Renal substrate metabolism.

Wirthensohn, Gabriele; Guder, W. G.

doi:10.1152/physrev.1986.66.2.469

Cited by 231 publications

(172 citation statements)

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“…Lipid is normally the major oxidative fuel of the kidney (57). In the present study, postprandial renal FFA net uptake was reduced by 65% (i.e., by 48 mol/ min).…”

Section: Discussionsupporting

confidence: 53%

Role of human liver, kidney, and skeletal muscle in postprandial glucose homeostasis

Meyer¹,

Dostou²,

Welle

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

237

163

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. Role of human liver, kidney, and skeletal muscle in postprandial glucose homeostasis. Am J Physiol Endocrinol Metab 282: E419-E427, 2002; 10.1152/ ajpendo.00032.2001.-Recent studies indicate a role for the kidney in postabsorptive glucose homeostasis. The present studies were undertaken to evaluate the role of the kidney in postprandial glucose homeostasis and to compare its contribution to that of liver and skeletal muscle. Accordingly, we used the double isotope technique along with forearm and renal balance measurements to assess systemic, renal, and hepatic glucose release as well as glucose uptake by kidney, skeletal muscle, and splanchnic tissues in 10 normal volunteers after ingestion of 75 g of glucose. We found that, during the 4.5-h postprandial period, 22 Ϯ 2 g (30 Ϯ 3% of the ingested glucose) were initially extracted by splanchnic tissues. Of the remaining 53 Ϯ 2 g that entered the systemic circulation, 19 Ϯ 3 g were calculated to have been taken up by skeletal muscle and 7.5 Ϯ 1.7 g by the kidney (26 Ϯ 3 and 10 Ϯ 2%, respectively, of the ingested glucose). Endogenous glucose release during the postprandial period (16 Ϯ 2 g), calculated as the difference between overall systemic glucose appearance and the appearance of ingested glucose in the systemic circulation, was suppressed 61 Ϯ 3%. Surprisingly, renal glucose release increased twofold (10.6 Ϯ 2.5 g) and accounted for ϳ60% of postprandial endogenous glucose release. Hepatic glucose release (6.7 Ϯ 2.2 g), the difference between endogenous and renal glucose release, was suppressed 82 Ϯ 6%. These results demonstrate a hitherto unappreciated contribution of the kidney to postprandial glucose homeostasis and indicate that postprandial suppression of hepatic glucose release is nearly twofold greater than had been calculated in previous studies (42 Ϯ 4%), which had assumed that there was no renal glucose release. We postulate that increases in postprandial renal glucose release may play a role in facilitating efficient liver glycogen repletion by permitting substantial suppression of hepatic glucose release.gluconeogenesis; glycogenolysis; glucose disposal CONSIDERABLE INFORMATION has recently accumulated regarding postprandial glucose homeostasis. It appears that about one-third of ingested carbohydrate is immediately taken up by splanchnic tissues (5, 22, 33-35, 37, 38, 44, 60). Of the remaining two-thirds of the ingested carbohydrate that enters the systemic circulation, some is extracted by the liver (23), but most is taken up by peripheral tissues. Limb balance measurements indicate that skeletal muscle is the predominant site for this peripheral glucose disposal, being responsible for about one-fourth of the ingested carbohydrate (5, 26, 33-35, 37, 38, 44). The fate of the remaining 40% of the ingested carbohydrate is less clear.In addition to tissue uptake of ingested carbohydrate, another important factor for postprandial glucose homeostasis is suppression of the release of glucose endogenously produced by gluconeogenesis and breakdown of ...

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“…Lipid is normally the major oxidative fuel of the kidney (57). In the present study, postprandial renal FFA net uptake was reduced by 65% (i.e., by 48 mol/ min).…”

Section: Discussionsupporting

confidence: 53%

Role of human liver, kidney, and skeletal muscle in postprandial glucose homeostasis

Meyer¹,

Dostou²,

Welle

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

237

163

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“…Uptake and release are distinct processes subject to separate regulation and occurring in different locations within the kidney. Glucose utilization occurs predominantly in the renal medulla, whereas glucose production is confined to the cortex [23,[26][27][28] (Fig. 1).…”

Section: Methodological Considerationsmentioning

confidence: 99%

“…3). The stimulatory effect of epinephrine on renal glucose production could be direct via In vitro and animal data summarized from [26,27] cAMP-mediated stimulation of renal key gluconeogenic enzymes, as shown in vitro [40], or indirect through increased substrate availability since epinephrine has been shown to increase the availability of gluconeogenic precursors [41].…”

Section: Hormonal Regulation Of Renal Glucose Productionmentioning

confidence: 99%

Renal glucose production and utilization: new aspects in humans

et al. 1997

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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].

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“…The kidney has long been the subject of metabolic studies (52)(53)(54)(55)(56). It has the capacity to metabolize a large variety of substrates (e.g.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Proteinuria through Podocyte Alkalinization

Altintas

Moriwaki

Wei

et al. 2014

Journal of Biological Chemistry

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Background: Podocyte injury can be caused by cytosolic cathepsin L activity, leading to foot process effacement and proteinuria. Results: Glutamine blunts the damaging activity of induced cytosolic cathepsin L in podocytes by modulating intracellular pH. Conclusion: Podocyte pH modulation is a novel way to tackle proteinuric kidney disease. Significance: The optimization of amino acid metabolism fluxes and associated pH i of podocytes may form a basis for novel therapeutic approaches.

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Renal substrate metabolism.

Cited by 231 publications

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Role of human liver, kidney, and skeletal muscle in postprandial glucose homeostasis

Role of human liver, kidney, and skeletal muscle in postprandial glucose homeostasis

Renal glucose production and utilization: new aspects in humans

Reduction of Proteinuria through Podocyte Alkalinization

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