Relationship of Insulin Secretion Rate to Blood Glucose Concentration in Newborn and Adult Dogs

Neonatology ◽  
1969 ◽  
Vol 14 (3-4) ◽  
pp. 194-202 ◽  
Author(s):  
P.A.J. Adam ◽  
D. Kornhauser ◽  
D. Link ◽  
R. Schwartz
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Secretion Rate ◽  
Relationship Of ◽  
Insulin Secretion Rate

scholarly journals Impaired glucose homeostasis in Shb−/− mice

2009 ◽  
Vol 203 (2) ◽  
pp. 271-279 ◽  
Author(s):  
Björn Åkerblom ◽  
Sebastian Barg ◽  
Gabriela Calounova ◽  
Dariush Mokhtari ◽  
Leif Jansson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Endothelial Cell ◽  
Glucose Homeostasis ◽  
Glucose Concentration ◽  
Cell Function ◽  
Blood Glucose Concentration ◽  
Β Cell ◽  
Islet Volume

Src homology 2 domain-containing protein B (SHB) is an adapter protein involved in the regulation of β-cell and endothelial cell function. We have recently obtained the Shb knockout mouse, and consequently, the aim of this study was to assess the effect of Shb deletion upon β-cell function and blood glucose homeostasis. Shb−/− mice display an elevated basal blood glucose concentration, and this increase is maintained during insulin challenge in insulin sensitivity tests. To assess glucose-induced insulin secretion, pancreata were perfused, and it was observed that Shb−/− first phase insulin secretion was blunted during glucose stimulation. Gene expression of Shb−/− islets shortly after isolation was altered, with increased pancreatic and duodenal homeobox gene-1 (Pdx1) gene expression and reduced expression of Vegf-A. Islet culture normalized Pdx1 gene expression. The microvascular density of the Shb−/− islets was reduced, and islet capillary endothelial cell morphology was changed suggesting an altered microvascular function as a contributing cause to the impaired secretory activity. Capacitance measurements of depolarization-induced exocytosis indicate a direct effect on the exocytotic machinery, in particular a dramatic reduction in readily releasable granules, as responsible for the insulin-secretory defect operating in Shb−/− islets. Shb−/− mice exhibited no alteration of islet volume or β-cell area. In conclusion, loss of Shb impairs insulin secretion, alters islet microvascular morphology, and increases the basal blood glucose concentration. The impaired insulin secretory response is a plausible underlying cause of the metabolic impairment observed in this mutant mouse.

STUDY OF GLUCOSE TOLERANCE AND THE DYNAMIC PROPERTY OF INSULIN SECRETION. ANALYSIS OF INTRAVENOUS GLUCOSE TOLERANCE TEST WITH THE AID OF A CONTROL THEORY

1979 ◽  
Vol 90 (2) ◽  
pp. 283-294 ◽  
Author(s):  
Ryuzo Kawamori ◽  
Motoaki Shichiri ◽  
Teishi Murata ◽  
Makoto Nomura ◽  
Yukio Shigeta ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Dynamic Property ◽  
Glucose Concentration ◽  
Weighting Function ◽  
Blood Glucose Concentration ◽  
Rate Of Change ◽  
Intravenous Glucose ◽  
K Value

ABSTRACT The dynamic property of insulin secretion in relation to glucose tolerance was investigated quantitatively during iv glucose tolerance tests in 237 cases. The following results were obtained; 1) Glucose clearance constant (k-value) was not constant but variable with time and should be expressed as a function of time, K(t). In normal glucose tolerance, K(t) became greater with time. 2) Glucose-induced insulin secretion was expressed as the function of a proportional plus derivative response to glucose concentration. A weighting function of derivative response, reflecting the insulin secretion per unit of rate of change in blood glucose concentration, was calculated from blood glucose concentration (input) and insulin concentration (output) by the deconvolution method. It was clearly shown that the gain in weighting function was small and the response was slow even in the individual whose glucose tolerance was slightly impaired. 3) The greater the weighting function, the larger the change in K(t).

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