Rat liver responsiveness to gluconeogenic substrates during insulin-induced hypoglycemia

Souza, Helenir Medri de; Borba-Murad, Glaucia Regina; Ceddia, Rolando B.; Curi, Rui; Vardanega-Peicher, M.; Bazotte, Roberto Barbosa

doi:10.1590/s0100-879x2001000600012

Cited by 29 publications

(26 citation statements)

References 30 publications

(31 reference statements)

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“…Alanine can additionally contribute to the supply of new carbon for gluconeogenesis. It appears that glutamine is a major gluconeogenic substrate predominantly in the kidney, whereas alanine dependent gluconeogenesis is essentially confined to the liver (de Souza et al, 2001). In support of this observation, Ikeda and Iwata (2003) confirmed gluconeogenesis from glutamine in the kidney had a significant role in whole body glucose homeostasis.…”

Section: Cell Metabolismmentioning

confidence: 68%

“…Intracellular glutamine concentration varies between 2 and 20 mM (depending on cell type) whereas its extracellular concentration averages 0.7 mM (Newsholme et al, 2003b). Glutamine plays an essential role, promoting and maintaining function of various organs and cells such as kidney (Conjard et al, 2002), intestine (Lima et al, 1992;Ramos Lima et al, 2002), liver (de Souza et al, 2001), heart (Khogali et al, 2002), neurons (Mates et al, 2002), lymphocytes , macrophages , neutrophils Pithon-Curi et al, 2002a, 2003bPithon-Curi et al, 2003), pancreatic b-cells (Skelly et al, 1998), and white adipocytes (Curi et al, 1987;Kowalchuk et al, 1988). At the most basic level, glutamine serves as important fuel in these cells and tissues.…”

mentioning

confidence: 99%

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Molecular mechanisms of glutamine action

Curi

Lagranha

Doi

et al. 2005

Journal Cellular Physiology

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411

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Glutamine is the most abundant free amino acid in the body and is known to play a regulatory role in several cell specific processes including metabolism (e.g., oxidative fuel, gluconeogenic precursor, and lipogenic precursor), cell integrity (apoptosis, cell proliferation), protein synthesis, and degradation, contractile protein mass, redox potential, respiratory burst, insulin resistance, insulin secretion, and extracellular matrix (ECM) synthesis. Glutamine has been shown to regulate the expression of many genes related to metabolism, signal transduction, cell defense and repair, and to activate intracellular signaling pathways. Thus, the function of glutamine goes beyond that of a simple metabolic fuel or protein precursor as previously assumed. In this review, we have attempted to identify some of the common mechanisms underlying the regulation of glutamine dependent cellular functions.

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Section: Cell Metabolismmentioning

confidence: 68%

mentioning

confidence: 99%

Molecular mechanisms of glutamine action

Curi

Lagranha

Doi

et al. 2005

Journal Cellular Physiology

Self Cite

411

300

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“…Thus, gluconeogenesis from glutamine may be a major consumer of glutamate-derived carbon in the liver, resulting in the formation and export of glucose (32).…”

Section: Glutamine/glutamate In the Livermentioning

confidence: 99%

“…The hepatocytes in this area are rich in glutamine synthetase (32). The substrate(s) for glutamine synthesis are of course glutamate and NH 4 + .…”

Section: Glutamine/glutamate In the Livermentioning

confidence: 99%

Glutamine and glutamate as vital metabolites

Newsholme

Lima

Procópio

et al. 2003

Braz J Med Biol Res

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307

225

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Glucose is widely accepted as the primary nutrient for the maintenance and promotion of cell function. This metabolite leads to production of ATP, NADPH and precursors for the synthesis of macromolecules such as nucleic acids and phospholipids. We propose that, in addition to glucose, the 5-carbon amino acids glutamine and glutamate should be considered to be equally important for maintenance and promotion of cell function. The functions of glutamine/glutamate are many, i.e., they are substrates for protein synthesis, anabolic precursors for muscle growth, they regulate acid-base balance in the kidney, they are substrates for ureagenesis in the liver and for hepatic and renal gluconeogenesis, they act as an oxidative fuel for the intestine and cells of the immune system, provide inter-organ nitrogen transport, and act as precursors of neurotransmitter synthesis, of nucleotide and nucleic acid synthesis and of glutathione production. Many of these functions are interrelated with glucose metabolism. The specialized aspects of glutamine/glutamate metabolism of different glutamineutilizing cells are discussed in the context of glucose requirements and cell function.

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“…Male Wistar fed rats (200-220 g), were anesthetized by an intraperitoneal injection of pentobarbital sodium (40 mg/kg). After laparotomy, livers were perfused in situ through the portal vein as previously described (Akimoto et al, 2000;Souza et al, 2001). After 10 min of perfusion isoproterenol, glucagon, cAMP or cAMP agonists were dissolved in the perfusion fluid and infused between 10 and 30 min of the perfusion period.…”

Section: Methodsmentioning

confidence: 99%

Comparative effect of glucagon and isoproterenol on hepatic glycogenolysis and glycolysis in isolated perfused liver

Vardanega-Peicher

Galletto

Silva

et al. 2003

Braz. arch. biol. technol.

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The effect of glucagon and isoproterenol (ß-adrenergic agonist) on hepatic glycogenolysis and glycolysis in isolated perfused liver was compared. The levels of isoproterenol and glucagon which promoted the maximal activation of glycogenolysis were 20 µM and 1nM respectively. However, glucagon (1 nM) not only increased glycogenolysis but also inhibited glycolysis. Because adenosine-3'-5'-cyclic monophosphate (cAMP) is a common second messenger to glucagon and isoproterenol, the level of cAMP that simulates the effect of these substances were investigated. The concentration of cAMP that inhibited glycolysis was five times higher (15 ìM) than that which stimulated glycogenolysis (3 ìM). Similar inhibition of glycolysis was obtained with cAMP agonists resistant to phosphodiesterases, i.e., 8-Br-cAMP and N 6 -monobutyryl-cAMP (6-MB-cAMP) at the concentration of 3 ìM. Thus, apparently glucagon could produce higher cellular levels of cAMP than that obtained with the activation of ß-adrenergic receptors. The higher amount of cAMP could be enough to overcome the action of phosphodiesterases and penetrate in the cytosol creating a favourable gradient to inhibit the enzymes of glycolysis.

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Rat liver responsiveness to gluconeogenic substrates during insulin-induced hypoglycemia

Cited by 29 publications

References 30 publications

Molecular mechanisms of glutamine action

Molecular mechanisms of glutamine action

Glutamine and glutamate as vital metabolites

Comparative effect of glucagon and isoproterenol on hepatic glycogenolysis and glycolysis in isolated perfused liver

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