Interaction between glucose metabolism and endogenous insulin release in hypertension

Metabolism ◽  
2002 ◽  
Vol 51 (3) ◽  
pp. 297-303 ◽  
Author(s):  
Silvia Natalucci ◽  
Massimo Boemi ◽  
Daniele Fumelli ◽  
Paolo Fumelli ◽  
Roberto Burattini
Keyword(s):  
Glucose Metabolism ◽  
Insulin Release ◽  
Endogenous Insulin

Temporal analysis of myocardial glucose metabolism by 2-[18F]fluoro-2-deoxy-D-glucose

1990 ◽  
Vol 259 (4) ◽  
pp. H1022-H1031 ◽  
Author(s):  
V. T. Nguyen ◽  
K. A. Mossberg ◽  
T. J. Tewson ◽  
W. H. Wong ◽  
R. W. Rowe ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Work Load ◽  
Temporal Analysis ◽  
Input Function ◽  
Graphical Analysis ◽  
Time Activity ◽  
Myocardial Glucose Metabolism ◽  
Fractional Rate ◽  
Endogenous Insulin

To assess kinetic changes of myocardial glucose metabolism after physiological interventions, we perfused isolated working rat hearts with glucose and 2-[18F]fluoro-2-deoxy-D-glucose (2-FDG). Tissue uptake of 2-FDG and the input function were measured on-line by external detection. The fractional rate of 2-FDG phosphorylation was determined by graphical analysis of time-activity curves. The steady-state uptake of 2-FDG was linear with time, and the tracer was retained predominantly in its phosphorylated form. Tissue accumulation of 2-FDG decreased with a reduction in work load and with the addition of competing substrates. Insulin caused a significant increase in 2-FDG accumulation in hearts from fasted but not from fed animals. We conclude that in the isolated working rat heart there is rapid adjustment of exogenous substrate utilization and that most interventions known to alter glucose metabolism induce parallel changes in 2-FDG uptake. Qualitative differences in the in vitro response to insulin may be affected by the presence of either endogenous insulin or glycogen.

Pancreatic Islet Function in ω3 Fatty Acid-Depleted Rats: Glucose Metabolism and Nutrient-Stimulated Insulin Release

Endocrine ◽  
2006 ◽  
Vol 29 (3) ◽  
pp. 457-466 ◽  
Author(s):  
Berrin Oguzhan ◽  
Ying Zhang ◽  
Karim Louchami ◽  
Philippe Courtois ◽  
Laurence Portois ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Glucose Metabolism ◽  
Insulin Release ◽  
Pancreatic Islet ◽  
Islet Function

Feedback inhibition by biosynthetic human insulin of insulin release in healthy human subjects

1982 ◽  
Vol 243 (6) ◽  
pp. E476-E482 ◽  
Author(s):  
W. K. Waldhausl ◽  
S. Gasic ◽  
P. Bratusch-Marrain ◽  
A. Korn ◽  
P. Nowotny
Keyword(s):  
Insulin Release ◽  
Human Insulin ◽  
Clearance Rate ◽  
Feedback Inhibition ◽  
Insulin Clearance ◽  
Metabolic Clearance ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Hepatic Insulin Clearance ◽  
Biosynthetic Human Insulin

To determine the impact of biosynthetic human insulin (BHI) on endogenous insulin release, splanchnic output and arterial concentrations of C-peptide were measured in eight healthy men after intravenous administration of 0, 0.5, 1.25, U BHI . m-2 . h-1 for 70 min each. Euglycemia was maintained by a variable glucose infusion. Arterial levels of serum insulin were 48 +/- 6 pmol/liter before and 135 +/- 12, 265 +/- 18, and 593 +/- 47 pmol/liter after BHI infusion. Splanchnic C-peptide output was reduced by BHI infusion from 88 +/- 10 pmol/min before to 50 +/- 9, 28 +/- 10, and 18 +/- 16 pmol/min (P less than 0.0025). Simultaneously, arterial concentrations of C-peptide fell from 539 +/- 54 pmol/liter by 29 and 43% when 1.25 and 2.5 U . m-2 . h-1 of BHI were administered. Hepatic insulin uptake was directly related with BHI infusion rate (r = 0.88) and rose during BHI administration from a basal value of 58 +/- 7 to an uptake of 265 +/- 31 pmol/min when 2.5 U . m-2 . h-1 were infused (P less than 0.0005). Basal hepatic insulin clearance was 4.75 +/- 0.60 ml . kg-1 . min-1 and remained unchanged after BHI infusion as did hepatic fractional extraction of insulin, which was 61 +/- 4% in the basal state. Metabolic clearance rate of immunoreactive insulin (MCRi) was dose-dependently reduced by BHI infusion, whereas the relative share of hepatic insulin clearance in total MCRi rose simultaneously (P less than 0.01). We conclude that feedback inhibition of endogenous insulin release may play an important role in vivo. Furthermore, it appears that nonhepatic insulin degradation is a saturable phenomenon as total MCRi fell in the presence of its unchanged hepatic clearance rate after the infusion of large amounts of BHI.

