INFLUENCE OF PROLONGED GLUCOSE INFUSIONS ON PLASMA INSULIN AND GROWTH HORMONE CONCENTRATIONS OF FOETAL LAMBS

1974 ◽  
Vol 62 (2) ◽  
pp. 299-309 ◽  
Author(s):  
J. M. BASSETT ◽  
DENISE MADILL

SUMMARY Chronically cannulated foetal lambs close to term were infused intravenously with glucose at rates of 40 or 70 mg/min for up to 5 days. Infusion at these rates increased the foetal plasma glucose concentration to values in the ranges 35–45 and 60–80 mg/100 ml respectively. There were related increases in plasma fructose and lactate concentrations. Foetal plasma insulin concentrations increased within the first hour and remained raised throughout infusion. Plasma insulin concentrations were significantly correlated with plasma glucose concentrations. The secretory response of insulin to subsequent glucose infusions at a rate of 140 mg/min was not increased by the previous prolonged glucose infusions. Glucose infusion resulted in decreased plasma growth hormone concentrations in three of the lambs infused, but over the total number of observations plasma glucose and growth hormone concentrations were not significantly correlated.

2003 ◽  
Vol 95 (1) ◽  
pp. 330-335 ◽  
Author(s):  
Antony D. Karelis ◽  
François Péronnet ◽  
Phillip F. Gardiner

Glucose infusion attenuates fatigue in rat plantaris muscle stimulated in situ, and this is associated with a better maintenance of electrical properties of the fiber membrane (Karelis AD, Péronnet F, and Gardiner PF. Exp Physiol 87: 585–592, 2002). The purpose of the present study was to test the hypothesis that elevated plasma insulin concentration due to glucose infusion (∼900 pmol/l), rather than high plasma glucose concentration (∼10–11 mmol/l), could be responsible for this phenomenon, because insulin has been shown to stimulate the Na+-K+ pump. The plantaris muscle was indirectly stimulated (50 Hz, for 200 ms, 5 V, every 2.7 s) via the sciatic nerve to perform concentric contractions for 60 min, while insulin (8 mU · kg-1 · min-1: plasma insulin ∼900 pmol/l) and glucose were infused to maintain plasma glucose concentration between 4 and 6 [6.2 ± 0.4 mg · kg-1 · min-1: hyperinsulinemic-euglycemic (HE)] or 10 and 12 mmol/l [21.7 ± 1.1 mg · kg-1 · min-1: hyperinsulinemic-hyperglycemic clamps (HH)] (6 rats/group). The reduction in submaximal dynamic force was significantly ( P < 0.05) less with HH (-53%) than with HE and saline only (-66 and -70%, respectively). M-wave characteristics were also better maintained in the HH than in HE and control groups. These results demonstrate that the increase in insulin concentration is not responsible for the increase in muscle performance observed after the elevation of circulating glucose.


1979 ◽  
Vol 237 (3) ◽  
pp. E214 ◽  
Author(s):  
R A DeFronzo ◽  
J D Tobin ◽  
R Andres

Methods for the quantification of beta-cell sensitivity to glucose (hyperglycemic clamp technique) and of tissue sensitivity to insulin (euglycemic insulin clamp technique) are described. Hyperglycemic clamp technique. The plasma glucose concentration is acutely raised to 125 mg/dl above basal levels by a priming infusion of glucose. The desired hyperglycemic plateau is subsequently maintained by adjustment of a variable glucose infusion, based on the negative feedback principle. Because the plasma glucose concentration is held constant, the glucose infusion rate is an index of glucose metabolism. Under these conditions of constant hyperglycemia, the plasma insulin response is biphasic with an early burst of insulin release during the first 6 min followed by a gradually progressive increase in plasma insulin concentration. Euglycemic insulin clamp technique. The plasma insulin concentration is acutely raised and maintained at approximately 100 muU/ml by a prime-continuous infusion of insulin. The plasma glucose concentration is held constant at basal levels by a variable glucose infusion using the negative feedback principle. Under these steady-state conditions of euglycemia, the glucose infusion rate equals glucose uptake by all the tissues in the body and is therefore a measure of tissue sensitivity to exogenous insulin.


2011 ◽  
Vol 106 (S1) ◽  
pp. S105-S109 ◽  
Author(s):  
Adrian K. Hewson-Hughes ◽  
Matthew S. Gilham ◽  
Sarah Upton ◽  
Alison Colyer ◽  
Richard Butterwick ◽  
...  

A charge made against feeding dry foods to cats is that the high carbohydrate (i.e. starch) content results in high blood glucose levels which over time may have detrimental health effects. The present study determined the post-meal concentrations of plasma glucose and insulin in adult cats (seven males and four females) and dogs (Labrador retrievers; four males and five females) fed dry diets with low-starch (LS), moderate-starch (MS) or high-starch (HS) levels. In a cross-over design with at least 7 d between the test meals, plasma glucose and insulin concentrations were measured following a single meal of a LS, MS and HS diet (209 kJ/kg bodyweight). Only the HS diet resulted in significant post-meal increases in plasma glucose concentration in cats and dogs although the time-course profiles were different between the species. In cats, plasma glucose concentration was significantly increased above the pre-meal concentration from 11 h until 19 h after the meal, while in dogs, a significant increase above baseline was seen only at the 7 h time point. Plasma insulin was significantly elevated in dogs 4–8 h following the MS diet and 2–8 h after the HS diet. In cats, plasma insulin was significantly greater than baseline from 3–7 and 11–17 h after the HS diet. The time lag (approximately 11 h) between eating the HS diet and the subsequent prolonged elevation of plasma glucose concentration seen in cats may reflect metabolic adaptations that result in a slower digestive and absorptive capacity for complex carbohydrate.


