Effects of somatostatin and glucose infusion on glucose kinetics in fetal sheep

1988 ◽  
Vol 255 (1) ◽  
pp. E87-E93
Author(s):  
C. A. Bloch ◽  
R. K. Menon ◽  
M. A. Sperling
Keyword(s):  
Steady State ◽  
Blood Glucose ◽  
Infusion Rate ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Plasma Glucagon ◽  
Glucose Kinetics ◽  
Fetal Sheep ◽  
Sequence Protocol

We examined the contribution of glucose, independently of insulin, on fetal glucose kinetics in the sheep by infusing somatostatin (SRIF), followed by SRIF plus glucose (protocol A) or reversing the initial infusion sequence (protocol B). In protocol A (n = 8), infusion of SRIF at 200 micrograms/h decreased plasma insulin (IRI) and blood glucose (G) by 2.8 +/- 1.0 microU/ml and 1.34 +/- 0.2 mg/dl from their respective basal concentrations of 6.8 +/- 1.4 microU/ml and 16.47 +/- 0.91 mg/dl (P less than 0.05; P less than 0.005). There were no significant changes in plasma glucagon (IRG) or the rates of umbilical G uptake or of G utilization, but G turnover decreased by 1.77 +/- 0.34 mg.kg-1.min-1 (P less than 0.005). Addition of G at a rate of 5.6 +/- 0.8 mg.kg-1.min-1 had no effect on IRI and IRG. Total G uptake (G infusion rate plus umbilical G uptake) increased from 6.37 +/- 0.77 to 10.25 +/- 1.0 mg.kg-1.min-1 (P less than 0.01), despite suppression of umbilical G uptake by 33%. Fetal G reached a new steady state of 23.08 +/- 1.37 mg/dl, and G turnover increased by 4.81 +/- 0.96 mg.kg-1.min-1 from its SRIF-induced nadir (P less than 0.005). Since G concentration was maintained at steady state, the rate of G utilization was equivalent to the rate of total G uptake, an increase of 60% from basal despite suppressed IRI.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin responsiveness, action and sensitivity in growing lambs and mature rams

1996 ◽  
Vol 76 (2) ◽  
pp. 203-208 ◽  
Author(s):  
H. Sano ◽  
K. Asanos ◽  
Y. Noguchi ◽  
K. Yoshimura ◽  
T. Senshu ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Infusion Rate ◽  
Plasma Insulin ◽  
Glucose Clamp ◽  
Glucose Infusion ◽  
Glucose Infusion Rate ◽  
Clamp Technique ◽  
Glucose Clamp Technique ◽  
Insulin Responsiveness ◽  
Blood Glucose Concentrations

Insulin responsiveness, action and sensitivity, using the glucose clamp technique, were measured in ruminating growing lambs (5 and 9 mo old) and mature rams (3 yr old). In the hyperglycemic clamp experiment, blood glucose concentrations were designed to remain 50 mg dL−1 above basal concentrations for more than 1 h. Plasma insulin concentrations during glucose infusion were lower (P < 0.05) for 5 mo-old lambs than for 9 mo-old lambs and mature rams and were higher (P < 0.05) for 9 mo-old lambs than for 5 mo-old lambs and mature rams. In the hyperinsulinemic euglycemic clamp experiment, insulin was infused over five sequential 1-h periods at rates from 0.64 to 25 mU kg−1 min−1 with concomitant glucose infusion to maintain preinfusion blood glucose concentrations. Glucose infusion rates during insulin infusion were lower (P < 0.05) for 5 mo-old lambs than for 9 mo-old lambs and plasma insulin concentration at half-maximal glucose infusion rate was numerically lower for 5 mo-old lambs, whereas maximal glucose infusion rate did not differ among growth stages. It is likely that in ruminating sheep insulin responsiveness, action and sensitivity may change with growth stage. Key words: Development, insulin response, insulin sensitivity, sheep, glucose clamp technique

