scholarly journals Effect of N G ‐monomethyl l ‐arginine on microvascular blood flow and glucose metabolism after an oral glucose load

2020 ◽  
Vol 27 (3) ◽  
Author(s):  
Alexandra Högstedt ◽  
Fredrik Iredahl ◽  
Erik Tesselaar ◽  
Simon Farnebo
2016 ◽  
Vol 23 (7) ◽  
pp. 597-605 ◽  
Author(s):  
Fredrik Iredahl ◽  
Alexandra Högstedt ◽  
Joakim Henricson ◽  
Folke Sjöberg ◽  
Erik Tesselaar ◽  
...  

2017 ◽  
Vol 6 (4) ◽  
pp. 243-252 ◽  
Author(s):  
Tao Yuan ◽  
Lanping Jiang ◽  
Chen Chen ◽  
Xiaoyan Peng ◽  
Min Nie ◽  
...  

Objective Impaired glucose metabolism and insulin sensitivity have been reported in patients with Gitelman syndrome (GS), but insulin secretion and the related mechanisms are not well understood. Design and methods The serum glucose levels, insulin secretion and insulin sensitivity were evaluated in patients with GS (n = 28), patients with type 2 diabetes mellitus (DM) and healthy individuals (n = 20 in both groups) using an oral glucose tolerance test. Serum and urine sodium, potassium and creatinine levels were measured at 0, 30, 60, 120 and 180 min after an oral glucose load was administered. Results The areas under the serum glucose curves were higher in the GS patients than those in the healthy controls (17.4 ± 5.1 mmol·h/L vs 14.5 ± 2.8 mmol·h/L, P = 0.02) but lower than those in the DM patients (24.8 ± 5.3 mmol·h/L, P < 0.001). The areas under the serum insulin curves and the insulin secretion indexes in GS patients were higher than those in DM patients and lower than those in healthy subjects. The insulin secretion-sensitivity index of GS patients was between that of healthy subjects and DM patients, but the insulin sensitivity indices were not different among the three groups. After one hour of glucose administration, the serum potassium level significantly decreased from baseline, and the urinary potassium-to-creatinine ratio increased gradually and peaked at 2 h. Conclusions Glucose metabolism and insulin secretion were impaired in GS patients, but insulin sensitivity was comparable between GS patients and patients with type 2 DM. After administration of an oral glucose load, the plasma potassium level decreased in GS patients due to the increased excretion of potassium in the urine.


2006 ◽  
Vol 290 (6) ◽  
pp. E1198-E1204 ◽  
Author(s):  
Vincent Rigalleau ◽  
Marie-Christine Beauvieux ◽  
Jean-Louis Gallis ◽  
Henri Gin ◽  
Phillippe Schneiter ◽  
...  

The plasma glucose excursion may influence the metabolic responses after oral glucose ingestion. Although previous studies adressed the effects of hyperglycemia in conditions of hyperinsulinemia, it has not been evaluated whether the route of glucose administration (oral vs. intravenous) plays a role. Our aim was to determine the effects of moderately controlled hyperglycemia on glucose metabolism before and after oral glucose ingestion. Eight normal men underwent two oral glucose clamps at 6 and 10 mmol/l plasma glucose. Glucose turnover and cycling rates were measured by infusion of [2H7]glucose. The oral glucose load was labeled by d-[6,6-2H2]glucose to monitor exogenous glucose appearance, and respiratory exchanges were measured by indirect calorimetry. Sixty percent of the oral glucose load appeared in the systemic circulation during both the 6 and 10 mmol/l plasma glucose tests, although less endogenous glucose appeared during the 10 mmol/l tests before glucose ingestion ( P < 0.05). This inhibitory effect of hyperglycemia was not detectable after oral glucose ingestion, although glucose utilization was increased (+28%, P < 0.05) due to increased nonoxidative glucose disposal [10 vs. 6 mmol/l: +20%, not significant (NS) before oral glucose ingestion; +40%, P < 0.05 after oral glucose ingestion]. Glucose cycling rates were increased by hyperglycemia (+13% before oral glucose ingestion, P < 0.001; +31% after oral glucose ingestion, P < 0.05) and oral glucose ingestion during both the 6 (+10%, P < 0.05) and 10 mmol/l (+26%, P < 0.005) tests. A moderate hyperglycemia inhibits endogenous glucose production and contributes to glucose tolerance by enhancing nonoxidative glucose disposal. Hyperglycemia and oral glucose ingestion both stimulate glucose cycling.


2014 ◽  
Vol 60 (1) ◽  
pp. S352-S353
Author(s):  
E. Vanni ◽  
L. Mezzabotta ◽  
C. Rosso ◽  
M. Gaggini ◽  
R. Gambino ◽  
...  

Diabetes ◽  
1975 ◽  
Vol 24 (12) ◽  
pp. 1066-1071 ◽  
Author(s):  
K. Yasuda ◽  
T. Sato ◽  
T. Furuyama ◽  
K. Yashinaga

Diabetes ◽  
1985 ◽  
Vol 34 (6) ◽  
pp. 580-588 ◽  
Author(s):  
E. Ferrannini ◽  
O. Bjorkman ◽  
G. A. Reichard ◽  
A. Pilo ◽  
M. Olsson ◽  
...  

Angiology ◽  
1998 ◽  
Vol 49 (9) ◽  
pp. 815-826 ◽  
Author(s):  
Shigeo Takata ◽  
Atsuhiro Shimakura ◽  
Satoru Sakagami ◽  
Yukio Nakamura ◽  
Hitoshi Ohkuwa ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document