Diminished arginine-stimulated insulin secretion in trained men

1990 ◽  
Vol 69 (1) ◽  
pp. 261-267 ◽  
Author(s):  
F. Dela ◽  
K. J. Mikines ◽  
B. Tronier ◽  
H. Galbo
Keyword(s):  
Growth Hormone ◽  
Insulin Secretion ◽  
Beta Cell ◽  
Insulin Response ◽  
Cell Secretion ◽  
Cell Adaptation ◽  
Glucose Stimulated Insulin Secretion ◽  
Beta Hydroxybutyrate ◽  
Beta Cell Adaptation ◽  
Beta Cell Secretion

Glucose-stimulated insulin secretion is depressed by training. To further elucidate the beta-cell adaptation to training, a nonglucose secretagogue was applied. Arginine was infused for 90 min to seven trained and seven untrained young men. Arginine and glucose concentrations increased identically in the groups. The insulin response was biphasic and waned despite increasing arginine concentrations. Both these phases as well as C-peptide responses were reduced in trained subjects, whereas proinsulin responses were similar in the groups. Identical increases were found in glucagon, growth hormone, catecholamines, and production and disappearance of glucose; identical decreases were found in free fatty acids, glycerol, and beta-hydroxybutyrate. In conclusion, in men training diminishes both arginine- and glucose-stimulated insulin secretion, indicating a profound beta-cell adaptation. Being enhanced, the effects of insulin on both production and disposal of glucose are changed in the opposite direction to beta-cell secretion by training. The responses of glucagon- and growth hormone-secreting cells to arginine do not change with training.

Effect of 7 days of bed rest on dose-response relation between plasma glucose and insulin secretion

1989 ◽  
Vol 257 (1) ◽  
pp. E43-E48 ◽  
Author(s):  
K. J. Mikines ◽  
F. Dela ◽  
B. Tronier ◽  
H. Galbo
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Insulin Response ◽  
Bed Rest ◽  
Glucose Disposal ◽  
Cell Secretion ◽  
Hyperglycemic Clamp ◽  
Peripheral Insulin Resistance ◽  
Glucose Stimulated Insulin Secretion ◽  
Beta Cell Secretion

Physical training decreases glucose-stimulated insulin secretion. To further explore the influence of the level of daily physical activity on beta-cell secretion, the effect of 7 days of bed rest was studied in six young, healthy men by sequential hyperglycemic clamp technique (7, 11, and 20 mM glucose, each step lasting 90 min). At 11 and 20 mM glucose, insulin concentrations in plasma were higher after (87 +/- 11 and 303 +/- 63 microU/ml) than before (63 +/- 5 and 251 +/- 50 microU/ml, P less than 0.05) bed rest. Also C-peptide levels were higher after bed rest than before during glucose stimulation. The responses of other hormones, metabolites, or electrolytes influencing beta-cell secretion were not influenced by bed rest. In spite of increased insulin levels after bed rest, glucose disposal at 20 mM of glucose was significantly lower after bed rest than before. It is concluded that bed rest for 7 days increases the glucose-stimulated insulin response, at least partly due to a beta-cell adaptation increasing glucose-stimulated insulin secretion. However, the insulin secretion does not increase adequately compared with the peripheral insulin resistance induced by bed rest.

scholarly journals Beta cell secretion of miR-375 to HDL is inversely associated with insulin secretion

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Leslie R. Sedgeman ◽  
Carine Beysen ◽  
Marisol A. Ramirez Solano ◽  
Danielle L. Michell ◽  
Quanhu Sheng ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Cell Secretion ◽  
Beta Cell Secretion

Effects of training and detraining on dose-response relationship between glucose and insulin secretion

1989 ◽  
Vol 256 (5) ◽  
pp. E588-E596 ◽  
Author(s):  
K. J. Mikines ◽  
B. Sonne ◽  
B. Tronier ◽  
H. Galbo
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Plasma Glucose ◽  
Response Relationship ◽  
Cell Secretion ◽  
Dose Response Relationship ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Beta Cell Secretion ◽  
Training And Detraining

We studied the effect of training and detraining on the dose-response relationship between plasma glucose and beta-cell secretion in seven trained young men using sequential hyperglycemic clamp technique (7, 11, and 20 mM). Experiments were performed in the habitual state 15 h after last training session (T) as well as after 5 days of detraining (DT). Results were compared to data from seven untrained subjects (UT). Glucose-stimulated insulin, proinsulin, and C-peptide levels were lower in T than in UT. They increased during detraining but not to levels seen in UT. Furthermore, in T and DT, but not in UT, increases in C-peptide and proinsulin leveled off with increasing glucose concentrations. Estimated by C-peptide-to-insulin ratios, clearance of endogenous insulin was not influenced by T. Glucose uptake in tissue was the same in T, DT, and UT during clamps, despite lower insulin levels in T and DT. Differences between groups in counterregulatory hormones, fat metabolites, alanine, or electrolytes did not account for these findings. Oxygen consumption was higher in the basal state in T and DT compared with UT but increased similarly in all groups in response to glucose. Conclusions: regular physical activity causes an adaptive decrease in glucose-mediated beta-cell secretion in humans. The training-induced decrease in glucose-stimulated insulin secretion is accurately matched to increased insulin action, keeping glucose disposal constant at any given plasma glucose concentration. Finally, training increases basal metabolic rate but does not influence glucose-induced thermogenesis or clearance of endogenous insulin.

scholarly journals The Role of Fatty Acid Signaling in Islet Beta-Cell Adaptation to Normal Pregnancy

