Reduction of Remnant Nephron Hypermetabolism by Protein Restriction

Jarusiripipat, Chokchai; Shapiro, Joseph I.; Chan, Laurence; Schrier, Robert W.

doi:10.1016/s0272-6386(12)80097-7

Cited by 16 publications

(11 citation statements)

References 28 publications

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“…In the isolated kidney, transport and metabo lism compete for ATP [20], and as sodium transport and the metabolic processes tested, in particular ammoniagenesis, were substrate dependent, a relative preservation of metab olism at the expense of transport could explain the apparent increase in nontransport metabolism. However, the in crease in nephron QO: was demonstrated for all substrates tested, and was in accord with previous ex vivo [1][2][3] and in vivo [4,5] studies of the remnant kidney. Thus, despite the shortcomings of isolated kidney perfusion, the data are of relevance to the remnant kidney in vivo.…”

Section: Discussionsupporting

confidence: 90%

“…The original observation was made in the isolated perfused kidney [1], and has since been confirmed by other investigators [2,3], and by in vivo experiments [2,4,5],…”

Section: Introductionmentioning

confidence: 62%

“…In both ex vivo and in vivo studies [1][2][3][4][5], the marked increment in nephron Q 0 2 was accompanied by a more modest elevation of net nephron Accepted: July 15.1992 sodium reabsorption (TNa+), suggesting the enhancement of metabolic processes in addition to TNa+. The nature of these other metabolic processes is unknown, but a number of possibilities exist.…”

Section: Introductionmentioning

confidence: 99%

“…The purpose of the present study was to define the basis of increased remnant kidney Q 0 2 further by examining: (1) the time-course of its development, (2) metabolic processes in addition to T Na+, and (3) the effect of variation of perfusion pressure and substrate.…”

Section: Introductionmentioning

confidence: 99%

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Altered Metabolism in the ex vivo Remnant Kidney

Harris

Tay²,

Egan³

et al. 1993

Nephron

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Oxygen consumption is increased in the rat remnant kidney (RK), but the basis of this enhanced metabolic activity has not been defined fully. To characterize the hypermetabolism further, isolated RK and normal kidneys (NK) were perfused using a range of perfusion pressures and substrates, and at varying times after 5/6 nephrectomy. Altered and increased RK metabolism was found as early as 1 week after 5/6 nephrectomy. The rate of net glucose consumption was higher in RK than NK (e.g., 0-30 min, 2.42 ± 0.28 vs. 1.21 ± 0.33 μmol·min^-1 g^-1), a difference not explained by changes in oxygen delivery or glycosuria. Ammonia production was significantly greater early in perfusion in RK than NK. Calculated nephron oxygen consumption (QO₂) was greater in RK than NK for all substrates tested (e.g., pyruvate 5 ml: 552.3 ± 43.1 vs. 173.3 ± 25.6 pmol min^-1, p < 0.001). When considered together, site I mitochondrial substrates supported QO₂ and net sodium reabsorption (T_Na+) better than site II substrates. In RK, QO₂ did not change with increasing perfusion pressure, and T_Na+ rose only slightly for pressures ≥ 120 mm Hg. In summary, RK hypermetabolism is characterized by increased oxygen consumption, glycolysis and ammoniagenesis, is not substrate-specific and does not appear to be an artefact of the altered physiology of remnant perfusion.

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Section: Discussionsupporting

confidence: 90%

“…The original observation was made in the isolated perfused kidney [1], and has since been confirmed by other investigators [2,3], and by in vivo experiments [2,4,5],…”

Section: Introductionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Altered Metabolism in the ex vivo Remnant Kidney

Harris

Tay²,

Egan³

et al. 1993

Nephron

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“…Other nontransport metabolic processes, such as prostanoid [7,8], lipid and protein synthesis [9] are also increased during renal hypertrophy. Several maneuvers with proven or possible efficacy in slowing the progression of chronic renal disease, including restriction of dietary phosphate [3,10] and protein [11,12] and the Chinese herbal drug rheum officinale [13,14], have been shown to reduce nephron oxygen consumption (QO:). In the case of phosphate restriction, this effect was not explained by reduction in TNa+, but rather by the inhibition of nontransport processes [3,10], Protein retriction has been shown to have multiple effects on renal metabolism in addition to the inhibition of sodium transport, and so its effect on nephron QCh may depend on its ability to dampen nontransport processes as well.…”

Section: Introductionmentioning

confidence: 99%

Altered Metabolism in the ex vivo Remnant Kidney

C²

1993

Nephron

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To understand further the contribution of heightened net sodium reabsorption (T_Na+) and other nontransport processes to increased and altered metabolic activity of the rat remnant kidney (RK), isolated RK and normal kidneys (NK) were perfused with and without metabolic inhibitors and following 4 weeks of low (12%)- or high (40%)-protein diet. 3-Mercaptopicolinate (200 μM) and 2-deoxyglucose (200 μM) reduced glucose production and consumption, respectively, without altering oxygen consumption (QO₂). Ouabain reduced T_Na+ and QO₂ in NK but not RK, and increased glucose consumption in RK (by 67%, p < 0.02, n = 12) and NK (by 54%, p < 0.05, n = 12). Raising perfusate pH by 0.3 U to 7.65 increased glucose production in RK but not NK and reduced T_Na+ in NK but not RK Dietary protein restriction reduced QO₂ (2.18 ± 0.29 vs. 4.13 ± 0.20 μmol^-1 min^-1 g^-1 p < 0.001), T_Na+ (8.74 ± 4.39 vs. 38.83 ± 8.32, p < 0.01) and ammoniagenesis (0-30 min, 0.16 ± 0.05 vs. 0.32 ± 0.10, p < 0.05) in RK, but not NK. In summary: (1) responses to ouabain and alkalosis, but not other metabolic inhibitors, were quite distinct in remnant versus normal kidneys, and (2) protein restriction limited sodium-transport-dependent and -independent hypermetabolism in RK.

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Nuclear magnetic resonance measurements of intracellular pH: Biomedical implications

Malhotra

Shapiro²

1993

Concepts Magn. Reson.

Self Cite

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The measurement of intracellular pH is of crucial importance in biomedical investigation. Nuclear magnetic resonance (NMR) spectroscopy methods allow investigators to monitor this essential parameter in a variety of experimental conditions. Although a number of NMR spectroscopy methods for measuring intracellular pH have been described, the method of using the chemical shift of inorganic phosphate has been employed most widely. In this review, we discuss the various NMR methodologies which allow for measurement of intracellular pH as well as selected topics where these measurements have been employed. Because of the volume of work which has been published using NMR to monitor intracellular pH, we have not attempted to be exhaustive in our review, but rather have tried to highlight the importance of this methodology by reviewing several topics in biology and medicine where NMR measurements of intracellular pH have played an important role in improving our understanding.

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Reduction of Remnant Nephron Hypermetabolism by Protein Restriction

Cited by 16 publications

References 28 publications

Altered Metabolism in the ex vivo Remnant Kidney

Altered Metabolism in the ex vivo Remnant Kidney

Altered Metabolism in the ex vivo Remnant Kidney

Nuclear magnetic resonance measurements of intracellular pH: Biomedical implications

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