In vivo insulin secretion and action in hyperglycemic rat

1989 ◽  
Vol 257 (2) ◽  
pp. E180-E184 ◽  
Author(s):  
M. C. Laury ◽  
L. Penicaud ◽  
A. Ktorza ◽  
H. Benhaiem ◽  
M. T. Bihoreau ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Insulin Level ◽  
Glucose Infusion ◽  
Short Term ◽  
Glucose Ratio ◽  
Tissue Sensitivity ◽  
Infusion Period

This work was designed to study the effects of insulin secretion and action in vivo of moderate hyperglycemia induced by glucose infusion during 4 days in unrestrained rats. The maintenance of a glycemia around 170 mg/dl throughout the infusion time necessitated a gradual increase of glucose infusion rate from 11.5 to 19 g/day. Throughout the infusion period, plasma insulin-to-glucose ratio remained much higher in hyperglycemic rats (HG) than in controls. Glucose tolerance and insulin secretion tests were performed 2 h after the end of the infusion, when glycemia and insulinemia were back to basal values. Incremental plasma glucose values were significantly lower in HG than in control rats without significant changes in incremental plasma insulin concentrations, suggesting an increased insulin efficiency. At the same insulin level, glucose utilization was higher in HG than in control rats during euglycemic-hyperinsulinemic clamps. These data show that short-term hyperglycemia and hyperinsulinemia do not induce a defect in insulin secretion in vivo and do increase tissue sensitivity to insulin.

Immediate in-vivo effect of corticosterone on glucose-induced insulin secretion in the rat

1982 ◽  
Vol 95 (3) ◽  
pp. 315-320 ◽  
Author(s):  
B. Billaudel ◽  
B. Ch. J. Sutter
Keyword(s):  
Insulin Secretion ◽  
Plasma Level ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Glucose Levels ◽  
Standard Pulse ◽  
Glucose Pulse

The effect of infused corticosterone (300 μg/h per kg body wt) on the concentrations of insulin in the plasma of the rat was examined (1) when glucose concentration was basal, (2) at standardized glucose levels attained by modulated glucose infusion and (3) in response to a standard or a modulated glucose pulse. There was no effect of corticosterone on the levels of plasma insulin when the glucose concentrations were either basal or raised in response to the standard pulse of glucose. However, when glucose was infused a significantly reduced plasma level of insulin was detected after 60 min when the glucocorticoid was present and this level remained significantly reduced after the modulated pulse of glucose. Thus the infusion of corticosterone leads to an acute depression of the concentrations of insulin in the plasma and of their response to a glucose pulse only when the hormone acts in the presence of a concentration of glucose in the plasma that is insulin-stimulatory.

Islet amyloid polypeptide inhibits insulin secretion in conscious rats

1994 ◽  
Vol 267 (2) ◽  
pp. E300-E305
Author(s):  
C. Furnsinn ◽  
H. Leuvenink ◽  
M. Roden ◽  
P. Nowotny ◽  
B. Schneider ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Muscle Glycogen ◽  
Plasma Insulin ◽  
Islet Amyloid Polypeptide ◽  
Term Effect ◽  
Short Term ◽  
Islet Amyloid ◽  
Conscious Rats ◽  
Group A

To investigate the effect of islet amyloid polypeptide (IAPP, amylin) exposure on insulin secretion in vivo, the plasma glucose level of conscious rats was clamped at 11.1 mmol/l (hyperglycemic clamp) during the last 2 h of a 24-h infusion study. Group parameters were A, 24-h saline; B and C, 22-h saline followed by 2-h IAPP (B, 8.5 pmol/min; C, 85 pmol/min), and D, 24-h IAPP (85 pmol/min). Induced hyperglycemia increased plasma insulin concentration by 426 +/- 34 pmol/l in control rats (group A). This effect on plasma insulin was reduced by 31% and 53% during short-term IAPP infusion (group B, 8.5 pmol/min, 294 +/- 41 pmol/l; C, 85 pmol/min, 202 +/- 25 pmol/l; short-term effect, P < 0.0001), whereas insulin levels tended to increase after 24 h of continuous IAPP exposure (group D, 682 +/- 120 pmol/l; P < 0.05 vs. group A). Glucose infusion rate required to maintain constant hyperglycemia fell dose dependently during short-term but not during long-term IAPP infusion (mumol.kg-1.min-1: group A, 203 +/- 11; B, 154 +/- 7; C, 119 +/- 7; D, 212 +/- 9; short-term effect, P < 0.0001). In parallel, muscle glycogen content was dose dependently reduced by short-term IAPP exposure. We conclude that IAPP inhibits glucose-stimulated insulin secretion and decreases muscle glycogen storage in conscious rats in vivo.

