Glucose Transport in the Renal Proximal Tubule

Silverman, Melvin; Turner, R. Jay

doi:10.1002/cphy.cp080243

Cited by 10 publications

(10 citation statements)

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“…3). Five millimolar glucose exceeds the 1.6 mM K m for glucose transport with Na in proximal tubule S1 and S2 segments (33). Therefore, raising glucose from 5 to 25 mM had no effect on phloridzin-inhibited Q O 2 .…”

Section: F290mentioning

confidence: 90%

Glucose stimulates O₂consumption, NOS, and Na/H exchange in diabetic rat proximal tubules

Baínes

2002

American Journal of Physiology-Renal Physiology

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Endothelial nitric oxide synthase (NOS) and neuronal NOS protein increased in proximal tubules of acidotic diabetic rats 3-5 wk after streptozotocin injection. NOS activity (citrulline production) was similar in nondiabetic and diabetic tubules incubated with low glucose (5 mM glucose + 20 mM mannitol); but after 30 min with high glucose (25 mM), Ca-sensitive citrulline production had increased 23% in diabetic tubules. Glucose concentration did not influence citrulline production in nondiabetic tubules. High glucose increased carboxy-2-phenyl-4,4,5,5,-tetramethylimidazoline 1-oxyl-3-oxide (cpt10)-scavenged NO sevenfold in a suspension of diabetic tubules but did not alter NO in nondiabetic tubules. Diabetes increased ouabain-sensitive 86Rb uptake (141 +/- 9 vs. 122 +/- 6 nmol x min(-1) x mg(-1)) and oligomycin-sensitive O2 consumption (QO2; 16.0 +/- 1.7 vs. 11.3 +/- 0.7 nmol x min(-1) x mg(-1)). Ethylisopropyl amiloride-inhibitable QO2 (6.5 +/- 0.6 vs. 2.4 +/- 0.3 nmol x min(-1) x mg(-1)) accounted for increased oligomycin-sensitive QO2 in diabetic tubules. N(G)-monomethyl-L-arginine methyl ester (L-NAME) inhibited most of the increase in 86Rb uptake and QO2 in diabetic tubules. L-NAME had little effect on nondiabetic tubules. Inhibition of QO2 by ethylisopropyl amiloride and L-NAME was only 5-8% additive. Uncontrolled diabetes for 3-5 wk increases NOS protein in proximal tubules and makes NOS activity sensitive to glucose concentration. Under these conditions, NO stimulates Na-K-ATPase and QO2 in proximal tubules.

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Section: F290mentioning

confidence: 90%

Glucose stimulates O₂consumption, NOS, and Na/H exchange in diabetic rat proximal tubules

Baínes

2002

American Journal of Physiology-Renal Physiology

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“…Figure 1 describes the renal handling of filtered glucose 32. Glucose is freely filtered in the glomerulus, so that, as plasma glucose levels increase, the amount of glucose in the glomerular filtrate increases linearly.…”

Section: Renal Glucose Reabsorptionmentioning

confidence: 99%

“…The ‘rounding’ of the titration curve seen around the transition from complete reabsorption to urinary excretion of excess glucose (shown in Fig. 1 as ‘splay’) can be accounted for by heterogeneity in the glomerular filtration rate and glucose reabsorptive capacity of different individual nephrons 32.…”

Section: Renal Glucose Reabsorptionmentioning

confidence: 99%

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Role of the kidney in normal glucose homeostasis and in the hyperglycaemia of diabetes mellitus: therapeutic implications

