Abnormal renal glucose handling in X-linked hypophosphataemic mice

1991 ◽  
Vol 80 (1) ◽  
pp. 71-76 ◽  
Author(s):  
R. C. Mühlbauer ◽  
H. Fleisch
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Glucose Concentration ◽  
Urinary Glucose Excretion ◽  
Renal Handling ◽  
Acute Response ◽  
Altered Glucose ◽  
Urinary Glucose ◽  
Glucagon And Insulin ◽  
Glucose Excretion

1. The renal handling of glucose was determined in male X-linked hypophosphataemic (Hyp/Y) mice and in control littermates (+/Y) aged 4 months. Plasma glucose concentration and urinary glucose excretion were measured before and during stepwise increase in glycaemia induced by an acute infusion of glucose. The relationship between plasma glucose concentration and urinary glucose excretion was monitored per ml of glomerular filtrate in mice fed high and low phosphate diets. 2. Hyp/Y mice fed the high phosphate diet showed a significantly higher glucosuria compared with +/Y littermates. When glycaemia was increased, Hyp/Y mice developed frank glucosuria earlier than +/Y animals. In Hyp/Y mice we could not find a threshold below which virtually no glucose was excreted in the urine, whereas this was clearly visible in +/Y mice. These differences persisted in animals fed the low phosphate diet. 3. Using the acute response to the glucoregulatory hormones, glucagon and insulin, administered exogenously, we found that the regulation of plasma glucose concentration did not differ between Hyp/Y and +/Y mice. 4. The significantly lower plasma glucose concentration observed in Hyp/Y as compared with +/Y mice decreased further during fasting. 5. We conclude that the renal reabsorptive capacity for glucose is defective in Hyp/Y mice and their low plasma glucose concentration may be explained by the renal leak. Therefore the X-linked phosphataemic mouse appears not only to be characterized by a defect in renal phosphate and calcium reabsorption but also by an altered glucose reabsorption.

THE EFFECT OF URINARY GLUCOSE EXCRETION ON THE PLASMA GLUCOSE CLEARANCES AND PLASMA INSULIN RESPONSES TO INTRAVENOUS GLUCOSE LOADS IN UNANAESTHESIZED DOGS

1978 ◽  
Vol 87 (1) ◽  
pp. 133-138 ◽  
Author(s):  
J. J. Kaneko ◽  
D. Mattheeuws ◽  
R. P. Rottiers ◽  
J. Van Der Stock ◽  
A. Vermeulen
Keyword(s):  
Plasma Glucose ◽  
Insulin Response ◽  
Immunoreactive Insulin ◽  
Glucose Load ◽  
Urinary Glucose Excretion ◽  
Intravenous Glucose ◽  
K Value ◽  
Urinary Glucose ◽  
Glucose Clearance ◽  
Glucose Excretion

ABSTRACT The effect of urinary glucose excretion on the plasma glucose clearance and insulin response to varying sizes of glucose loads was studied in normal unanaesthesized dogs. Glucose loads ranging from 0.15 to 1.25 g/kg b.w. were infused intravenously in a standard time period of 30 seconds. Plasma glucose and plasma immunoreactive insulin (IRI) concentrations were determined during one-hour after infusion. All urine excreted during the one-hour was collected by a catheterization and bladder wash-out procedure. The urinary glucose excretion was expressed as the percent of the glucose load. The urinary glucose excretion varied directly with the size of the glucose load and ranged from minimal to 12 %. This would indicate that urinary losses play a considerable role proportionate to the degree of hyperglycaemia above the renal threshold. Thus, urinary loss of glucose must be recognized as an important factor influencing the plasma glucose clearance and hence the plasma IRI response. A glucose load of 0.5 g/kg b.w. given in 30 seconds with the k-value calculated between 15–45 min would minimize the influence of urinary loss and provide more accurate plasma clearance values.

scholarly journals Regulation of renal tubular glucose reabsorption by Akt2/PKBβ

2010 ◽  
Vol 298 (5) ◽  
pp. F1113-F1117 ◽  
Author(s):  
Daniela S. Kempe ◽  
Gulab Siraskar ◽  
Henning Fröhlich ◽  
Anja T. Umbach ◽  
Michael Stübs ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Epithelial Transport ◽  
Plasma Glucose Concentration ◽  
Xenopus Laevis Oocytes ◽  
Renal Tubules ◽  
Glucose Reabsorption ◽  
Urinary Glucose ◽  
Renal Tubular

Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Nothing is known, however, of the role of Akt/PKB in the regulation of renal epithelial transport. To explore whether Akt2/PKBβ influences the Na+-coupled glucose cotransporter SGLT1, human SGLT1 was expressed in Xenopus laevis oocytes with or without Akt/PKB, and electrogenic glucose transport was determined by dual-electrode voltage clamp. The coexpression of Akt/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. To study the functional significance of Akt/PKB-sensitive renal glucose transport, further experiments were performed in gene-targeted mice lacking functional Akt2/PKBβ ( akt2−/−) and in their wild-type littermates ( akt2+/+). Plasma glucose concentration was significantly higher in akt2−/− mice than in akt2+/+ mice but was virtually identical to the plasma glucose concentration in fructose-treated akt2+/+ mice. Urinary glucose excretion was significantly higher in akt2−/− mice compared with akt2+/+ mice with or without fructose treatment. Moreover, the glucose-induced depolarization of proximal tubular cells was significantly smaller in isolated, perfused renal tubules from akt2−/− mice than in those from akt2+/+ mice. In conclusion, Akt2/PKBβ plays a role in the regulation of renal glucose transport.

155-LB: The Increase in Endogenous Glucose Production with SGLT2 Inhibition Is Unchanged by Renal Denervation but Highly Correlates to Urinary Glucose Excretion

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 155-LB
Author(s):  
CAROLINA SOLIS-HERRERA ◽  
MARIAM ALATRACH ◽  
CHRISTINA AGYIN ◽  
HENRI HONKA ◽  
RUPAL PATEL ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Urinary Glucose Excretion ◽  
Urinary Glucose ◽  
Sglt2 Inhibition ◽  
Endogenous Glucose ◽  
Glucose Excretion

scholarly journals Direct Chemical Measurement of the λ of the Lumped Constant of the [14C]Deoxyglucose Method in Rat Brain: Effects of Arterial Plasma Glucose Level on the Distribution Spaces of [14C]Deoxyglucose and Glucose and on λ

1989 ◽  
Vol 9 (3) ◽  
pp. 304-314 ◽  
Author(s):  
Kentaro Mori ◽  
Nancy Cruz ◽  
Gerald Dienel ◽  
Thomas Nelson ◽  
Louis Sokoloff
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Severe Hypoglycemia ◽  
Plasma Glucose Concentration ◽  
Operational Equation ◽  
Chemical Measurements ◽  
Lumped Constant ◽  
Dg Method ◽  
Arterial Plasma ◽  
Distribution Spaces

The lumped constant in the operational equation of the 2-[14C]deoxyglucose (DG) method contains the factor λ that represents the ratio of the steady-state tissue distribution spaces for [14C]DG and glucose. The lumped constant has been shown to vary with arterial plasma glucose concentration. Predictions based mainly on theoretical grounds have suggested that disproportionate changes in the distribution spaces for [14C]DG and glucose and in the value of λ are responsible for these variations in the lumped constant. The influence of arterial plasma glucose concentration on the distribution spaces for DG and glucose and on λ were, therefore, determined in the present studies by direct chemical measurements. The brain was maintained in steady states of delivery and metabolism of DG and glucose by programmed intravenous infusions of both hexoses designed to produce and maintain constant arterial concentrations. Hexose concentrations were assayed in acid extracts of arterial plasma and freeze-blown brain. Graded hyperglycemia up to 28 m M produced progressive decreases in the distribution spaces of both hexoses from their normoglycemic values (e.g., ∼ – 20% for glucose and – 50% for DG at 28 m M). In contrast, graded hypoglycemia progressively reduced the distribution space for glucose and increased the space for [14C]DG. The values for λ were comparatively stable in normoglycemic and hyperglycemic conditions but rose sharply (e.g., as much as 9–10-fold at 2 m M) in severe hypoglycemia.

scholarly journals Comparative Study of Fasting Plasma Glucose Concentration and Glucose Challenge Test for Screening Gestational Diabetes Mellitus

