scholarly journals SAT-166 Techniques For Direct Imaging Of Beta-cell Activity And Glucose Homeostasis In Zebrafish

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Jennifer Ikle ◽  
Rob Tryon ◽  
Christopher Emfinger ◽  
Kryzysztof Hyrc ◽  
Maria Remedi ◽  
...  
Keyword(s):  
Beta Cell ◽  
Glucose Homeostasis ◽  
Cell Activity ◽  
Direct Imaging

scholarly journals β-cells operate collectively to help maintain glucose homeostasis

2019 ◽  
Author(s):  
Boris Podobnik ◽  
Dean Korošak ◽  
Maša Skelin Klemen ◽  
Andraž Stožer ◽  
Jurij Dolenšek ◽  
...  
Keyword(s):  
Beta Cell ◽  
Beta Cells ◽  
Glucose Homeostasis ◽  
Cell Activity ◽  
Cell Communication ◽  
Calcium Oscillations ◽  
Homeostatic Function ◽  
Entire Cell ◽  
Collective Phenomenon ◽  
Gap Junctional

Residing in the islets of Langerhans in the pancreas, beta cells contribute to glucose homeostasis by managing the body’s insulin supply. A circulating hypothesis has been that healthy beta cells heavily engage in cell-to-cell communication to perform their homeostatic function. We provide strong evidence in favor of this hypothesis in the form of (i) a dynamical network model that faithfully mimics fast calcium oscillations in response to above-threshold glucose stimulation and (ii) empirical data analysis that reveals a qualitative shift in the cross-correlation structure of measured signals below and above the threshold glucose concentration. Combined together, these results point to a glucose-induced transition in beta-cell activity thanks to increasing coordination through gap-junctional signaling and paracrine interactions. The model further suggests how the conservation of entire cell-cell conductance, observed in coupled but not uncoupled beta cells, emerges as a collective phenomenon. An overall implication is that improving the ability to monitor beta-cell signaling should offer means to better understand the pathogenesis of diabetes mellitus.

Age-dependent reduction in insulin secretion and insulin mRNA in isolated islets from rats

1995 ◽  
Vol 269 (6) ◽  
pp. E983-E990 ◽  
Author(s):  
R. Perfetti ◽  
C. M. Rafizadeh ◽  
A. S. Liotta ◽  
J. M. Egan
Keyword(s):  
Beta Cell ◽  
Wistar Rats ◽  
Cell Activity ◽  
Insulin Content ◽  
Dependent Diabetes Mellitus ◽  
Etiologic Factor ◽  
Mrna Levels ◽  
Age Dependent ◽  
Insulin Mrna ◽  
Old Rats

Aging is an etiologic factor in non-insulin-dependent diabetes mellitus. To characterize the beta-cell abnormalities that occur with age, we investigated glucose-stimulated insulin release, pancreatic insulin content, and mRNA levels for islet-specific genes in aging Wistar rats. Ten minutes after glucose stimulation, 6-mo-old islets had approximately 40% more cells secreting insulin than 24-mo-old islets (P < 0.0001); after 1 h, 67 +/- 1.0% islets from 6-mo-old rats secreted insulin, compared with 51 +/- 3.5% from 24-mo-old rats (P < 0.0001). The amount of insulin secreted by each beta-cell was also less in the older animals (P < 0.0001). Despite increases in islet size (P < 0.0001) and beta-cell number (P < 0.0001) with age, whole pancreas insulin content showed that 24-mo-old pancreas had less insulin than 6-mo-old pancreas (0.61 +/- 0.06 vs. 0.84 +/- 0.08 microgram/mg pancreatic protein; P < 0.05). Finally, insulin mRNA levels declined to 50% of the newborn value in 24-mo-old islets (P < 0.0001), whereas glucagon mRNA levels showed a very modest decline with age. Somatostatin mRNA levels did not vary significantly. In summary, it appears that in Wistar rats there is a progressive decline in beta-cell activity with age. This decline may represent the biological features of the age-dependent risk of developing diabetes.

scholarly journals Difference in the influence of maternal and paternal NIDDM on pancreatic beta-cell activity and blood lipids in normoglycaemic non-diabetic adult offspring

Diabetologia ◽  
1996 ◽  
Vol 39 (7) ◽  
pp. 831-837 ◽  
Author(s):  
T. Kasperska-Czyzyk ◽  
K. Jedynasty ◽  
R. R. Bowsher ◽  
D. L. Holloway ◽  
I. Stradowska ◽  
...  
Keyword(s):  
Beta Cell ◽  
Blood Lipids ◽  
Pancreatic Beta Cell ◽  
Cell Activity ◽  
Adult Offspring

scholarly journals Genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis

Diabetologia ◽  
2016 ◽  
Vol 59 (5) ◽  
pp. 1012-1020 ◽  
Author(s):  
Joan Mir-Coll ◽  
Jordi Duran ◽  
Felipe Slebe ◽  
Mar García-Rocha ◽  
Ramon Gomis ◽  
...  
Keyword(s):  
Beta Cell ◽  
Glucose Homeostasis ◽  
Genetic Models ◽  
Rule Out

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.

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