Quantifying gluconeogenesis during fasting

1997 ◽  
Vol 273 (6) ◽  
pp. E1209-E1215 ◽  
Author(s):  
Visvanathan Chandramouli ◽  
Karin Ekberg ◽  
William C. Schumann ◽  
Satish C. Kalhan ◽  
John Wahren ◽  
...  
Keyword(s):  
Steady State ◽  
Blood Glucose ◽  
Healthy Subjects ◽  
Glucose Production ◽  
Body Water ◽  
Glucose Infusion ◽  
Apparent Change ◽  
State 1

The use of2H2O in estimating gluconeogenesis’ contribution to glucose production (%GNG) was examined during progressive fasting in three groups of healthy subjects. One group ( n = 3) ingested2H2O to a body water enrichment of ≈0.35% 5 h into the fast. %GNG was determined at 2-h intervals from the ratio of the enrichments of the hydrogens at C-5 and C-2 of blood glucose, assayed in hexamethylenetetramine. %GNG increased from 40 ± 8% at 10 h to 93 ± 6% at 42 h. Another group ingested2H2O over 2.25 h, beginning at 11 h ( n = 7) and 19 h ( n = 7) to achieve ≈0.5% water enrichment. Enrichment in plasma water and at C-2 reached steady state ≈1 h after completion of2H2O ingestion. The C-5-to-C-2 ratio reached steady state by the completion of 2H2O ingestion. %GNG was 54 ± 2% at 14 h and 64 ± 2% at 22 h. A 3-h [6,6-2H2]glucose infusion was also begun to estimate glucose production from enrichments at C-6, again in hexamethylenetetramine. Glucose produced by gluconeogenesis was 0.99 ± 0.06 mg ⋅ kg−1 ⋅ min−1at both 14 and 22 h. In a third group ( n = 3) %GNG reached steady state ≈2 h after2H2O ingestion to only ≈0.25% enrichment. In conclusion, %GNG by 2 h after2H2O ingestion and glucose production using [6,6-2H2]glucose infusion, begun together, can be determined from hydrogen enrichments at blood glucose C-2, C-5, and C-6. %GNG increases gradually from the postabsorptive state to 42 h of fasting, without apparent change in the quantity of glucose produced by gluconeogenesis at 14 and 22 h.

scholarly journals Effects of supplemental chromium and heat exposure on glucose metabolism and insulin action in sheep

2000 ◽  
Vol 134 (3) ◽  
pp. 319-325 ◽  
Author(s):  
H. SANO ◽  
S. KONNO ◽  
A. SHIGA
Keyword(s):  
Blood Glucose ◽  
Glucose Metabolism ◽  
Infusion Rate ◽  
Insulin Action ◽  
Heat Exposure ◽  
Glucose Infusion ◽  
Glucose Infusion Rate ◽  
Isotope Dilution Method ◽  
Glucose Turnover ◽  
Dilution Method

An isotope dilution method using [U-13C]glucose and a glucose clamp approach were applied to determine the effects of supplemental chromium (Cr) and heat exposure on blood glucose metabolism and tissue responsiveness and sensitivity to insulin in sheep. The sheep consumed diets with either 0 or 1 mg of Cr/kg (Control and +Cr diet, respectively) from high-Cr-yeast, and were exposed from a thermoneutral environment (20 °C) to a hot environment (30 °C) for 5 days. Blood glucose turnover rate did not differ between the diets, and was lower (P < 0·05) during heat exposure than in the thermoneutral environment. The maximal glucose infusion rate (tissue responsiveness to insulin) tended to be lower (P = 0·06) for the +Cr diet than for the Control diet, but did not change with heat exposure. The plasma insulin concentration at half maximal glucose infusion rate (tissue sensitivity to insulin) did not differ between the diets, and was greater (P < 0·05) during heat exposure than in the thermoneutral environment. No significant diet × environment interactions were observed. There was no significant evidence that Cr supplementation moderated heat stress in sheep from the measures of blood glucose metabolism and insulin action.

