Renal glucose reabsorption

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Relationship of Sodium Reabsorption and Glomerular Filtration Rate to Renal Glucose Reabsorption

Relationship of Sodium Reabsorption and Glomerular Filtration Rate to Renal Glucose Reabsorption

sodium diuresis (C Na /GFR>0.1) are plotted on the same graph, glucose reabsorption at any given glomerular filtration rate is much less than during antidiuresis. Glucose reabsorption divided by glomerular filtration rate varies inversely with fractional sodium excretion. This study demonstrates that glomerular tubular balance for glucose exists in the dog and that this balance is changed when sodium reabsorption changes.

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The influence of saline loading on renal glucose reabsorption in the rat

The influence of saline loading on renal glucose reabsorption in the rat

Glucose titration studies were performed in normal rats under control conditions and during expansion of the extracellular fluid volume. In association with expansion, the maximal rate of glucose transport (Tm glucose ) decreased while glomerular filtration rate (GFR) typically increased; thus there was a consistent increase in the GFR/Tm glucose ratio. In previous studies, marked reduction of the nephron population was associated with an alteration in the kinetics of glucose transport and GFR/Tm glucose ratios were observed to increase. In both volume-expanded rats and in animals and human beings with uremia, the splay in the titration curve is increased. Finally in both volume-expanded animals and uremic animals fractional reabsorption of sodium is depressed. One interpretation of the present data is that the natriuretic “third factor” may influence a key rate-limiting step in glucose transport; and it is possible that this step is shared by or coupled to a rate-limiting step in sodium transport.
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Update on developments with SGLT2 inhibitors in the management of type 2 diabetes

Update on developments with SGLT2 inhibitors in the management of type 2 diabetes

Abstract: The importance of the kidney’s role in glucose homeostasis has gained wider understanding in recent years. Consequently, the development of a new pharmacological class of anti-diabetes agents targeting the kidney has provided new treatment options for the management of type 2 diabetes mellitus (T2DM). Sodium glucose co-transporter type 2 (SGLT2) inhibitors, such as dapagliflozin, canagliflozin, and empagliflozin, decrease renal glucose reabsorption, which results in enhanced urinary glucose excretion and subsequent reductions in plasma glu- cose and glycosylated hemoglobin concentrations. Modest reductions in body weight and blood pressure have also been observed following treatment with SGLT2 inhibitors. SGLT2 inhibitors appear to be generally well tolerated, and have been used safely when given as monotherapy or in combination with other oral anti-diabetes agents and insulin. The risk of hypoglycemia is low with SGLT2 inhibitors. Typical adverse events appear to be related to the presence of glucose in the urine, namely genital mycotic infection and lower urinary tract infection, and are more often observed in women than in men. Data from long-term safety studies with SGLT2 inhibi- tors and from head-to-head SGLT2 inhibitor comparator studies are needed to fully determine their benefit–risk profile, and to identify any differences between individual agents. However, given current safety and efficacy data, SGLT2 inhibitors may present an attractive option for T2DM patients who are failing with metformin monotherapy, especially if weight is part of the underlying treatment consideration.
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“Sodium Glucose Co-Transporter-2 (SGLT2) Inhibitors as a New Class of Anti-diabetic Drugs: Pharmacokinetics, Efficacy and Clinical significance” by Harsharan Pal Singh, Ishpreet Kaur, Gunjan Sharma, India.

“Sodium Glucose Co-Transporter-2 (SGLT2) Inhibitors as a New Class of Anti-diabetic Drugs: Pharmacokinetics, Efficacy and Clinical significance” by Harsharan Pal Singh, Ishpreet Kaur, Gunjan Sharma, India.

Sodium-dependent glucose co-transporters (SGLT) belong to the family of glucose transporter found in the intestinal mucosa of small intestine (SGLT1) and in the proximal tube of nephron (SGLT2 in PCT and SGLT1 in PST) which contribute to renal glucose reabsorption. In kidneys, 100% of the filtered glucose in the glomerulus has to be reabsorbed along the nephron via SGLT2 5,6 . In case of high plasma glucose concentration (hyperglycemia), glucose is excreted in urine (glucosuria); because SGLT are saturated with the filtered monosaccharide 7 . Diabetes mellitus is the most common metabolic disorder characterized by hyperglycaemia which is associated with long term complications affecting kidney, heart, eyes and nerves 8-10 . Insulin regulates carbohydrate metabolism by aiding the transport of glucose and amino acid from the blood stream into the storage organs such as liver and muscles. In diabetes mellitus, hindrance in glucose transport takes place of such a degree that threatens or impairs health 11 .
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Salt handling and hypertension