2014 ◽  
Vol 6 (2) ◽  
pp. 75-78
Author(s):  
Sujaya Sham ◽  
B Poornima R Bhat ◽  
Aruna Kamath
Keyword(s):  
Diabetes Mellitus ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Glucose Concentration ◽  
Challenge Test ◽  
Plasma Glucose Concentration ◽  
Fasting Plasma ◽  
Glucose Challenge Test ◽  
Glucose Challenge ◽  
Fasting Plasma Glucose Concentration

ABSTRACT Background To compare the sensitivity and specificity of fasting plasma glucose (FPG) with that of standard glucose challenge test (GCT). Materials and methods Eighty-nine eligible pregnant women underwent GCT between 24th and 28th gestational week, followed by a diagnostic 3 hours 100 gm oral glucose tolerance test within 1 week. Out patient clinic in Father Muller Medical College Hospital, Mangalore. Data was analyzed for significance by chi-square test. Results Fasting plasma glucose concentration at a threshold value of 90 mg/dl and GCT at recommended standard threshold of 140 mg/dl yielded sensitivities of 66.7% and 100% respectively and specificities of 87.3% and 46.5% respectively. Reducing the threshold value of FPG to 80 mg/dl increased the sensitivity of test to 91.7% with specificity of 54.9% which was comparable to standard GCT, in our study. Conclusion Measuring FPG concentration using a cut-off of. 80 mg/dl is an easier, tolerable and more cost effective procedure than GCT for detecting more severe cases of GDM, i.e. the diabetes mellitus group. In resource poor settings with population belonging to average risk or high risk category, FPG at a cut-off of 90 mg/dl can be used to screen GDM. How to cite this article Sham S, Bhat BPR, Kamath A. Comparative Study of Fasting Plasma Glucose Concentration and Glucose Challenge Test for Screening Gestational Diabetes Mellitus. J South Asian Feder Obst Gynae 2014;6(2):75-78.

A single bolus infusion of C-reactive protein increases gluconeogenesis and plasma glucose concentration in humans

Metabolism ◽  
2007 ◽  
Vol 56 (11) ◽  
pp. 1576-1582 ◽  
Author(s):  
Rakesh S. Birjmohun ◽  
Radjesh J. Bisoendial ◽  
Sander I. van Leuven ◽  
Mariette Ackermans ◽  
Aelko Zwinderman ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Glucose Concentration ◽  
C Reactive Protein ◽  
Bolus Infusion ◽  
Single Bolus ◽  
Reactive Protein

Overnight inhibition of insulin secretion restores pulsatility and proinsulin/insulin ratio in type 2 diabetes

2000 ◽  
Vol 279 (3) ◽  
pp. E520-E528 ◽  
Author(s):  
Thomas Laedtke ◽  
Lise Kjems ◽  
Niels Pørksen ◽  
Ole Schmitz ◽  
Johannes Veldhuis ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Glucose Concentration ◽  
Molar Ratio ◽  
Β Cell ◽  
First Phase Insulin Secretion ◽  
Clinical Experiments

Impaired insulin secretion in type 2 diabetes is characterized by decreased first-phase insulin secretion, an increased proinsulin-to-insulin molar ratio in plasma, abnormal pulsatile insulin release, and heightened disorderliness of insulin concentration profiles. In the present study, we tested the hypothesis that these abnormalities are at least partly reversed by a period of overnight suspension of β-cell secretory activity achieved by somatostatin infusion. Eleven patients with type 2 diabetes were studied twice after a randomly ordered overnight infusion of either somatostatin or saline with the plasma glucose concentration clamped at ∼8 mmol/l. Controls were studied twice after overnight saline infusions and then at a plasma glucose concentration of either 4 or 8 mmol/l. We report that in patients with type 2 diabetes, 1) as in nondiabetic humans, insulin is secreted in discrete insulin secretory bursts; 2) the frequency of pulsatile insulin secretion is normal; 3) the insulin pulse mass is diminished, leading to decreased insulin secretion, but this defect can be overcome acutely by β-cell rest with somatostatin; 4) the reported loss of orderliness of insulin secretion, attenuated first-phase insulin secretion, and elevated proinsulin-to-insulin molar ratio also respond favorably to overnight inhibition by somatostatin. The results of these clinical experiments suggest the conclusion that multiple parameters of abnormal insulin secretion in patients with type 2 diabetes mechanistically reflect cellular depletion of immediately secretable insulin that can be overcome by β-cell rest.

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