scholarly journals Glucose-Dependent Insulinotropic Polypeptide (GIP) Inhibits Bone Resorption Independently of Insulin and Glycemia

2017 ◽  
Vol 103 (1) ◽  
pp. 288-294 ◽  
Author(s):  
Mikkel B Christensen ◽  
Asger Lund ◽  
Salvatore Calanna ◽  
Niklas R Jørgensen ◽  
Jens J Holst ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Insulin Release ◽  
Plasma Glucose ◽  
Saline Infusion ◽  
Bone Homeostasis ◽  
Collagen Crosslinks ◽  
Procollagen Type ◽  
Endogenous Insulin ◽  
Gut Hormone

Abstract Context The gut hormone glucose-dependent insulinotropic polypeptide (GIP) causes postprandial insulin release and inhibits bone resorption assessed by carboxy-terminal collagen crosslinks (CTX). Objective To study if GIP affects bone homeostasis biomarkers independently of insulin release and glycemic level. Design Randomized, double-blinded, crossover study with 5 study days. Patients Ten male C-peptide-negative patients with type 1 diabetes. Interventions On 3 matched days with “low glycemia” (plasma glucose in the interval 3 to 7 mmol/L for 120 minutes), we administered intravenous (IV) GIP (4 pmol × kg−1 × min−1), glucagon-like peptide 1 (1 pmol × kg−1 × min−1), or placebo (saline), and on 2 matched days with “high glycemia” (plasma glucose 12 mmol/L for 90 minutes), we administered either GIP or saline. Main Outcome Measures CTX, procollagen type 1 N-terminal propeptide (P1NP), and parathyroid hormone (PTH). Results During low glycemia: GIP progressively suppressed CTX from baseline by up to 59 ± 18% compared with 24 ± 10% during saline infusion (P < 0.0001). Absolute values of P1NP and PTH did not differ between days. During high glycemia: GIP suppressed CTX from baseline by up to 59 ± 19% compared with 7 ± 9% during saline infusion (P < 0.0001). P1NP did not differ between days. GIP suppressed PTH after 60 minutes compared with saline (P < 0.01), but this difference disappeared after 90 minutes. Conclusions Short-term GIP infusions robustly reduce bone resorption independently of endogenous insulin secretion and during both elevated and low plasma glucose, but have no effect on P1NP or PTH after 90 minutes.

POTENTIATION OF INSULIN RELEASE BY GLUCOSE IN MAN

1975 ◽  
Vol 79 (3) ◽  
pp. 502-510 ◽  
Author(s):  
Erol Cerasi
Keyword(s):  
Glucose Metabolism ◽  
Adenylate Cyclase ◽  
Beta Cell ◽  
Insulin Release ◽  
Insulin Response ◽  
Glucose Infusion ◽  
Insulin Responses

ABSTRACT If two consecutive glucose infusions are administered with 40 min of rest between, the insulin response to the second challenge is markedly potentiated. When the insulin response to the first glucose infusion was suppressed by 65 % with the aid of adrenaline, potentiation of the insulin response to the second infusion was not modified. This suggests that the generation of a state of enhancement in the islet does not necessitate that glucose exerts its insulin releasing action. It is postulated that islet glucose metabolism may be involved in producing the potentiation. Pretreatment of the subjects with a glucose infusion enhanced also the insulin responses to glucagon and to tolbutamide, given intravenously 50 min later. Thus, the potentiation generated by glucose is not restricted to the insulinogenic signal induced by glucose. The eventual role that the beta-cell adenylate cyclase may play in this respect is discussed.

scholarly journals Abnormal glucose metabolism accompanies failure of glucose to stimulate insulin release from a rat pancreatic cell line (RINm5F)

1983 ◽  
Vol 212 (2) ◽  
pp. 439-443 ◽  
Author(s):  
P A Halban ◽  
G A Praz ◽  
C B Wollheim
Keyword(s):  
Glucose Metabolism ◽  
Cell Line ◽  
Insulin Release ◽  
Glucose Utilization ◽  
Rinm5f Cells ◽  
Pancreatic Cell ◽  
Abnormal Glucose Metabolism ◽  
Isolated Rat Islets ◽  
Stimulate Insulin Release ◽  
Stimulation Of

Glucose metabolism and insulin release were studied in isolated rat islets and in an insulin-producing rat cell-line (RINm5F). Intact islets displayed two components of glucose utilization, with glucose stimulation of insulin release being associated with the high-Km component (reflecting glucokinase-like activity). Glucose failed to stimulate insulin release from RINm5F cells, which only displayed a single low-Km component of glucose utilization. Only low-Km (hexokinase-like) glucose-phosphorylating activity was found for disrupted RINm5F cells. These changes in glucose metabolism may contribute towards the failure of glucose to stimulate insulin release from RINm5F cells.