Salt handling and hypertension

Bartter and Gitelman syndromes were originally described as vari- ations of a single disease process (21, 22) resulting in hypokalemic metabolic alkalosis. More recent biochemical and latterly genetic studies have permitted their separation into distinct disorders, with separable phenotypic characteristics. The genetic defects involve either the salt transporters that are targets of diuretics, or other transporters that are their essential cellular partners. In both diseases, the mode of inheritance is autosomal recessive. To date, four genes have been implicated in the pathogenesis of Bartter syn- drome in different kindreds, whereas all cases of Gitelman syn- drome studied, now numbering several hundred, are accounted for by mutations in a single gene. In all these variants, the net effect is renal salt wasting, leading to low BP, reduced serum potassium, and an activated renin-angiotensin system.
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Bench to bedside review: Glucose production from the kidney

Bench to bedside review: Glucose production from the kidney

Data obtained from net organ balance studies of glucose production lead to the classic view according to which glucose homeostasis is mainly ensured by the liver, and renal glucose production only plays a significant role during acidosis and prolonged starvation. Renal glucose release and uptake, as well as the participation of gluconeogenic substrates in renal gluconeogenesis, were recently re-evaluated using systemic and renal arteriovenous balance of substrates in combination with deuterated glucose dilution. Data obtained using these methods lead one to reconsider the magnitude of renal glucose production as well as its role in various physiological and pathological circumstances. These findings now conduce one to consider that renal gluconeogenesis substantially participates in postabsorptive glucose production, and that its role in glucose homeostasis is of first importance.
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On the Mechanism of the Splay in the Glucose Titration Curve in Advanced Experimental Renal Disease in the Rat

On the Mechanism of the Splay in the Glucose Titration Curve in Advanced Experimental Renal Disease in the Rat

Glucose titration studies were performed in rats with unilateral chronic pyelonephritis before and after removal of the contralateral control kidneys. Identical studies were performed in animals with unilateral partial renal infarction in which the experimental kidneys had a marked reduction in nephron population but no anatomic deformation in the surviving nephrons. In the initial studies, both groups of animals were free of clinical and chemical abnormalities of uremia. In the follow-up studies uremic abnormalities were present. Minimal splay was observed in the titration curves in the initial studies; marked splay was present in the group data from the same kidneys in the subsequent studies. Thus a marked reduction in the nephron population was associated with the evolution of splay in both groups of animals. In association with the increase in splay, the mean values for maximal glucose transport increased; thus a defect in glucose transport can be excluded as the basis of the splay. Glomerular filtration rate increased proportionately more than the maximal transport of glucose; hence the ratios of glomerular filtration rate to maximal glucose transport increased consistently. The possibility of asymmetric hypertrophy of glomerular and tubular functions among the nephron population imposed by scar tissue or other anatomic deformities was considered, but the results in the animals with partially infarcted kidneys militate against this explanation. The splay also […]
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The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium

The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium

However, since each of these pressor agents produced natriuresis only in the presence of induced renal vasodilatation, it is apparent that some critical level of renal blood flow or rena[r]

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Renal Reabsorption of Phosphate in Normal Human Subjects and in Patients with Parathyroid Disease

Renal Reabsorption of Phosphate in Normal Human Subjects and in Patients with Parathyroid Disease

THE QUANTITIES OF PHOSPHATE FILTERED, glomerular filtration rate; RPF, effective renal plasma flow; Tm, maximal rate of renal tubular reabsorption; ExCRETED, AND REABSORBED DURING INTRAV[r]

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RENAL REABSORPTION OF BICARBONATE DURING ACUTE RESPIRATORY ALKALOSIS

RENAL REABSORPTION OF BICARBONATE DURING ACUTE RESPIRATORY ALKALOSIS

In contrast,, during acute respiratory acidosis the reabsorption of bicarbonate increases as a curvilinear function of plasma concentration 3, suggesting that the transport limits impose[r]

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RENAL TUBULAR SECRETION AND REABSORPTION OF ORGANIC BASES IN THE DOG

RENAL TUBULAR SECRETION AND REABSORPTION OF ORGANIC BASES IN THE DOG

In assessing the relative roles of these two processes on the net excretion of a weak base, the following factors warrant consideration: 1 the magnitude of active secretion, 2 the extent[r]

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A micropuncture study of the effect of parathyroid hormone on renal bicarbonate reabsorption

A micropuncture study of the effect of parathyroid hormone on renal bicarbonate reabsorption

tubule. Measurements of urinary ammonium and titratable acid indicate that net acid excretion (NH+/4 + TA -- HCO-/3) increases significantly after PTH administration. These results do not provide support for the view that PTH excess causes metabolic acidosis by reducing renal acid […]

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Effects of N-Acetyl Cysteine on Oxidative Stress Biomarkers in End-stage Renal Disease

Effects of N-Acetyl Cysteine on Oxidative Stress Biomarkers in End-stage Renal Disease

Reactive Oxygen Species (ROS) have a central role in the etiology of numerous worldwide diseases [1-5]. ROS play an important role in the pathophysiological processes of a surprisingly wide variety of renal diseases. In renal disease patients, there are good evidences indicating that the interaction of blood with artificial membranes leads to activation of several cellular pathways, which include the plasma cascade systems of complement, coagulation and kinins together with activation of polymorphonuclear leukocytes (PMN), monocytes, lymphocytes and platelets. Thus, activation of these pathways promotes the production of ROS [6-11].
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Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat

Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat

dependent alterations in Pi reabsorption may play a significant role in establishing the rate of Pi excretion per nephron under certain circumstances and should be considered in the interpretation of studies investigating renal Pi handling. The ability of phosphorus-depleted animals to maintain a phosphate-free urine during Pi loading would favor the rapid repletion of body phosphorus stores.

