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Cytosolic phosphoenolpyruvate carboxykinase as a cataplerotic pathway in the small intestine.
Potts, Austin; Uchida, Aki; Deja, Stanislaw; Berglund, Eric D; Kucejova, Blanka; Duarte, Joao A; Fu, Xiaorong; Browning, Jeffrey D; Magnuson, Mark A; Burgess, Shawn C.
Afiliação
  • Potts A; Advanced Imaging Research Center, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Uchida A; Advanced Imaging Research Center, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Deja S; Center for Human Nutrition, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Berglund ED; Advanced Imaging Research Center, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Kucejova B; Center for Human Nutrition, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Duarte JA; Advanced Imaging Research Center, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Fu X; Center for Human Nutrition, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Browning JD; Department of Clinical Nutrition, The University of Texas Southwestern Medical Center , Dallas, Texas.
  • Magnuson MA; Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine , Nashville, Tennessee.
  • Burgess SC; Advanced Imaging Research Center, The University of Texas Southwestern Medical Center , Dallas, Texas.
Am J Physiol Gastrointest Liver Physiol ; 315(2): G249-G258, 2018 08 01.
Article em En | MEDLINE | ID: mdl-29631378
ABSTRACT
Cytosolic phosphoenolpyruvate carboxykinase (PEPCK) is a gluconeogenic enzyme that is highly expressed in the liver and kidney but is also expressed at lower levels in a variety of other tissues where it may play adjunct roles in fatty acid esterification, amino acid metabolism, and/or TCA cycle function. PEPCK is expressed in the enterocytes of the small intestine, but it is unclear whether it supports a gluconeogenic rate sufficient to affect glucose homeostasis. To examine potential roles of intestinal PEPCK, we generated an intestinal PEPCK knockout mouse. Deletion of intestinal PEPCK ablated ex vivo gluconeogenesis but did not significantly affect glycemia in chow, high-fat diet, or streptozotocin-treated mice. In contrast, postprandial triglyceride secretion from the intestine was attenuated in vivo, consistent with a role in fatty acid esterification. Intestinal amino acid profiles and 13C tracer appearance into these pools were significantly altered, indicating abnormal amino acid trafficking through the enterocyte. The data suggest that the predominant role of PEPCK in the small intestine of mice is not gluconeogenesis but rather to support nutrient processing, particularly with regard to lipids and amino acids. NEW & NOTEWORTHY The small intestine expresses gluconeogenic enzymes for unknown reasons. In addition to glucose synthesis, the nascent steps of this pathway can be used to support amino acid and lipid metabolisms. When phosphoenolpyruvate carboxykinase, an essential gluconeogenic enzyme, is knocked out of the small intestine of mice, glycemia is unaffected, but mice inefficiently absorb dietary lipid, have abnormal amino acid profiles, and inefficiently catabolize glutamine. Therefore, the initial steps of intestinal gluconeogenesis are used for processing dietary triglycerides and metabolizing amino acids but are not essential for maintaining blood glucose levels.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Glicemia / Fosfoenolpiruvato Carboxiquinase (ATP) / Aminoácidos / Gluconeogênese / Glucose / Intestino Delgado Limite: Animals Idioma: En Revista: Am J Physiol Gastrointest Liver Physiol Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Glicemia / Fosfoenolpiruvato Carboxiquinase (ATP) / Aminoácidos / Gluconeogênese / Glucose / Intestino Delgado Limite: Animals Idioma: En Revista: Am J Physiol Gastrointest Liver Physiol Ano de publicação: 2018 Tipo de documento: Article