Insulin secretion and substrate homeostasis in prolonged hypothermia in rats

1988 ◽  
Vol 255 (6) ◽  
pp. R1035-R1040
Author(s):  
R. Hoo-Paris ◽  
M. L. Jourdan ◽  
L. C. Wang ◽  
R. Rajotte
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Low Temperatures ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Exogenous Insulin ◽  
Metabolic Substrate ◽  
Endogenous Insulin ◽  
Dose Dependent Decrease ◽  
Dose Dependent

In hypothermia, impairment of metabolic substrate mobilization and utilization may be a factor limiting survival. By use of a newly developed technique, substrate profiles and their regulation by insulin were examined in hypothermic rats (body temperature 19 degrees C) over 24 h. Plasma glucose concentrations increased to approximately 300 mg/dl during cooling and remained high throughout the period of hypothermia. Free fatty acid (FFA) concentration was not altered during cooling or during the first 10 h of hypothermia (approximately 700 mu eq/l) but progressively decreased thereafter, reaching 420 mu eq/l by 20 h. Plasma insulin decreased dramatically during cooling and remained very low (9 +/- 2 microU/ml) during the whole period of hypothermia, reflecting the suppression of insulin secretion by isolated islets at low temperatures. To test he hypothesis that suppression of endogenous insulin secretion may hamper glucose utilization and thus limit survival in hypothermia, exogenous insulin was administered. At doses of 0.1, 0.5, and 1 U/kg intravenously, insulin slowly decreased plasma glucose and FFA. However, at 0.1 and 1 U/kg intraperitoneally, insulin resulted in a dose-dependent decrease in survival time in the hypothermic rat. It is possible that the antilipolytic effect of insulin may have outweighed any beneficial effect of improving glucose utilization in hypothermia.

scholarly journals Effect of early dietary restriction on insulin action and secretion in the GK rat, a spontaneous model of NIDDM

2000 ◽  
Vol 278 (6) ◽  
pp. E1097-E1103 ◽  
Author(s):  
Carmen Alvarez ◽  
Danielle Bailbe ◽  
Françoise Picarel-Blanchot ◽  
Eric Bertin ◽  
Ana-Maria Pascual-Leone ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Weight Gain ◽  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Insulin Level ◽  
Gk Rat ◽  
Basal Plasma

The availability of the Goto-Kakisaki (GK) rat model of non-insulin-dependent diabetes mellitus prompted us to test the effect of a limited period of undernutrition in previously diabetic young rats on their insulin secretion and insulin action during adult age. Four-week-old female GK rats were either food restricted (35% restriction, 15% protein diet) or protein and energy restricted (35% restriction, 5% protein diet) for 4 wk. Food restriction in the young GK rat lowered weight gain but did not aggravate basal hyperglycemia or glucose intolerance, despite a decrease in basal plasma insulin level. Furthermore, the insulin-mediated glucose uptake by peripheral tissues in the GK rat was clearly improved. We also found that food restriction, when it is coupled to overt protein deficiency in the young GK rat, altered weight gain more severely and slightly decreased basal hyperglycemia but conversely aggravated glucose tolerance. Improvement of basal hyperglycemia was related to repression of basal hepatic glucose hyperproduction, despite profound attenuation of basal plasma insulin level. Deterioration of tolerance to glucose was related to severe blunting of the residual glucose-induced insulin secretion. It is, however, likely that the important enhancement of the insulin-mediated glucose uptake helped to limit the deterioration of glucose tolerance.

Effect of gestational hyperglycemia on insulin secretion in vivo and in vitro by fetal rat pancreas

1986 ◽  
Vol 251 (1) ◽  
pp. E86-E91 ◽  
Author(s):  
M. T. Bihoreau ◽  
A. Ktorza ◽  
A. Kervran ◽  
L. Picon
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Cell Function ◽  
Pregnant Rats ◽  
Fetal Rat ◽  
Gestational Hyperglycemia

The effects of gestational hyperglycemia on B-cell function were studied in near-term fetuses from unrestrained pregnant rats made slightly or highly hyperglycemic using continuous glucose infusion during the last week of pregnancy. Pancreatic and plasma insulin and insulin secretion in vitro were studied in the fetuses. Compared with controls, slightly hyperglycemic fetuses showed increased pancreatic and plasma insulin concentrations and similar insulin release in response to glucose in vitro. In highly hyperglycemic fetuses, pancreatic and plasma insulin concentrations were unchanged compared with controls, and insulin release in vitro was insensitive to glucose and to the mixture glucose plus theophylline. These results confirm that glucose is able to stimulate insulin secretion in normal or slightly hyperglycemic fetuses and suggest that severe hyperglycemia per se, without association of other metabolic disorders or toxic injuries, profoundly alters the stimulus-secretion coupling of the fetal rat B-cell.

