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).

scholarly journals Glucose Tolerance and Insulin Release in Malnourished Rats

1976 ◽  
Vol 50 (3) ◽  
pp. 153-163 ◽  
Author(s):  
C. Weinkove ◽  
E. A. Weinkove ◽  
B. L. Pimstone
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Protein Energy

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.

Endogenous and Exogenous Insulin Responses in Patients With Cystic Fibrosis

PEDIATRICS ◽  
1975 ◽  
Vol 55 (1) ◽  
pp. 75-82
Author(s):  
Errol G. Wilmshurst ◽  
J. Stuart Soeldner ◽  
Douglas S. Holsclaw ◽  
Robert L. Kaufmann ◽  
Harry Shwachman ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Serum Insulin ◽  
Lower Serum ◽  
Intravenous Glucose ◽  
Family History Of Diabetes ◽  
Insulin Levels

Eight male patients with cystic fibrosis, normal nutrition, normal physical activity, relatively mild pulmonary disease, no evidence of liver disease and no family history of diabetes mellitus underwent a series of carbohydrate tolerance tests in comparison with a group of 18 normal male subjects matched for age and body weight. Compared with the normal group, the patients with cystic fibrosis had significantly impaired glucose tolerance and significantly lower serum immunoreactive insulin levels during oral and intravenous glucose tolerance tests; serum insulin levels were also significantly lower after intravenous administration of tolbutamide in the patients with cystic fibrosis, but the reduction in blood glucose concentration in each group was not significantly different. During an intravenous insulin test, the decrease in blood glucose concentration was the same for both groups, in spite of significantly lower serum insulin levels in the patients with cystic fibrosis. The percentage fall in plasma free fatty acids was at least as great in the patients with cystic fibrosis as in normals during the test procedures, while a significant decrease in plasma alpha-amino nitrogen after intravenously administered insulin was seen only in the patients with cystic fibrosis. These studies suggest that the carbohydrate intolerance of cystic fibrosis is consequent upon an impaired insulin response to glucose, but that this insulin deficiency is partly compensated for by increased peripheral tissue sensitivity to insulin.

IMPORTANCE OF INSULIN SECRETION BASED ON THE RATE OF CHANGE IN BLOOD GLUCOSE CONCENTRATION IN GLUCOSE TOLERANCE, ASSESSED BY THE ARTIFICIAL BETA CELL

1978 ◽  
Vol 87 (2) ◽  
pp. 339-351 ◽  
Author(s):  
Ryuzo Kawamori ◽  
Motoaki Shichiri ◽  
Yoshikazu Goriya ◽  
Yoshimitsu Yamasaki ◽  
Yukio Shigeta ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Glucose Concentration ◽  
Insulin Infusion ◽  
Insulin Pump ◽  
Blood Glucose Concentration ◽  
Rate Of Change ◽  
Glucose Regulation ◽  
Physiological Level ◽  
Artificial Beta Cell

ABSTRACT The dynamic property of glucose-induced insulin secretion was simulated with the aid of a control theory, and the relationship between the stepwise input of glucose concentration and the biphasic response of insulin as an output was expressed in the transfer function of proportional plus derivative action to glucose concentration. By utilizing this model, the following computer algorithm for the artificial beta cell was made; rate of insulin infusion = Kp BG + Kd ΔBG+ Kc, where BG was the abbreviation for glucose concentration, ΔBG was the rate of change in BG, Kp and Kd were the coefficient for the proportional and derivative action, respectively, and Kc the constant for basal insulin secretion. Microcomputer, insulin pump and digital printer were packed in small case, which was connected with glucose analyzer. Experiments were carried out in the depancreatized dogs to validate the importance of infused insulin based on derivative action to glucose concentration in glucose regulation. Kd/Kp ratio was changed when insulin was infused following iv glucose bolus injection. The results revealed that when the derivative action was added to the proportional action properly in insulin infusion regulatory system, insulin requirement was the smallest and glucose regulation was the best. The characteristics of the system recognized in clinical application were 1) rate of insulin infusion was small enough to keep the plasma concentration of insulin at a physiological level, then insulin requirements were reduced to around a half of those given subcutaneously, 2) glucose or glucagon to restore hypoglycaemia was not essential.

Influence of Dihydromyricetin on Lowering Blood Glucose Concentration and Reducing Early Kidney Damage in Imparied Glucose Tolerance Rats

2014 ◽  
Vol 1004-1005 ◽  
pp. 857-863 ◽  
Author(s):  
Yong Qiang Zhou ◽  
Tao Yan Mao
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Early Stage ◽  
Fasting Blood Glucose ◽  
Kidney Damage ◽  
Postprandial Blood Glucose ◽  
Control Groups ◽  
Dose Levels

Diabetic nephropathy (DN) is a common complication of diabetes and it is related to irreversible kidney damages and chronic renal failure. Impaired glucose tolerance (IGT) is an early stage in the development of diabetes and DN. Early detection of IGT and treatment of its associated early kidney damage can effectively prevent the development of DN. In this paper, the influence of dihydromyricetin (DHM) on lowering blood glucose concentration and reducing early kidney damage in IGT rats was studied. Animal model of IGT rats was built by two week intragastric injection of D-galactose and treated with eight weeks of intragastric injection of DHM at two dose levels. The concentrations of fasting blood glucose (FBG), two-hour postprandial blood glucose (2hBG), insulin levels, contents of microalbuminuia (mAlb) and blood urea nitrogen (BUN), and activities of lactate dehydrogenase (LDH) in kidney were analysed and compared with those in control groups. Experimental results indicated that DHM treatment can significantly lower the levels of two-hour postprandial blood glucose and insulin, decrease the content of mAlb and the activities of LDH in kidney, but does not influence the level of BUN. The study suggested that DHM can effectively improve the states of IGT rats and provide a protective effect against early kidney damage.

scholarly journals Glucocorticoid-Induced Preterm Birth and Neonatal Hyperglycemia Alter Ovine β-Cell Development

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3763-3776 ◽  
Author(s):  
Amita Bansal ◽  
Frank H. Bloomfield ◽  
Kristin L. Connor ◽  
Mike Dragunow ◽  
Eric B. Thorstensen ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Preterm Birth ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Cell Mass ◽  
Β Cell ◽  
High Blood Glucose ◽  
Increased Risk

Adults born preterm are at increased risk of impaired glucose tolerance and diabetes. Late gestation fetuses exposed to high blood glucose concentration also are at increased risk of impaired glucose tolerance as adults. Preterm babies commonly become hyperglycemic and are thus exposed to high blood glucose concentration at an equivalent stage of pancreatic maturation. It is not known whether preterm birth itself, or complications of prematurity, such as hyperglycemia, alter later pancreatic function. To distinguish these, we made singleton preterm lambs hyperglycemic (HYPER) for 12 days after birth with a dextrose infusion and compared them with vehicle-treated preterm and term controls and with HYPER lambs made normoglycemic with an insulin infusion. Preterm birth reduced β-cell mass, apparent by 4 weeks after term and persisting to adulthood (12 mo), and was associated with reduced insulin secretion at 4 months (juvenile) and reduced insulin mRNA expression in adulthood. Hyperglycemia in preterm lambs further down-regulated key pancreatic gene expression in adulthood. These findings indicate that reduced β-cell mass after preterm birth may be an important factor in increased risk of diabetes after preterm birth and may be exacerbated by postnatal hyperglycemia.

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.

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