scholarly journals Detrimental actions of metabolic syndrome risk factor, homocysteine, on pancreatic β-cell glucose metabolism and insulin secretion

2006 ◽  
Vol 189 (2) ◽  
pp. 301-310 ◽  
Author(s):  
S Patterson ◽  
P R Flatt ◽  
L Brennan ◽  
P Newsholme ◽  
N H McClenaghan
Keyword(s):  
Metabolic Syndrome ◽  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Insulin Release ◽  
Cell Function ◽  
Tca Cycle ◽  
Gastric Inhibitory Polypeptide ◽  
Β Cell ◽  
The Metabolic Syndrome ◽  
Cell Glucose

Elevated plasma homocysteine has been reported in individuals with diseases of the metabolic syndrome including vascular disease and insulin resistance. As homocysteine exerts detrimental effects on endothelial and neuronal cells, this study investigated effects of acute homocysteine exposure on β-cell function and insulin secretion using clonal BRIN-BD11 β-cells. Acute insulin release studies in the presence of various test reagents were performed using monolayers of BRIN-BD11 cells and samples assayed by insulin radioimmunoassay. Cellular glucose metabolism was assessed by nuclear magnetic resonance (NMR) analysis following 60-min exposure of BRIN-BD11 cell monolayers to glucose in either the absence or presence of homocysteine. Homocysteine dose-dependently inhibited insulin release at moderate and stimulatory glucose concentrations. This inhibitory effect was reversible at all but the highest concentration of homocysteine. 13C-glucose NMR demonstrated decreased labelling of glutamate from glucose at positions C2, C3 and C4, indicating that the tricarboxylic acid (TCA) cycle-dependent glucose metabolism was reduced in the presence of homocysteine. Homocysteine also dose-dependently inhibited insulinotropic responses to a range of glucose-dependent secretagogues including nutrients (alanine, arginine, 2-ketoisocaproate), hormones (glucagon-like peptide-1 (7–36)amide, gastric inhibitory polypeptide and cholecystokinin-8), neurotransmitter (carbachol), drug (tolbutamide) as well as a depolarising concentration of KCl or elevated Ca2+. Insulin secretion induced by activation of adenylate cyclase and protein kinase C pathways with forskolin and phorbol 12-myristate 13-acetate were also inhibited by homocysteine. These effects were not associated with any adverse action on cellular insulin content or cell viability, and there was no increase in apoptosis/necrosis following exposure to homocysteine. These data indicate that homocysteine impairs insulin secretion through alterations in β-cell glucose metabolism and generation of key stimulus-secretion coupling factors. The participation of homocysteine in possible β-cell demise merits further investigation.

Glucose metabolism and insulin release in mouse beta HC9 cells, as model for wild-type pancreatic beta-cells

1996 ◽  
Vol 270 (5) ◽  
pp. E846-E857 ◽  
Author(s):  
Y. Liang ◽  
G. Bai ◽  
N. Doliba ◽  
C. Buettger ◽  
L. Wang ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Beta Cell ◽  
Cell Line ◽  
Insulin Release ◽  
Cell Lines ◽  
Pancreatic Beta Cells ◽  
Pancreatic Beta Cell ◽  
Glucose Sensing ◽  
Cell Functions ◽  
Glucose Phosphorylation

Glucose metabolism and its relationship with glucose-induced insulin release were studied in beta HC9 and beta TC3 cells to identify and characterize key factors controlling the intermediary metabolism of glucose and glucose-induced insulin release. The beta HC9 cell line, derived from pancreatic islets with beta-cell hyperplasia, is characterized by a normal concentration-dependency curve for glucose-stimulated insulin release, whereas the beta TC3 cell line, derived from pancreatic beta-cell tumors, shows a marked leftward shift of this curve. Maximum velocity and the Michaelis-Menten constant of glucose uptake in beta HC9 and beta TC3 cells were similar, even though GLUT-2 expression in these two cell lines differed. In both cell lines, the kinetic characteristics of glucose usage, glucose oxidation, and glucose-induced oxygen consumption were similar to those of glucose phosphorylation, indicating that the kinetics of glucose metabolism from the glucose phosphorylation step in the cytosol to the mitochondrial process of oxidative phosphorylation are determined by the glucose-phosphorylating enzyme, that is, by glucokinase in beta HC9 cells and by hexokinase in beta TC3 cells. Thus beta HC9 cells provide an opportunity for the quantitative analysis of glucose metabolism, the associated generation of coupling factors, and other essential beta-cell functions involved in glucose sensing and insulin secretion.

Sign in / Sign up

Export Citation Format

Share Document