ArticleAmerican journal of physiology. Renal physiology2009
SGK1-sensitive renal tubular glucose reabsorption in diabetes.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Effect of Insulin on Proximal Tubules Handling of Glucose: A Systematic Review.Journal of diabetes research · 2020Pooled it
- Update on Pathogenesis of Glomerular Hyperfiltration in Early Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
- Crosstalk between Sodium-Glucose Cotransporter Inhibitors and Sodium-Hydrogen Exchanger 1 and 3 in Cardiometabolic Diseases.International journal of molecular sciences · 2021Review
- Glucose transporters in the kidney in health and disease.Pflugers Archiv : European journal of physiology · 2020Review
- The functional duality of SGK1 in the regulation of hyperglycemia.Endocrine connections · 2020Review
- Renal tubule insulin receptor modestly promotes elevated blood pressure and markedly stimulates glucose reabsorption.JCI insight · 2018Article
- Sodium glucose cotransporter SGLT1 as a therapeutic target in diabetes mellitus.Expert opinion on therapeutic targets · 2016Review
- Sodium-retaining effect of insulin in diabetes.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Review
- Serum- and glucocorticoid-inducible kinase 1 in the regulation of renal and extrarenal potassium transport.Clinical and experimental nephrology · 2012Review
- Chronic intrarenal insulin replacement reverses diabetes mellitus-induced natriuresis and diuresis.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney.Annual review of physiology · 2012Review
- Pathophysiology of the diabetic kidney.Comprehensive Physiology · 2011Review
- The proximal tubule in the pathophysiology of the diabetic kidney.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
- Chronic sodium-retaining action of insulin in diabetic dogs.American journal of physiology. Renal physiology · 2011Article
- Renal glucose transporters: novel targets for hyperglycemia management.Nature reviews. Nephrology · 2010Review
- Regulation of renal tubular glucose reabsorption by Akt2/PKBβ.American journal of physiology. Renal physiology · 2010Article
- Targeting SGK1 in diabetes.Expert opinion on therapeutic targets · 2009Review
- The physiological impact of the serum and glucocorticoid-inducible kinase SGK1.Current opinion in nephrology and hypertension · 2009Review
- SGK, renal function and hypertension.Journal of nephrologyArticle
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
The hyperglycemia of diabetes mellitus increases the filtered glucose load beyond the maximal tubular transport rate and thus leads to glucosuria. Sustained hyperglycemia, however, may gradually increase the maximal renal tubular transport rate and thereby blunt the increase of urinary glucose excretion. The mechanisms accounting for the increase of renal tubular glucose transport have remained ill-defined. A candidate is the serum- and glucocorticoid-inducible kinase SGK1. The kinase has been shown to stimulate Na(+)-coupled glucose transport in vitro and mediate the stimulation of electrogenic intestinal glucose transport by glucocorticoids in vivo. SGK1 expression is confined to glomerula and distal nephron in intact kidneys but may extend to the proximal tubule in diabetic nephropathy. To explore whether SGK1 modifies glucose transport in diabetic kidneys, Akita mice (akita(+/-)), which develop spontaneous diabetes, have been crossbred with gene-targeted mice lacking SGK1 on one allele (sgk1(+/-)) to eventually generate either akita(+/-)/sgk1(-/-) or akita(+/-)/sgk1(+/+) mice. Both akita(+/-)/sgk1(-/-) and akita(+/-)/sgk1(+/+) mice developed profound hyperglycemia (>20 mM) within approximately 6 wk. Body weight and plasma glucose concentrations were not significantly different between these two genotypes. However, urinary excretion of glucose and urinary excretion of fluid, Na(+), and K(+), as well as plasma aldosterone concentrations, were significantly higher in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. Studies in isolated perfused proximal tubules revealed that the electrogenic glucose transport was significantly lower in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. The data provide the first evidence that SGK1 participates in the stimulation of renal tubular glucose transport in diabetic kidneys.
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