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.

scholarly journals Chronic Prednisolone Treatment Reduces Hepatic Insulin Sensitivity while Perturbing the Fed-to-Fasting Transition in Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (5) ◽  
pp. 2171-2178 ◽  
Author(s):  
Anke J. Laskewitz ◽  
Theo H. van Dijk ◽  
Vincent W. Bloks ◽  
Dirk-Jan Reijngoud ◽  
Marie-José van Lierop ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Plasma Insulin ◽  
Fasting Blood Glucose ◽  
Whole Body ◽  
Fibroblast Growth Factor 21 ◽  
Glucose Kinetics ◽  
Prednisolone Treatment ◽  
Hepatic Glucose ◽  
Blood Glucose Concentrations

Chronic glucocorticoid use for treatment of inflammatory diseases is accompanied by severe side effects in humans (e.g. hyperglycemia and insulin resistance). The present studies were conducted to characterize consequences of chronic treatment with the synthetic glucocorticoid prednisolone on insulin sensitivity and blood glucose kinetics in mice. Prednisolone treatment increased fasting blood glucose and plasma insulin concentrations, but this apparently reduced insulin sensitivity could not be confirmed in hyperinsulinemic euglycemic clamp studies. Therefore, a novel method to study whole body glucose kinetics was used. This method revealed that prednisolone-treated mice show an increased hepatic glucose production (HGP). The increased HGP was accompanied by elevated plasma insulin concentrations, indicating reduced insulin sensitivity of hepatic glucose metabolism in prednisolone-treated mice. Compared with vehicle, prednisolone-treated mice had lower blood glucose concentrations, higher plasma free fatty acids, and higher plasma fibroblast growth factor-21 concentrations in the fed condition, i.e. mimicking a fasting situation. Next, the effects of 24-h fasting on energy metabolism were studied. Compared with controls, fasted prednisolone-treated mice had higher blood glucose concentrations and lower plasma β-hydroxybutyrate concentrations. In conclusion, these results indicate that chronic prednisolone treatment reduces insulin sensitivity of HGP, induces a fasting-like phenotype in fed mice, and perturbs the fed-to-fasting transition.

An analogue computer model for the insulin response to glucose infusion

SIMULATION ◽  
1971 ◽  
Vol 16 (6) ◽  
pp. 243-255 ◽  
Author(s):  
Erol Cerasi ◽  
Bertil Andersson
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Computer Model ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Quantitative Information ◽  
Glucose Infusion ◽  
Analogue Computer ◽  
Dynamic Factors ◽  
Insulin Response To Glucose

An analogue computer model has been constructed for the analysis of the interrelationship between blood glucose and plasma insulin concentrations during glucose infusion. The model presented gives quantitative information on the effect of plasma insulin on glucose uptake, the total amount of glucose taken up by the tissues at a given time, the effect of blood glucose on the release of stored and newly formed insulin, and the rapidity by which plasma insulin is increased in response to hyperglycaemia. Such an analogue computer model might be a useful tool in the investigation of the various dynamic factors involved in the glucose- insulin interrelationship.

Blood Glucose, Plasma Insulin and Plasma Glucagon in NZO Mice

1980 ◽  
Vol 12 (04) ◽  
pp. 173-174 ◽  
Author(s):  
J. Upton ◽  
J. G. T. Sneyd ◽  
J. Livesey
Keyword(s):  
Blood Glucose ◽  
Plasma Insulin ◽  
Plasma Glucagon ◽  
Nzo Mice ◽  
Glucose Plasma

scholarly journals OR26-07 Mild Physiologic Hyperglycemia Does Not Affect Glucose Mediated but Impairs Insulin-Mediated Suppression of Plasma Glucagon in Healthy Normal Glucose Tolerant Subjects

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Devjit Tripathy ◽  
Xi chen ◽  
aurora merovci ◽  
Jonathan Trejo ◽  
Ralph DeFronzo
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Plasma Glucagon ◽  
Euglycemic Clamp ◽  
Hyperglycemic Clamp ◽  
Before And After ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Plasma Insulin Levels