2010

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Considerable data have accumulated over the past 20 years, indicating that the human kidney is involved in the regulation of glucose via gluconeogenesis, taking up glucose from the circulation, and by reabsorbing glucose from the glomerular filtrate. In light of the development of glucose-lowering drugs involving inhibition of renal glucose reabsorption, this review summarizes these data. Medline was searched from 1989 to present using the terms ‘renal gluconeogenesis’, ‘renal glucose utilization’, ‘diabetes mellitus’ and ‘glucose transporters’. The human liver and kidneys release approximately equal amounts of glucose via gluconeogenesis in the post-absorptive state. In the postprandial state, although overall endogenous glucose release decreases substantially, renal gluconeogenesis increases by approximately twofold. Glucose utilization by the kidneys after an overnight fast accounts for ∼10% of glucose utilized by the body. Following a meal, glucose utilization by the kidney increases. Normally each day, ∼180 g of glucose is filtered by the kidneys; almost all of this is reabsorbed by means of sodium–glucose co-transporter 2 (SGLT2), expressed in the proximal tubules. However, the capacity of SGLT2 to reabsorb glucose from the renal tubules is finite and, when plasma glucose concentrations exceed a threshold, glucose appears in the urine. Handling of glucose by the kidney is altered in Type 2 diabetes mellitus (T2DM): renal gluconeogenesis and renal glucose uptake are increased in both the post-absorptive and postprandial states, and renal glucose reabsorption is increased. Specific SGLT2 inhibitors are being developed as a novel means of controlling hyperglycaemia in T2DM.Diabet. Med. 27, 136–142 (2010)

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“…This mechanism may account for hypoglycaemic activity of LS. Blood glucose is filtered in glomeruli and then reabsorbed in epithelial cells of the renal proximal tubules via sodium-glucose cotransporters (Deetjen et al, 1995;Silverman and Turner, 1992). It has been reported that phlorizin, a specific inhibitor of Na + -glucose cotransporter, promotes the excretion of glucose into the urine and lower blood glucose levels in several animal models of diabetes mellitus (Abutt et al, 1995;Crofford, 1995;Krook et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Effect of Lepidium sativum L. on renal glucose reabsorption and urinary TGF‐β1 levels in diabetic rats

Eddouks¹,

Maghrani²

2007

Phytotherapy Research

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The purpose of this study was to determine the mechanism underlying the hypoglycaemic activity of the aqueous extract perfusion of Lepidium sativum L. (LS) in normal and streptozotocin-induced diabetic rats. The aqueous LS extract was administered intravenously and the blood glucose levels were determined within 4 h of treatment. Plasma insulin concentrations and glycosuria were determined. The 24 h urinary transforming growth factor-β β β β β 1 (ELISA) was evaluated in diabetic and control rats 15 days after oral treatment with the aqueous LS extract at a dose of 20 mg/kg.The study showed that LS at a dose of 10 mg/kg/h reduced blood glucose levels both in normal and diabetic rats ( p < < < < < 0.001). At the same time as a potent increase of glycosuria was observed both in normal and diabetic rats (p < < < < < 0.001). In addition, oral administration of LS for 15 days normalized glycaemia (p < < < < < 0.001), enhanced glycosuria ( p < < < < < 0.05 vs diabetic control) and decreased the amount of urinary TGF-β β β β β 1 (p < < < < < 0.01) in diabetic rats. It is concluded that the aqueous LS extract caused a potent inhibition of renal glucose reabsorption which in turn reduced blood sugar. This renal effect is at least one mechanism explaining the observed hypoglycaemic activity of this plant in normal and diabetic rats.

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Glucose Transport in the Renal Proximal Tubule

Cited by 10 publications

References 98 publications

Glucose stimulates O₂consumption, NOS, and Na/H exchange in diabetic rat proximal tubules

Glucose stimulates O₂consumption, NOS, and Na/H exchange in diabetic rat proximal tubules

Role of the kidney in normal glucose homeostasis and in the hyperglycaemia of diabetes mellitus: therapeutic implications

Effect of Lepidium sativum L. on renal glucose reabsorption and urinary TGF‐β1 levels in diabetic rats

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Glucose Transport in the Renal Proximal Tubule

Cited by 10 publications

References 98 publications

Glucose stimulates O2consumption, NOS, and Na/H exchange in diabetic rat proximal tubules

Glucose stimulates O2consumption, NOS, and Na/H exchange in diabetic rat proximal tubules

Role of the kidney in normal glucose homeostasis and in the hyperglycaemia of diabetes mellitus: therapeutic implications

Effect of Lepidium sativum L. on renal glucose reabsorption and urinary TGF‐β1 levels in diabetic rats

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Glucose stimulates O₂consumption, NOS, and Na/H exchange in diabetic rat proximal tubules

Glucose stimulates O₂consumption, NOS, and Na/H exchange in diabetic rat proximal tubules