scholarly journals A dynamic model to analyse intravenous glucose and insulin tolerance tests performed on dairy cows

2001 ◽  
Vol 86 (3) ◽  
pp. 359-369 ◽  
Author(s):  
Sophie Lemosquet ◽  
Philippe Faverdin
Keyword(s):  
Insulin Secretion ◽  
Dairy Cows ◽  
Dynamic Model ◽  
Plasma Insulin ◽  
Interstitial Fluid ◽  
Glucose Utilization ◽  
Utilization Rate ◽  
Sigmoidal Function ◽  
Entry Rate ◽  
Insulin Secretion Rate

A dynamic model was developed to assess insulin sensitivity and pancreatic response in lactating dairy cows. The model is based on a simultaneous analysis of insulin and glucose intravenous tolerance tests. It comprises five compartments corresponding to insulin in portal–hepatic plasma, and insulin or glucose in both systemic plasma and in interstitial fluid. Insulin secretion rate is a sigmoidal function of glucose in plasma. Insulin is cleared from hepatic plasma and from the interstitial fluid. The glucose entry rate is constant and glucose utilization rate is a sigmoidal function of insulin in the interstitial fluid. Six parameters were estimated: two for insulin secretion rate, two for insulin clearance, one for glucose entry rate and one for glucose utilization rate. After integration of the functions, the model yielded a relative estimate of the quantities of insulin secreted and cleared, as well as the glucose entering and utilized during each test. Using an experimental dataset composed of ten pairs of tolerance tests, the explained variations for plasma insulin and glucose concentrations were 96·0 and 98·3 % and standard errors of estimates were 0·032 nmol/l and 0·14 mmol/l respectively. Except in the early stages after injection, residual errors were low. A Jackknife analysis showed that the estimated parameters exhibited low statistical bias. This model simplifies the interpretation of both tests through a simulation based on six common parameters. Compared to a classical analysis of tolerance tests, it may improve the analysis of modifications in the key functions regulating glucose homeostasis in ruminants.

REGULATION OF INSULIN SECRETION IN THE OVINE FOETUS IN UTERO. EFFECTS OF SODIUM VALERATE ON SECRETION AND OF ADRENOCORTICOTROPHIN-INDUCED PREMATURE PARTURITION ON THE INSULIN SECRETORY RESPONSE TO GLUCOSE

1973 ◽  
Vol 56 (1) ◽  
pp. 13-25 ◽  
Author(s):  
J. M. BASSETT ◽  
G. D. THORBURN ◽  
DIANNE H. NICOL
Keyword(s):  
Insulin Secretion ◽  
Plasma Insulin ◽  
Short Chain Fatty Acid ◽  
Plasma Concentrations ◽  
Insulin Level ◽  
In Utero ◽  
Secretory Response ◽  
Lower Plasma ◽  
Insulin Secretory Response ◽  
Corticosteroid Secretion

SUMMARY Intravenous infusions of glucose into lambs in utero (130–150 days) and after birth, confirmed the marked post-natal increase in the magnitude of the response of plasma insulin to glucose. These studies also suggest that insulin secretion in foetal lambs is stimulated by glucose at lower plasma concentrations than in lambs after birth. The short-chain fatty acid, valeric acid, given as the sodium salt, caused a very rapid increase in the plasma insulin level of foetal lambs, when given either by intravenous injection or infusion. When birth was induced after only 135 days of gestation by i.v. infusion of a synthetic adrenocorticotrophin preparation (Synacthen) into foetal lambs there was also a prematurely induced maturation of the insulin secretory response to glucose. In these prematurely born lambs the insulin secretory response to i.v. glucose infusion was similar to that of normal lambs after birth and differed greatly from that of normal foetuses of similar age. The results indicate that maturation of the insulin secretory mechanism in the lamb is associated with parturition and suggest that these changes may be consequences of the increasing corticosteroid secretion in the foetus during the last few days of gestation.

