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Doctoral Thesis
DOI
10.11606/T.42.2016.tde-06092016-092140
Document
Author
Full name
Aline David Silva
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2016
Supervisor
Committee
Machado, Ubiratan Fabres (President)
Caperuto, Luciana Chagas
Festuccia, William Tadeu Lara
Ribeiro, Eliane Beraldi
Zorn, Telma Maria Tenorio
Title in Portuguese
A esteato-hepatite não alcoólica acompanha-se de superexpressão de SLC2A2, PCK1 e G6PC o que aumenta o efluxo hepático de glicose.
Keywords in Portuguese
Diabetes mellitus
Fígado gorduroso
Glicose
Obesidade
Abstract in Portuguese
A esteato-hepatite não alcoólica (EHNA) apresenta maior efluxo hepático de glicose e hiperglicemia. Estudamos o papel da hiperglicemia e as alterações do metabolismo da glicose em fígado de camundongos obesos (MSG) com EHNA, tratados com dieta hiperlipídica (DH) ou florizina. No fígado dos MSG, independentemente da DH, observou-se: 1) diagnóstico de EHNA; 2) aumento dos mRNAs Tnfa, Il6 e Rela; 3) aumento dos mRNAs Slc2a2, Pck1, G6pc e suas proteínas GLUT2, PEPCK e G6Pase; 4) redução do mRNA Gck e sua proteína GCK; 5) aumento do glicogênio e efluxo de glicose; 6) resistência insulínica, hiperinsulinemia, hiperglicemia; e 7) aumento na atividade dos fatores transcricionais HNF4A, HNF3B, HNF1A e NFKB. A florizina: 1) normalizou a glicemia; 2) atenuou a EHNA; e 3) reverteu as alterações relacionadas ao metabolismo de carboidrato e do efluxo de glicose. A EHNA aumenta a expressão do GLUT2 e das enzimas gliconeogênicas, promovendo maior efluxo de glicose e hiperglicemia. Essas alterações revertem pela queda glicêmica, revelando a hiperglicemia como fator etiopatogênico.
Title in English
The nonalcoholic steatohepatitis is accompanied by Slc2a2, Pck1 and G6pc superexpression and increased glucose liver eflux.
Keywords in English
Diabetes mellitus
Fatty liver
Glucose
Obesity
Abstract in English
The non-alcoholic steatohepatitis (NASH) has higher hepatic glucose efflux and hyperglycemia. We studied the role of hyperglycemia and glucose metabolism in liver of obese mice (MSG) with NASH treated with high fat diet (HFD) or phlorizin. In the liver MSG independently of HFD, we observed: 1) diagnosis of NASH; 2) increased TNFa, IL6 and Rela mRNAs; 3) increased Slc2a2, pCK1, G6pc mRNAs and their GLUT2, PEPCK and G6Pase proteins; 4) reduction of GCK mRNA and its protein GCK; 5) increased glycogen and glucose efflux; 6) insulin resistance, hyperinsulinaemia, hyperglycaemia; and 7) increased activity of transcription factors HNF4A, HNF3B, HNF1A and NFKB. The phlorizin: 1) normalized blood glucose; 2) attenuated NASH; and 3) reversed the changes related to carbohydrate metabolism and glucose efflux. The NASH increases the expression of the GLUT2 and gluconeogenic enzymes, promoting higher glucose efflux and hyperglycemia. These changes are reversed by glycemic fall, revealing hyperglycemia as pathogenetic factor.
 
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Release Date
2018-09-06
Publishing Date
2016-09-06
 
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