scholarly journals Novel extrapancreatic effects of incretin

2016 ◽  
Vol 7 (S1) ◽  
pp. 76-79 ◽  
Author(s):  
Yuichiro Yamada ◽  
Katsushi Tsukiyama ◽  
Takehiro Sato ◽  
Tatsunori Shimizu ◽  
Hiroki Fujita ◽  
...  
Keyword(s):  
Extrapancreatic Effects

Extrapancreatic effects of sulfonylurea drugs

1995 ◽  
Vol 28 ◽  
pp. S105-S108 ◽  
Author(s):  
Kohei Kaku ◽  
Yasushi Inoue ◽  
Toshio Kaneko
Keyword(s):  
Extrapancreatic Effects ◽  
Sulfonylurea Drugs

scholarly journals Pancreatic and Extrapancreatic Effects of Gastric Inhibitory Polypeptide

Diabetes ◽  
2006 ◽  
Vol 55 (Supplement 2) ◽  
pp. S86-S91 ◽  
Author(s):  
Y. Yamada ◽  
K. Miyawaki ◽  
K. Tsukiyama ◽  
N. Harada ◽  
C. Yamada ◽  
...  
Keyword(s):  
Gastric Inhibitory Polypeptide ◽  
Extrapancreatic Effects

1052-P: Investigation of the Extrapancreatic Effects of the DPP-4 Inhibitor Sitagliptin: A Randomized, Double-Blinded, Placebo-Controlled Crossover Trial in Totally Pancreatectomized Patients

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1052-P
Author(s):  
MILLE BAEKDAL ◽  
ASGER LUND ◽  
SOPHIE W. NIELSEN ◽  
CARSTEN HANSEN ◽  
JAN H. STORKHOLM ◽  
...  
Keyword(s):  
Crossover Trial ◽  
Double Blinded ◽  
Extrapancreatic Effects

Extrapancreatic effects of L-leucine infusion in leucine-sensitive and control subjects

Metabolism ◽  
1987 ◽  
Vol 36 (7) ◽  
pp. 697-702 ◽  
Author(s):  
John T. Devlin ◽  
Naji N. Abumrad ◽  
Benjamin Hoxworth ◽  
Randall Buckspan ◽  
Edward S. Horton
Keyword(s):  
Control Subjects ◽  
Extrapancreatic Effects ◽  
And Control

Extrapancreatic Effects of GIP and GLP-1

2004 ◽  
Vol 36 (11/12) ◽  
pp. 830-836 ◽  
Author(s):  
A. Vella ◽  
R. A. Rizza
Keyword(s):  
Extrapancreatic Effects

scholarly journals The Extrapancreatic Effects of Glucagon-Like Peptide-1 and Related Peptides

2009 ◽  
Vol 94 (6) ◽  
pp. 1843-1852 ◽  
Author(s):  
Rania Abu-Hamdah ◽  
Atoosa Rabiee ◽  
Graydon S. Meneilly ◽  
Richard P. Shannon ◽  
Dana K. Andersen ◽  
...  
Keyword(s):  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Extrapancreatic Effects

scholarly journals GLP-1-induced renal vasodilation in rodents depends exclusively on the known GLP-1 receptor and is lost in prehypertensive rats

2020 ◽  
Vol 318 (6) ◽  
pp. F1409-F1417 ◽  
Author(s):  
Elisa P. Jensen ◽  
Sophie Møller ◽  
Aleksander Vauvert Hviid ◽  
Simon Veedfald ◽  
Jens J. Holst ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Vascular Function ◽  
Vascular Effects ◽  
Renal Vasculature ◽  
Renal Effects ◽  
Vasodilatory Effect ◽  
Glucagon Like Peptide 1 ◽  
Extrapancreatic Effects ◽  
And Function ◽  
Renal Vascular

Glucagon-like peptide-1 (GLP-1) is an incretin hormone known to stimulate postprandial insulin release. However, GLP-1 also exerts extrapancreatic effects, including renal effects. Some of these renal effects are attenuated in hypertensive rats, where renal expression of GLP-1 receptors is reduced. Here, we assessed the expression and vascular function of GLP-1 receptors in kidneys from young prehypertensive rats. We also examined GLP-1-induced vasodilation in the renal vasculature in wild-type (WT) and GLP-1 receptor knockout mice using wire and pressure myography and the isolated perfused juxtamedullary nephron preparation. We investigated whether GLP-1 and the metabolite GLP-1(9–36)amide had renal vascular effects independent of the known GLP-1 receptor. We hypothesized that hypertension decreased expression of renal GLP-1 receptors. We also hypothesized that GLP-1-induced renal vasodilatation depended on expression of the known GLP-1 receptor. In contrast to normotensive rats, no immunohistochemical staining or vasodilatory function of GLP-1 receptors was found in kidneys from prehypertensive rats. In WT mice, GLP-1 induced renal vasodilation and reduced the renal autoregulatory response. The GLP-1 receptor antagonist exendin 9–39 inhibited relaxation, and GLP-1(9–36)amide had no vasodilatory effect. In GLP-1 receptor knockout mice, no relaxation induced by GLP-1 or GLP-1(9–36)amide was found, the autoregulatory response in afferent arterioles was normal, and no GLP-1-induced reduction of autoregulation was found. We conclude that in prehypertensive kidneys, expression and function of GLP-1 receptors is lost. The renal vasodilatory effect of GLP-1 is mediated exclusively by the known GLP-1 receptor. GLP-1(9–36)amide has no renal vasodilatory effect. GLP-1 attenuates renal autoregulation by reducing the myogenic response.

Population-based modeling to demonstrate extrapancreatic effects of tolbutamide

1998 ◽  
Vol 274 (4) ◽  
pp. E758-E771 ◽  
Author(s):  
A. Rostami-Hodjegan ◽  
S. R. Peacey ◽  
E. George ◽  
S. R. Heller ◽  
G. T. Tucker
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Population Based ◽  
Hypoglycemic Effect ◽  
Sensitivity Index ◽  
Intravenous Glucose ◽  
Glucose Effectiveness ◽  
Intravenous Glucose Tolerance ◽  
Extrapancreatic Effects

Tolbutamide is used increasingly as an investigative tool in in vivo studies of the physiology of glucose tolerance. Its hypoglycemic effect in nondiabetic subjects is widely variable, reflecting possible variability in its pharmacokinetics, an insulinergic response, an extrapancreatic effect of the drug, or the hypoglycemic effect of insulin itself. Using population-based modeling, we have investigated the kinetics and dynamics of tolbutamide and assessed covariates in two groups of healthy subjects. The results indicate a high variability in insulinergic effect, measured by the area under of the curve of insulin (0–60 min), in response to tolbutamide injection (coefficient of variation = 29–96%). However, it appears that impaired insulin sensitivity is compensated by higher insulin secretion in response to tolbutamide. Thus the hypoglycemic effect of high insulin secretion is minimal in insulin-resistant subjects. Application of the model indicated that tolbutamide has appreciable extrapancreatic effects mediated by prolongation of the residence time of insulin in a remote effect and by enhancement of glucose effectiveness. An effect in increasing the insulin sensitivity index is also possible but could not be confirmed statistically for all groups of subjects studied. These observations may explain inconsistencies between the results of tolbutamide and insulin injection in the frequently sampled intravenous glucose tolerance test and call for further study of insulin- vs. tolbutamide-modified frequently sampled intravenous glucose tolerance tests in the assessment of the insulin sensitivity and glucose effectiveness indexes.

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