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THE EFFECT OF PARATHYROID EXTRACT ON RENAL TUBULAR CALCIUM REABSORPTION IN THE DOG

THE EFFECT OF PARATHYROID EXTRACT ON RENAL TUBULAR CALCIUM REABSORPTION IN THE DOG

If the data of Walser 6, derived from clearance experiments, can be extrapolated to stop-flow studies, the observed increase in sodium concentration would be expected to result in an inc[r]

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Salt sensitive hypertension is associated with dysfunctional Cyp4a10
               gene and kidney epithelial sodium channel

Salt sensitive hypertension is associated with dysfunctional Cyp4a10 gene and kidney epithelial sodium channel

Based on the results discussed, we propose that under conditions of balanced salt intake and excretion, locally generated EETs participate in nonstimulated ENaC gating and the regulation of distal sodium reabsorption. Dietary­induced increases in plasma sodium cause com­ pensatory volume changes and rapid and delayed epoxygenase­medi­ ated responses (Figure 5). The rapid phase involves phospholipase­ dependent AA release and metabolism to EETs. The delayed phase requires an upregulated AA epoxygenase expression and increased EET synthase activity in the CDs (Figure 5). Augmented EET levels cause an EET­mediated inactivation of ENaC, a reduction in inward sodium transport, and increased sodium excretion (Figure 5). Reductions in epoxygenase expression or activity increase ENaC­ dependent sodium reabsorption and, to maintain plasma sodium levels within physiologically compatible levels, there is increased water retention and expansion of the plasma volume. These epoxy­ genase­mediated increases in ENaC­dependent sodium reabsorption and the attendant changes in plasma volume result in increased sys­ temic blood pressure (Figure 5) and, ultimately, hypertension. The proposal in Figure 5 is consistent with the normotensive effects of amiloride and Wy on Cyp4a10 –/– mice as well as the ENaC normal­
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THE REGULATION OF RENAL BICARBONATE REABSORPTION BY PLASMA CARBON DIOXIDE TENSION

THE REGULATION OF RENAL BICARBONATE REABSORPTION BY PLASMA CARBON DIOXIDE TENSION

There is a direct, approximately linear relationship between plasma carbon dioxide tension and renal bicarbonate reabsorption in the anesthetized dog which can be demonstrated in the pre[r]

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EVIDENCE FOR ACTIVE CHLORIDE REABSORPTION IN THE DISTAL RENAL TUBULE OF THE RAT

EVIDENCE FOR ACTIVE CHLORIDE REABSORPTION IN THE DISTAL RENAL TUBULE OF THE RAT

The mechanism of Cl- reabsorption in the distal tubule was examined by determining the relationship between the distal transtubular potential difference ET and the ratio of peritubular C[r]

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The Effects of Infusion of Water on Renal Hemodynamics and the Tubular Reabsorption of Sodium

The Effects of Infusion of Water on Renal Hemodynamics and the Tubular Reabsorption of Sodium

We suggest that volume expansion with water depresses proximal tubular reabsorption of sodium in a manner qualitatively similar to infusions of saline and that the extent to which sodium excretion is increased during water loading is dependent upon 1) the absolute extent to which proximal reabsorption is […]

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Renal Bicarbonate Reabsorption and Hydrogen Ion Excretion in Normal Infants

Renal Bicarbonate Reabsorption and Hydrogen Ion Excretion in Normal Infants

threshold ranging from 21.5 to 22.5 mmoles per L, maximal rate of reabsorption from 2.6 to 2.9 mmoles per 100 ml glomerular filtrate, and marked titration splay. A nephronic frequency distribution curve of the ratio of glomerular filtration rate to tubular reabsorptive capacity demonstrated both heterogeneity and skewing to the right, suggesting the presence of significant numbers of nephrons with low tubular transport capacity relative to filtration rate. It is suggested that the “physiologic acidosis” of the infant is due neither to a limited renal capacity to excrete hydrogen ion nor to a reduced capacity for reabsorption of bicarbonate, but rather to a low renal plasma bicarbonate threshold. Although the level of the threshold may relate to the kinetics of bicarbonate reabsorption during this period, it appears to be due at least in part to functional and morphologic heterogeneity of nephrons.
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