Beta-Cell Secretion in Glucose-Intolerant Subjects with High or Low Insulin Response to Glucose

2015 ◽  
pp. 226-230
Author(s):  
Enzo Bonora ◽  
Carlo Coscelli ◽  
Ugo Butturini
Keyword(s):  
Beta Cell ◽  
Insulin Response ◽  
Cell Secretion ◽  
Insulin Response To Glucose ◽  
Beta Cell Secretion ◽  
Low Insulin Response

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.

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 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.

Role of Ca2+ in impaired insulin release from islets of diabetic (C57BL/KsJ-db/db) mice

1980 ◽  
Vol 239 (2) ◽  
pp. E132-E138
Author(s):  
E. G. Siegel ◽  
C. B. Wollheim ◽  
G. W. Sharp ◽  
L. Herberg ◽  
A. E. Renold
Keyword(s):  
Tissue Culture ◽  
Beta Cell ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Insulin Response ◽  
Isolated Islets ◽  
Diabetic Mice ◽  
Impaired Insulin ◽  
Insulin Response To Glucose

The involvement of Ca2+ in the impaired insulin release of diabetic C57BL/KsJ-db/db mice was studied. Twenty-week-old severely hyperglycemic mice were compared to nondiabetic C57BL/KsJ mice as controls. Collagenase-isolated islets were maintained for 46 h in tissue culture allowing for equilibration at the same glucose concentration (8.3) mM). The insulin content of both types of islets was similar. In control islets preloaded during culture with 45Ca2+ glucose-induced insulin release was associated with increased 45Ca2+ effux. Islets from diabetic mice showed markedly reduced insulin response to glucose and a smaller increase in 45Ca2+ efflux. Because insulin release was strikingly potentiated by 3-isobutyl-1-methylxanthine (IBMX), even more than in control islets, there was no generalized release defect. In both types of islets, IBMX potentiation was accompanied by a further enhanced 45Ca2+ efflux, possibly suggesting that cAMP effects are associated with increased cytosol Ca2+% concentrations. As Ca2+ uptake was stimulated by glucose in both types of islets, a defect may lie in the mechanism by which glucose uses cellulr calcium to raise cytosol Ca2+ in the beta-cell of these diabetic mice.

INSULIN RESPONSE TO GLUCOSE INFUSION IN DIABETIC AND NON-DIABETIC MONOZYGOTIC TWIN PAIRS. GENETIC CONTROL OF INSULIN RESPONSE?

1967 ◽  
Vol 55 (2) ◽  
pp. 330-345 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft
Keyword(s):  
Diabetes Mellitus ◽  
Chronic Pancreatitis ◽  
Healthy Subjects ◽  
Insulin Response ◽  
Monozygotic Twin ◽  
Glucose Infusion ◽  
Striking Similarity ◽  
Insulin Response To Glucose ◽  
Genetically Determined ◽  
Low Insulin Response

ABSTRACT The insulin response during a standardized glucose infusion (GIT) was studied in a group of 13 monozygotic twin pairs previously registered as consisting of one diabetic/one non-diabetic member. At the time of the study three of the non-diabetic subjects had developed overt diabetes and three decreased glucose tolerance only. Of the non-diabetic members all but one (with diabetes due possibly to chronic pancreatitis in the sibling) showed an insulin response similar to that seen in diabetic subjects, and in healthy subjects previously assumed to be potential diabetics. The present study therefore supports our earlier suggestion that a low insulin response characterizes potential diabetes. There was a striking similarity between the insulin curves in the twin pairs, irrespective whether diabetes occurred in one, in both or in none of the members. It is suggested as a working hypothesis that the type of insulin response to glucose infusion is genetically determined, and that a low insulin response is a prerequisite for the development of diabetes mellitus.

Integrated mathematical model to assess beta-cell activity during the oral glucose test

1996 ◽  
Vol 270 (3) ◽  
pp. E522-E531 ◽  
Author(s):  
K. Thomaseth ◽  
A. Kautzky-Willer ◽  
B. Ludvik ◽  
R. Prager ◽  
G. Pacini
Keyword(s):  
Beta Cell ◽  
Cell Activity ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Cell Secretion ◽  
Islet Amyloid ◽  
Concentration Data ◽  
C Peptide ◽  
Fractional Clearance ◽  
Beta Cell Secretion

A model describing beta-cell secretion during an oral glucose tolerance test (OGTT) is introduced. The aim was to quantify beta-cell activity in different pathologies by analyzing peripheral concentration data of insulin, C-peptide, and islet amyloid polypeptide (IAPP). Insulin appearance in periphery is given by the fraction of C-peptide secretion, CPS(t), which accounts for liver degradation. A novelty of this study is the inclusion of IAPP delivery assumed proportional to CPS(t). Although IAPP fractional clearance is estimated in every subject, the clearances of insulin and C-peptide are assigned from a wide set of previous independent studies. Sensitivity analysis was performed to quantify the "error" in the estimated variables due to these assignments. All parameters relating to beta-cell secretion increased in the glucose-intolerant states [integrated CPS(t)=56 +/- 8 nmol/l in 180 min vs. 32 +/- 3 of controls, P<0.05; total IAPP delivery= 83 +/- 21 pmol/l in 180 min vs. 41 +/- 6, P<0.05]. Elevated plasma IAPP concentration of the patients was due to augmented secretion since IAPP clearance was found to be even slightly greater than in controls, (0.053 +/- 0.011 vs. 0.034 +/- 0.004 min-1) and markedly lower than that of insulin (0.14 +/- 0.02, P<0.01). In conclusion, the model introduced here allows the characterization of beta-cell secretory parameters during a simple test such as OGTT.

2126-P: Physiological Concentrations of IL-1 Beta Promote Islet Amyloid Deposition by Increasing Beta-Cell Secretion of Human Islet Amyloid Polypeptide

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2126-P
Author(s):  
ANDREW T. TEMPLIN ◽  
MAHNAZ MELLATI ◽  
DANIEL ZEMAN-MEIER ◽  
MEGHAN F. HOGAN ◽  
NATHALIE ESSER ◽  
...  
Keyword(s):  
Beta Cell ◽  
Islet Amyloid Polypeptide ◽  
Amyloid Deposition ◽  
Human Islet ◽  
Cell Secretion ◽  
Islet Amyloid ◽  
Human Islet Amyloid Polypeptide ◽  
Beta Cell Secretion
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