2022 ◽  
Vol 12 ◽  
Author(s):  
Jee-Hye Kim ◽  
Viviane Delghingaro-Augusto ◽  
Jeng Yie Chan ◽  
D. Ross Laybutt ◽  
Joseph Proietto ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
Beta Cell ◽  
Liver Glycogen ◽  
Oral Glucose ◽  
Pregnant Rat ◽  
Islet Beta Cell ◽  
Glucose Stimulated Insulin Secretion ◽  
Beta Cell Adaptation

BackgroundMaintenance of a normal fetal nutrient supply requires major adaptations in maternal metabolic physiology, including of the islet beta-cell. The role of lipid signaling processes in the mechanisms of islet beta-cell adaptation to pregnancy has been minimally investigated.ObjectiveTo determine the effects of pregnancy on islet fatty acid (FA) metabolic partitioning and FA augmentation of glucose-stimulated insulin secretion (GSIS).MethodsAge matched virgin, early pregnant (gestational day-11, G11) and late pregnant (G19) Sprague-Dawley rats were studied. Fasted and fed state biochemistry, oral glucose tolerance tests (OGTT), and fasted and post-OGTT liver glycogen, were determined to assess in vivo metabolic characteristics. In isolated islets, FA (BSA-bound palmitate 0.25 mmol/l) augmentation of GSIS, FA partitioning into esterification and oxidation processes using metabolic tracer techniques, lipolysis by glycerol release, triacylglycerols (TG) content, and the expression of key beta-cell genes were determined.ResultsPlasma glucose in pregnancy was lower, including during the OGTT (glucose area under the curve 0-120 min (AUC0-120); 655±24 versus 849±13 mmol.l-1.min; G19 vs virgin; P<0.0001), with plasma insulin concentrations equivalent to those of virgin rats (insulin AUC0-120; 97±7 versus 83±7 ng.ml-1.min; G19 vs virgin; not significant). Liver glycogen was depleted in fasted G19 rats with full recovery after oral glucose. Serum TG increased during pregnancy (4.4±0.4, 6.7±0.5; 17.1±1.5 mmol/l; virgin, G11, G19, P<0.0001), and islet TG content decreased (147±42, 172±27, 73±13 ng/µg protein; virgin, G11, G19; P<0.01). GSIS in isolated islets was increased in G19 compared to virgin rats, and this effect was augmented in the presence of FA. FA esterification into phospholipids, monoacylglycerols and TG were increased, whereas FA oxidation was reduced, in islets of pregnant compared to virgin rats, with variable effects on lipolysis dependent on gestational age. Expression of Ppargc1a, a key regulator of mitochondrial metabolism, was reduced by 51% in G11 and 64% in G19 pregnant rat islets compared to virgin rat islets (P<0.001).ConclusionA lowered set-point for islet and hepatic glucose homeostasis in the pregnant rat has been confirmed. Islet adaptation to pregnancy includes increased FA esterification, reduced FA oxidation, and enhanced FA augmentation of glucose-stimulated insulin secretion.

Beta Cell Function is Disrupted in Patients with Systemic Lupus Erythematosus

Rheumatology ◽  
2020 ◽  
Author(s):  
Alicia García-Dorta ◽  
Juan Carlos Quevedo-Abeledo ◽  
Íñigo Rua-Figueroa ◽  
Antonia M de Vera-González ◽  
Alejandra González-Delgado ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Beta Cell ◽  
Lupus Erythematosus ◽  
Cell Function ◽  
Multivariable Analysis ◽  
Serum Levels ◽  
Cell Secretion ◽  
Systemic Lupus ◽  
Proinsulin Processing ◽  
Beta Cell Secretion

Abstract Introduction To investigate how markers of beta cell secretion (proinsulin-processing metabolites) are expressed in systemic lupus erythematosus (SLE) patients and their potential relation to features associated with the disease such as activity or damage. Methods 144 SLE patients and 69 nondiabetic sex- and age-matched controls were assessed. Beta-cell secretion molecules, as measured by insulin, split and intact proinsulins, and C-peptide levels were analyzed in both groups. Multiple regression analysis was performed to compare proinsulin propeptides between groups and to explore the interrelations with SLE features. Analyses were adjusted for glucocorticoid intake and for insulin resistance classic risk factors. Results Fully multivariable analysis demonstrated that regardless of glucocorticoid use, SLE patients exhibited higher levels of split proinsulin. Likewise, the split proinsulin-to-insulin ratio was upregulated in patients with SLE undergoing glucocorticoid therapy (beta coef. 0.19 [95%CI 0.07–0.30], p= 0.002) or not (beta coef. 0.09 [95%CI 0.01–0.17), p= 0.025). Similar results were found for the intact proinsulin-to-insulin ratio, although differences were only statistically significant for patients taking glucocorticoids (beta coef. 0.08 [95%CI 0.03–0.12], p= 0.001). SLE damage score was associated with higher serum levels of intact (beta coef. 0.51 [95%CI 0.17–0.86] pmol/l, p= 0.004) and split proinsulins (beta coef. 1.65 [95%CI 0.24–3.06] pmol/l, p= 0.022) after multivariable analysis, including disease duration and prednisone use. Conclusion Among patients with SLE, proinsulin-processing metabolites, a marker of beta-cell disruption, are upregulated compared with matched controls. This disproportionate hyperproinsulinemia can be explained by the damage produced by the disease and occurs independently of prednisone use.

scholarly journals Incretin Receptor Null Mice Reveal Key Role of GLP-1 but Not GIP in Pancreatic Beta Cell Adaptation to Pregnancy

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e96863 ◽  
Author(s):  
R. Charlotte Moffett ◽  
Srividya Vasu ◽  
Bernard Thorens ◽  
Daniel J. Drucker ◽  
Peter R. Flatt
Keyword(s):  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Cell Adaptation ◽  
Beta Cell Adaptation
Sign in / Sign up

Export Citation Format

Share Document