Impaired Renal Tubular Function Induced by Sugar Infusion in Man

Fox, M. R. Spivey; Thier, Samuel O.; Rosenberg, León E.; Segal, Stanton; Coleman, Amy; Downing, Sylvia J.; Fisher, Lillian J.

doi:10.1210/jcem-24-12-1318

Cited by 55 publications

(18 citation statements)

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“…Prior studies in man (23)(24)(25) and dog (26)(27)(28) had suggested that hyperglycemia increases renal phosphate excretion. In contrast to our studies, however, significant glucosuria was present in all of these previous studies.…”

Section: Discussionmentioning

confidence: 99%

The effects of glucose and insulin on renal electrolyte transport.

DeFronzo¹,

Goldberg²,

Agus³

1976

J. Clin. Invest.

425

197

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A B S T R A C r The effects of hyperglycemia and hyperinsulinemia on renal handling of -sodium, calcium, and phosphate were studied in dogs employing the r.ecollection micropuncture technique. Subthreshold sustained hyperglycemia resulted in an isonatric inhibition of proximal tubular sodium, fluid, calcium, and phosphate reabsorption by 8-14%. Fractional excretion of sodium and phosphate, however, fell (P < 0.01) indicating that the increased delivery of these ions was reabsorbed in portions of the nephron distal to the site of puncture and in addition net sodium and phosphate transport was enhanced resulting in a significant antinatriuresis and antiphosphaturia.The creation of a steady state plateau of hyperinsulinemia while maintaining the blood glucose concentration at euglycemic levels mimicked the effects of hyperglycemia on proximal tubular transport and fractional excretion of sodium and calcium. Tubular fluid to plasma inulin ratio fell, similar to the hyperglycemic studies. These results suggest that the effects of hyperglycemia on renal handling of sodium and calcium may be mediated through changes in plasma insulin concentration. In contrast to hyperglycemia, however, hyperinsulinemia caused a significant fall in tubular fluid to plasma phosphate ratio with enhanced proximal tubular phosphate reabsorption (P < 0.02). This occurred concomitantly with a significant inhibition of proximal tubular sodium transport. These data indicate that insulin has a direct effect on proximal tubular phosphate reabsorption, and this effect of insulin is masked by the presence of increased amounts of unreabsorbed glucose in the tubule that ensues when hyperinsulinemia occurs -secondary to hyperglycemia. Fractional excretion Dr. Agus is a Clinical Investigator of the Veteran's Administration.

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Section: Discussionmentioning

confidence: 99%

The effects of glucose and insulin on renal electrolyte transport.

DeFronzo¹,

Goldberg²,

Agus³

1976

J. Clin. Invest.

425

197

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“…Aminoaciduria exists with the mellituria of diabetes mellitus (1), galactosemia (2), fructose intolerance (3), and the Fanconi syndrome (4); galactose feeding to rats (5) and hexose infusion into humans produces aminoaciduria (6). Previous reports from this laboratory have substantiated an interaction of amino acids and sugars in the kidney by the demonstration in vitro that glucose, galactose, and fructose inhibit the accumulation of some amino acids by rat kidney cortex slices (7,8).…”

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confidence: 99%

Separate Transport Systems for Sugars and Amino Acids in Developing Rat Kidney Cortex

Segal

Rea

Smith

1971

Proc. Natl. Acad. Sci. U.S.A.

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The ability of renal cortical slices of newborn and young rats to accumulate a nonmetabolizable sugar, a-methylglucoside, is slight and does not reach adult capacity until 25 days of age. However, a rudimentary sugar transport system is present, as indicated by a further decrease in accumulation in the presence of phlorizin or absence of sodium ion.Amino acid uptake in immature kidney tissue is not deficient;on the contrary,the tissue tookup and concentrated more glycine and lysine than adult tissue. Decreased amino acid efflux from the immature cells appears to be the explanation. Concentration dependence of amino acid uptake was the same in 5-day-old and adult tissue.These differences between the transport characteristics of a model sugar and representative amino acids during development indicate separate transport systems for the two types of substrate.

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“…However, both patients with diabetes mellitus in the absence of poor metabolic control and those individuals with the rare genetic disease familial renal glycosuria [36], who excrete massive amounts of glucose secondary to a defective brushborder transporter, fail to demonstrate the renal Fanconi syndrome. In support of the former mechanism, increased glomerular filtration of glucose secondary to the induction of acute experimental hyperglycemia in human subjects has been shown to result in impaired renal tubular reabsorption of phosphate and amino acids, independent of glomerular filtration rate or any osmotic diuretic effect [37]. The putative abnormality in proximal renal tubular cell handling of glucose in the Fanconi-Bickel syndrome is shown in Fig.…”

Section: Discussionmentioning

confidence: 83%

Diabetes-like renal glomerular disease in Fanconi-Bickel syndrome

et al. 1995

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The Fanconi-Bickel syndrome is a rare inherited disorder of metabolism characterized by hepatic glyconeogenesis, galactose intolerance, renal Fanconi syndrome with nephromegaly, and glycogen accumulation in proximal renal tubular cells. An 8-year-old patient with this disease and severe rickets due to medically resistant hypophosphatemia was found to have the previously unrecognized complication of renal glomerular hyperfiltration, microalbuminuria, and diffuse glomerular mesangial expansion. Similar to patients with glucose-6-phosphatase deficiency, the glomerular disease in this patient resembles incipient diabetic nephropathy. The Fanconi syndrome may be due to the defective transport of glucose at the proximal tubular basolateral membrane, which results in accumulation of glucose and secondarily glycogen within tubular cells. Since the metabolic defect, as evidenced by glycogen accumulation, selectively involves proximal renal tubular cells in the kidney of patients with Fanconi-Bickel syndrome and glucose-6-phosphatase deficiency, the abnormalities in renal glomerular hemodynamics and mesangial construct in these rare diseases are likely due to renal tubular factors, if the mechanism originates in the kidney. A delineation of these phenomena may further our understanding of the pathogenesis of diabetic nephropathy.

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Impaired Renal Tubular Function Induced by Sugar Infusion in Man

Cited by 55 publications

References 0 publications

The effects of glucose and insulin on renal electrolyte transport.

The effects of glucose and insulin on renal electrolyte transport.

Separate Transport Systems for Sugars and Amino Acids in Developing Rat Kidney Cortex

Diabetes-like renal glomerular disease in Fanconi-Bickel syndrome

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