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Sweet changes: glucose homeostasis can be altered by manipulating genes controlling hepatic glucose metabolism.
Collier, James J; Scott, Donald K.
Afiliación
  • Collier JJ; Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, 1901 Perdido Street, New Orleans, Louisiana 70112, USA.
Mol Endocrinol ; 18(5): 1051-63, 2004 May.
Article en En | MEDLINE | ID: mdl-14694084
The liver is responsible for glucose synthesis in the fasting state, and glucose uptake, storage, and utilization in the fed state. A phenotypic switch, normally initiated by insulin or glucagon, controls the transition between the two states, which includes transcriptional alterations that regulate metabolic enzyme abundance for multiple metabolic pathways in a coordinated manner. A network of transcription factors, coactivators, and corepressors direct these changes, thus acting as transcriptional sensors of the nutritional status of an organism. The inability of the hepatocyte to undergo this metabolic reprogramming is characteristic of diabetes mellitus. Modulations that control the amount of individual metabolic enzymes or transcription factors can initiate the fasting-to-fed transition of the hepatocyte in an insulin-independent manner. Alternatively, overexpression of key regulators of metabolism can lock hepatocytes in the fasted state. These manipulations alter hepatic glucose flux, leading to either amelioration or induction of diabetes mellitus. These maneuvers reveal the complexity of the coordinated mechanisms used by the liver to alter its phenotype and provide evidence for the control strength of metabolic signaling.
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Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Diabetes Mellitus / Glucosa / Homeostasis / Insulina / Hígado Límite: Animals / Humans Idioma: En Revista: Mol Endocrinol Asunto de la revista: BIOLOGIA MOLECULAR / ENDOCRINOLOGIA Año: 2004 Tipo del documento: Article País de afiliación: Estados Unidos
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Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Diabetes Mellitus / Glucosa / Homeostasis / Insulina / Hígado Límite: Animals / Humans Idioma: En Revista: Mol Endocrinol Asunto de la revista: BIOLOGIA MOLECULAR / ENDOCRINOLOGIA Año: 2004 Tipo del documento: Article País de afiliación: Estados Unidos