Importance of blood glucose concentration in regulating lipolysis during fasting in humans

1990 ◽  
Vol 258 (1) ◽  
pp. E32-E39 ◽  
Author(s):  
S. Klein ◽  
O. B. Holland ◽  
R. R. Wolfe
Keyword(s):  
Blood Glucose ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Glucose Infusion ◽  
Short Term ◽  
Epinephrine Infusion ◽  
Isotopic Studies ◽  
Fasting Plasma Insulin

The importance of the decline in blood glucose concentration on lipolysis and the lipolytic effect of epinephrine was evaluated during short-term fasting. Lipolytic rates were determined by infusing [2H5]glycerol and [1-13C]palmitic acid. Five volunteers were studied after 12 h of fasting before and during epinephrine infusion and after 84 h of fasting, before and during glucose infusion when plasma glucose was restored to postabsorptive values, and during glucose plus epinephrine infusion. In another protocol, five volunteers were given glucose intravenously throughout fasting to maintain plasma glucose at postabsorptive levels and isotopic studies were performed after 12 and 84 h of fasting before and during epinephrine infusion. Glucose infusion after 84 h of fasting restored glucose and insulin concentrations and lipolytic rates toward 12-h fasting values. When euglycemia was maintained throughout fasting, plasma insulin still declined (P less than 0.05) and lipolytic rates still increased (P less than 0.05). Despite similar glucose concentrations, the lipolytic response to epinephrine infusion was greater after 84 h than after 12 h of fasting in both protocols (P less than 0.05). These studies demonstrate that the decline in plasma glucose contributes to, but is not required for, the increase in lipolysis during fasting. The increase in epinephrine-stimulated lipolysis that occurs during fasting is not dependent on a decrease in plasma glucose concentration.

Estimation of insulin secretion using extracts of plasma from mice injected with anti-insulin serum: effects of arginine, glucose and anti-insulin serum

1982 ◽  
Vol 95 (1) ◽  
pp. 125-135
Author(s):  
L. V. Beck ◽  
Ilora Basu ◽  
Sally L. Hegeman
Keyword(s):  
Insulin Secretion ◽  
Plasma Insulin ◽  
Plasma Sample ◽  
Fixed Time ◽  
Endogenous Insulin ◽  
Insulin In Plasma ◽  
Plasma Insulin Levels ◽  
Time Required ◽  
Secretion Rates

Anti-insulin serum (AIS) injected intravenously into adult male mice was allowed to complex endogenous plasma insulin for a fixed time before blood samples were taken. In each plasma sample, insulin was separated from antibody using acid alcohol and the free insulin was estimated by radioimmunoassay. We consider AIS to be most useful for the estimations of in-vivo insulin secretion rates over the period 0·5–5 min after its injection. The lower limit is governed by the time required for mixing and complexing of endogenous insulin. The use of a short upper limit is because antibody complexed with antigen leaves plasma more rapidly than does free antibody, carrying antigen with it. Increases in insulin per ml plasma were appreciably greater in mice injected with glucose or l-arginine plus AIS than in mice injected with glucose or l-arginine only. Hence more realistic values for in-vivo insulin secretion rates may be obtained by the use of AIS to retain most insulin in plasma than by estimations of plasma insulin levels.

Disappearance of insulin in man: variation with the plasma insulin level

1981 ◽  
Vol 97 (3) ◽  
pp. 391-397 ◽  
Author(s):  
Karl-Göran Tranberg ◽  
Per Hagander ◽  
Jan Thorell
Keyword(s):  
Clearance Rate ◽  
Pancreatic Secretion ◽  
Plasma Insulin ◽  
Insulin Level ◽  
Glucose Infusion ◽  
Plasma Insulin Level ◽  
Exogenous Insulin ◽  
Fasting State ◽  
Endogenous Insulin ◽  
Arterial Blood

Abstract. Clearance rates of unlabelled insulin were studied in 45 unanaesthetized non-diabetic humans. The clearance rate, as well as the pancreatic secretion rate, of endogenous insulin was estimated from steady-state concentrations in portal and arterial blood. The clearance rate of exogenous insulin was determined after brief intraportal infusion. In the basal fasting state, the endogenous plasma insulin level varied as closely with the clearance of endogenous insulin as with the rate of pancreatic secretion. During elevation of insulin by glucose infusion, it varied predominantly with the rate of insulin secretion. Clearance of exogenous insulin did not vary with the pre-test endogenous insulin level. The clearance of endogenous insulin increased from 11 ml · min−1 · kg−1 in the basal fasting state to 17 ml · min−1 · kg−1 during glucose infusion. Clearance of exogenous insulin fell progressively with increasing dose, from 35 (8 mU/kg) to 14 (43 mU/kg) ml · min−1 · kg−1 at normoglycaemia and from 23 (8 mU/kg) to 17 (34 mU/kg) ml · min−1 · kg−1 at hyperglycaemia. The clearance of endogenous insulin was lower than that of exogenous insulin at normoglycaemia, but of similar size during glucose infusion. It is concluded that variation in clearance rate is partly responsible for variation in plasma insulin concentration, particularly in the basal fasting state, and that the clearance rate is lower in the basal state than otherwise. To some extent, the low clearance values for endogenous insulin in the basal state may reflect poor specificity of the insulin radioimmunoassay.

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