exercício agudo /

• Ano de defesa: 2017
• Autor(a) principal: Mamus, Guilherme Brescancin
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Estadual de Maringá.; Departamento de Ciências Fisiológicas.; Programa de Pós-Graduação em Ciências Fisiológicas; Maringá, PR; Centro de Ciências Biológicas.
• Palavras-chave em Português: Apolipoproteína CIII; Metabolismo hepático - Camundongos; Gliconeogênese; Hipertrigliceridemia; Área de Concentração: Fisiologia Integrativa
• Link de acesso: http://repositorio.uem.br:8080/jspui/handle/1/4705

Dyslipidemias change the peripheral glucose uptake and lead to blood glucose dysregulation and the propensity to develop metabolic diseases in the population. However, these diseases express several systemic alterations which make it difficult to understand the isolated effect of each one, thus limiting the treatment. Experimental models where the gene expression of apolipoprotein CIII (apoCIII), a protein from the very low density lipoprotein, is altered, change the liver production of this protein and the peripheral uptake of triglycerides, leading to hypertriglyceridemia and allowing the study of its direct effect on glucose metabolism, without the interference of other factors such as insulin alterations. In addition, exercise influences triglycerides and glucose metabolism, and may protect the organism from the degenerative effects of dyslipidemias. Therefore, we verified the effect of hypertriglyceridemia induced by overexpression of the apoCIII gene and of an exercise session on the liver glucose production and on the liver and muscle stores of glycogen. With this purpose, C57BL6 non-transgenic (NTG ? triglyceridemia < 100mg/dL) and transgenic (CIII ? triglyceridemia > 200mg/dL) male mice had their liver glucose production assessed after overnight fasting using in situ liver perfusion. Muscle and liver glycogen content, plasma triglycerides, free fatty acids and cholesterol were assessed as well under this condition. It was noted that the regulatory mechanisms and the hepatic and muscular metabolism of glucose are altered by hypertriglyceridemia in the CIII group. Despite the plasma compounds being elevated in the CIII group, there was no difference in running time, body weight and pre- and post-exercise blood glucose between the groups, demonstrating a good capacity of group CIII of regulating blood glucose homeostasis when subjected to metabolic challenges such as fasting and exercise. However, the regulatory mechanisms and the liver and muscle glucose metabolism were altered by hypertriglyceridemia, because in the absence of exercise there was a decrease of liver gluconeogenesis and increase in muscle glycogen content in group CIII. On the other hand, with exercise group CIII did not change liver gluconeogenesis, but muscle glycogen content was reduced. In this way, it is possible that the increased triglyceridemia per se, in the absence of other metabolic factors, may be one of the triggering agents of the metabolic syndrome, and liver and muscle can be the first organs to exhibit it