Distribution along the rat nephron of three enzymes of gluconeogenesis in acidosis and starvation

Burch, Helen B.; Narins, Robert G.; Chu, Carmen; Fagioli, Sabrina; Choi, Sang-Bang; McCarthy, W.; Lowry, Oliver H.

doi:10.1152/ajprenal.1978.235.3.f246

Cited by 77 publications

(70 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Moreover, renal cells which have appreciable glucose phosphorylating capacity and thus the ability to accumulate glycogen have relatively little glucose 6-phosphatase activity, whereas cells having little phosphorylating capacity possess abundant activity of glucose 6-phosphatase and other gluconeogenic enzymes [28,34]. It is thus likely that release of glucose by the normal kidney is due mainly if not exclusively to gluconeogenesis.…”

Section: Methodological Considerationsmentioning

confidence: 99%

Renal glucose production and utilization: new aspects in humans

et al. 1997

View full text Add to dashboard Cite

Summary According to current textbook wisdom the liver is the exclusive site of glucose production in humans in the postabsorptive state. Although many animal and in vitro data have documented that the kidney is capable of gluconeogenesis, production of glucose by the human kidney in the postabsorptive state has generally been regarded as negligible. This traditional view is based on net balance measurements which, other than after a prolonged fast or during metabolic acidosis, showed no significant net renal glucose release. However, recent studies have refuted this view by combining isotopic and balance techniques, which have demonstrated that renal glucose production accounts for 25 % of systemic glucose production. Moreover, these studies indicate that glucose production by the human kidney is stimulated by epinephrine, inhibited by insulin and is excessive in diabetes mellitus. Since renal glucose release is largely, if not exclusively, due to gluconeogenesis, it is likely that the kidney is as important a gluconeogenic organ as the liver. The most important renal gluconeogenic precursors appear to be lactate, glutamine and glycerol. The implications of these recent findings on the understanding of the physiology and pathophysiology of human glucose metabolism are discussed. [Diabetologia (1997) 40: 749-757].

show abstract

Section: Methodological Considerationsmentioning

confidence: 99%

Renal glucose production and utilization: new aspects in humans

et al. 1997

View full text Add to dashboard Cite

show abstract

“…Several key enzymes and proteins involved in ammoniagenesis and gluconeogenesis are specifically induced in the proximal tubule cells during acidosis (3,30). This includes the activities of PAG, GDH, and phosphoenolpyruvate carboxykinase (4,31).…”

Section: Sn1 Is Induced In Cortical Tubule Cells During Chronic Metabmentioning

confidence: 99%

Induction and Targeting of the Glutamine Transporter SN1 to the Basolateral Membranes of Cortical Kidney Tubule Cells during Chronic Metabolic Acidosis Suggest a Role in pH Regulation

Solbu

Boulland

Zahid

et al. 2005

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

“…These changes in tubule function are associated with changes in the activities of a number of proteins, including the apical membrane Na ϩ /H ϩ antiporter (7), glutaminase and glutamate dehydrogenase (8), and phosphoenolpyruvate carboxykinase (9), which may affect intracellular substrate availability for protein turnover, amino acid metabolism and/or transport, and gluconeogenesis. It has been shown that in tubule epithelial cells, the associated increase in ammonia production, rather than the acidosis per se, is responsible for favoring tubular hypertrophy (10 -12).…”

mentioning

confidence: 99%

Kidney Protein Dynamics and Ammoniagenesis in Humans with Chronic Metabolic Acidosis

Garibotto

Asioli²,

Robaudo³

et al. 2004

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abstract. To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ( 14 C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesis, so net protein leucine balance was markedly negative. In acidemic subjects, kidney protein degradation was no different from protein synthesis and was significantly lower (P Ͻ 0.05) than in controls. Kidney leucine oxidation was similar in both groups. Urinary ammonia excretion and total ammonia production were 186% and 110% higher, respectively, and more of the ammonia that was produced was shifted into urine (82% versus 65% in acidemic subjects versus controls). In all studies, protein degradation and net protein balance across the kidney were inversely related to urinary ammonia excretion and to the partition of ammonia into urine, but not to total ammonia production, arterial pH, , urinary flow, the uptake of glutamine by the kidney, or the ammonia released into the renal veins. The data show that response of the human kidney to metabolic acidosis includes both changes in amino acid uptake and suppression of protein degradation. The latter effect, which is likely induced by the increase in ammonia excretion and partition into the urine, is potentially responsible for kidney hypertrophy.Both in vitro and in vivo studies in animals have shown that metabolic acidosis causes several biochemical and morphologic changes in tubule cells, which are ultimately associated with kidney hypertrophy (1,2). Protein synthesis and degradation, the determinants of protein metabolism, are key factors in the hypertrophy process. However, information regarding the signals and mechanisms by which metabolic acidosis might cause kidney hypertrophy is still incomplete, and whether these effects take place in the human kidney is unknown. A further complicating element is that the effects of acidosis on protein turnover rates vary in different tissue types, with catabolic events occurring in peripheral tissues and splanchnic organs (3,4).Chronic acidosis causes several metabolic alterations in the renal proximal tubule, including increased H ϩ secretion (1,5), ammonia synthesis (6), and citrate reabsorption (6,7). These changes in tubule function are associated with changes in the activities of a number of proteins, including the apical membrane Na ϩ /H ϩ antiporter (7), glutaminase and glutamate dehydrogenase (8), and phosphoenolpyruvate carboxykinase (9), which may affect intracellular substrate availability for protein turnover, amino acid metabolism and/or transport, and gluconeogenesis. It has been shown that in tubule epithelial cells, the associated increase in ammonia production, rather than the acidosis per se, is responsible for favoring tubular hyper...

show abstract

Distribution along the rat nephron of three enzymes of gluconeogenesis in acidosis and starvation

Cited by 77 publications

References 0 publications

Renal glucose production and utilization: new aspects in humans

Renal glucose production and utilization: new aspects in humans

Induction and Targeting of the Glutamine Transporter SN1 to the Basolateral Membranes of Cortical Kidney Tubule Cells during Chronic Metabolic Acidosis Suggest a Role in pH Regulation

Kidney Protein Dynamics and Ammoniagenesis in Humans with Chronic Metabolic Acidosis

Contact Info

Product

Resources

About