Abstract Plasma glucagon levels are regulated by plasma glucose concentrations as well as intra-islet and circulating insulin concentrations. Hyperglycemia adversely affects skeletal muscle and hepatic insulin sensitivity (glucotoxicity). However, the effect of physiologic hyperglycemia on glucose-mediated and insulin-mediated suppression of glucagon is not known. The aim of the present study was to evaluate effect of chronic (48 or 72 hours) physiologic increase (+45 mg/dl) in plasma glucose concentration on the suppression of plasma glucagon concentration in healthy NGT individuals: 12 without family history of T2DM (FH-) (9M/3F, age = 50± 4 yrs, BMI = 27 ± 1 kg/m2) and 8 with FH of T2DM (FH+) (4M/4F, age = 48±2, BMI = 26±1 kg/m2). Subjects received an OGTT and 2-step hyperglycemic (+125 and +300 mg/dl) clamp (duration of each step = 80 minutes) before and after 72 hour glucose infusion. On another occasion subjects participated in a 3-step hyperinsulinemic (10, 20, 40 mU/m2·min) euglycemic clamp before and after a 48 hour glucose infusion. Plasma insulin and C-peptide concentrations were obtained every 2-5 minutes during each hyperglycemic clamp step and plasma glucagon concentrations were measured every 10 minutes. The ratio of insulin/glucagon was measured and used as an index of insulin-medicated suppression of plasma glucagon. FPG concentration increased from 97±4 to 140±4 mg/dl during the 72 hour glucose infusion. Following chronic glucose infusion, plasma insulin levels were significantly higher during the basal state and during each hyperglycemic clamp step (by 59% and 78%). There was no difference in plasma glucagon levels following chronic glucose infusion and the degree of suppression of glucagon during 2-step hyperglycemic (+125 and +300 mg/dl) were similar. However, the plasma insulin/glucagon ratio was significantly higher during the fasting state (by 76%) and during the first (by 128%) and second (by 178%) hyperglycemic clamp steps. Similarly during the three step euglycemic clamp (10, 20, 40 mU/m2·min) studies following 48 hr glucose infusion, despite similar plasma glucose concentrations during each clamp step, plasma insulin and glucagon concentrations were higher following chronic glucose infusion. These results demonstrate that sustained physiologic hyperglycemia for 48 hrs or 72 hours (i.e. glucotoxicity) does not affect the glucose mediated suppression of glucagon, but impairs insulin-mediated suppression of glucagon, and could contribute to fasting and post-prandial hyperglycemia in T2DM patients.

Differential effects of epinephrine on glucose production and disposal in man.

1979 ◽  
Vol 237 (4) ◽  
pp. E356 ◽  
Author(s):  
R Rizza ◽  
M Haymond ◽  
P Cryer ◽  
J Gerich
Keyword(s):  
Infusion Rate ◽  
Plasma Insulin ◽  
Glucose Production ◽  
Normal Subjects ◽  
Plasma Glucagon ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Glucose Clearance ◽  
Physiological Regulator ◽  
Gluconeogenic Substrates

Normal subjects were infused 1) with epinephrine (50 ng/(kg.min)) for 180 min followed by epinephrine plus glucagon (3 ng/(kg.min)) for 60 min after which the epinephrine infusion rate was increased (125 ng/(kg.min)) or 2) with epinephrine plus somatostatin (500 microgram/h) for 180 min. Epinephrine increased glucose production and plasma glucagon transiently but caused persistent suppression of glucose clearance and sustained hyperglycemia (despite increased plasma insulin and gluconeogenic substrates); glucose production increased again on addition of glucagon and on increasing the epinephrine infusion rate. During epinephrine plus somatostatin, glucose production still increased transiently, but further suppression of glucose clearance caused more marked hyperglycemia. In conclusion, 1) in man hyperepinephrinemia within the physiological range caused sustained suppression of glucose clearance but only a transient increase in glucose production; 2) this transient hepatic response a) was not due to glycogen or substrate depletion, b) occurred without changes in plasma glucagon or insulin, c) was specific for epinephrine but permitted subsequent responses to changes in plasma epinephrine; 3) epinephrine can serve as a physiological regulator of glucose homeostasis in man both by increasing glucose production and by decreasing glucose clearance.

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