Effects of taurine on plasma glucose concentration and active glucose transport in the small intestine

2017 ◽  
Vol 88 (11) ◽  
pp. 1763-1767 ◽  
Author(s):  
Yo Tsuchiya ◽  
Koichi Kawamata
2010 ◽  
Vol 298 (5) ◽  
pp. F1113-F1117 ◽  
Author(s):  
Daniela S. Kempe ◽  
Gulab Siraskar ◽  
Henning Fröhlich ◽  
Anja T. Umbach ◽  
Michael Stübs ◽  
...  

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.


1998 ◽  
Vol 18 (6) ◽  
pp. 632-638 ◽  
Author(s):  
William J. Powers ◽  
Joan L. Rosenbaum ◽  
Carmen S. Dence ◽  
Joanne Markham ◽  
Tom O. Videen

Few data regarding early developmental changes in cerebral (blood-to-brain) glucose transport (CTXglc) and CMRglc are available for humans. We measured CBF, CTXglc, and CMRglc with positron emission tomography at 4 to 7 days of life in six preterm human infants whose estimated gestational age was 25 to 34 weeks. The Michaelis-Menten constants Kt and Tmax were estimated from CTXglc and the calculated cerebral capillary plasma glucose concentration. Mean CMRglc was 8.8 μmol 100 g−1 min−1. The CMRglc did not correlate with plasma glucose concentration ( r = .315, P = .543), whereas CTXglc showed a significant correlation with plasma glucose concentration ( r = .836, P = .038). Estimation of the Michaelis-Menten constants from the best fit to the measured data produced values of Kt = 6.0 μmol mL−1 and Tmax = 32.6 μmol 100 g−1 min−1. These values for Kt in the developing human brain are similar to those that have been reported for the mature brain of adolescent and adult humans and adult nonhuman primates, indicating the affinity of the glucose transport protein for d-glucose is similar. However, Tmax is approximately one third to one half of the comparable values for mature brain, indicating a reduced number of available luminal transporters.


1989 ◽  
Vol 9 (3) ◽  
pp. 304-314 ◽  
Author(s):  
Kentaro Mori ◽  
Nancy Cruz ◽  
Gerald Dienel ◽  
Thomas Nelson ◽  
Louis Sokoloff

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.


2014 ◽  
Vol 6 (2) ◽  
pp. 75-78
Author(s):  
Sujaya Sham ◽  
B Poornima R Bhat ◽  
Aruna Kamath

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.


Metabolism ◽  
2007 ◽  
Vol 56 (11) ◽  
pp. 1576-1582 ◽  
Author(s):  
Rakesh S. Birjmohun ◽  
Radjesh J. Bisoendial ◽  
Sander I. van Leuven ◽  
Mariette Ackermans ◽  
Aelko Zwinderman ◽  
...  

2000 ◽  
Vol 279 (3) ◽  
pp. E520-E528 ◽  
Author(s):  
Thomas Laedtke ◽  
Lise Kjems ◽  
Niels Pørksen ◽  
Ole Schmitz ◽  
Johannes Veldhuis ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document