1990 ◽  
Vol 258 (1) ◽  
pp. E32-E39 ◽  
Author(s):  
S. Klein ◽  
O. B. Holland ◽  
R. R. Wolfe

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.


1995 ◽  
Vol 82 (5) ◽  
pp. 1154-1159 ◽  
Author(s):  
Dounia Sbai ◽  
Philippe Jouvet ◽  
Anne Soulier ◽  
Luc Penicaud ◽  
Jacques Merckx ◽  
...  

Background It should be possible to avoid variations in plasma glucose concentration during anesthesia by adjusting glucose infusion rate to whole-body glucose uptake. To study this hypothesis, we measured glucose utilization and production, before and during halothane anesthesia. Methods After an overnight fast, six adolescents between 12 and 17 yr of age were infused with tracer doses of [6,6-2H2]glucose for 2 h before undergoing anesthesia, and the infusion was continued after induction, until the beginning of surgery. Plasma glucose concentration was monitored throughout, and free fatty acids, lactate, insulin, and glucagon concentrations were measured before and during anesthesia. Results Despite the use of a glucose-free maintenance solution, plasma glucose concentration increased slightly but significantly 5 min after induction (5.3 +/- 0.4 vs. 4.5 +/- 0.4 mmol.l-1, P &lt; 0.05). This early increase corresponded to a significant increase in endogenous glucose production over basal conditions (4.1 +/- 0.4 vs. 3.6 +/- 0.2 mg.kg-1.min-1, P &lt; 0.05), with no concomitant change in peripheral glucose utilization. Fifteen minutes after induction, both glucose utilization and production rates decreased steadily and were 20% less than basal values by 35 min after induction (2.9 +/- 0.3 vs. 3.6 +/- 0.2 mg.kg-1.min-1, P &lt; 0.05). Similarly, glucose metabolic clearance rate decreased by 25% after 35 min. Despite the increase in blood glucose concentration, anesthesia resulted in a significant decrease in plasma insulin concentration. Conclusions These data suggest that halothane anesthesia per se affects glucose metabolism. The decrease in peripheral glucose utilization and metabolic clearance rates and the blunted insulin release question the relevance of glucose infusion in these clinical settings.


2000 ◽  
Vol 164 (1) ◽  
pp. 1-6 ◽  
Author(s):  
CT Musabayane ◽  
O Munjeri ◽  
P Bwititi ◽  
EE Osim

We report successful oral administration of insulin entrapped in amidated pectin hydrogel beads in streptozotocin (STZ)-diabetic rats, with a concomitant reduction in plasma glucose concentration. The pectin-insulin (PI) beads were prepared by the gelation of humilin-pectin solutions in the presence of calcium. Separate groups of STZ-diabetic rats were orally administered two PI beads (30 micrograms insulin) once or twice daily or three beads (46 micrograms) once daily for 2 weeks. Control non-diabetic and STZ-diabetic rats were orally administered pectin hydrogel drug-free beads. By comparison with control non-diabetic rats, untreated STZ-diabetic rats exhibited significantly low plasma insulin concentration (0.32+/-0. 03 ng/ml, n=6, compared with 2.60+/-0.44 ng/ml in controls, n=6) and increased plasma glucose concentrations (25.84+/-1.44 mmol/l compared with 10.72+/- 0.52 mmol/l in controls). Administration of two PI beads twice daily (60 micrograms active insulin) or three beads (46 micrograms) once a day to STZ-diabetic rats increased plasma insulin concentrations (0.89+/-0.09 ng/ml and 1.85+/- 0.26 ng/ml, respectively), with a concomitant reduction in plasma glucose concentration (15.45+/-1.63 mmol/l and 10.56+/-0.26 mmol/l, respectively). However, a single dose of PI beads (30 micrograms) did not affect plasma insulin concentrations, although plasma glucose concentrations (17.82+/-2.98 mmol/l) were significantly reduced compared with those in untreated STZ-diabetic rats. Pharmacokinetic parameters in STZ-diabetic rats show that the orally administered PI beads (30 micrograms insulin) were more effective in sustaining plasma insulin concentrations than was s.c. insulin (30 micrograms). The data from this study suggest that this insulin-loaded amidated pectin hydrogel bead formulation not only produces sustained release of insulin, but may also reduce plasma glucose concentration in diabetes mellitus.


1979 ◽  
Vol 236 (4) ◽  
pp. E328 ◽  
Author(s):  
R A DeFronzo ◽  
A D Beckles

The effect of chronic metabolic acidosis (0.1 g/(kg . day) X 3 days) on carbohydrate metabolism was examined with the glucose-clamp technique in 16 healthy volunteers. Hyperglycemic clamp. Plasma glucose concentration is acutely raised and maintained 125 mg/dl above the basal level. Because the glucose concentration is held constant, the glucose infusion rate is an index of glucose metabolism (M). Following NH4Cl, M decreased from 8.95 +/- 1.12 to 7.35 +/- 0.76 (P less than 0.05) despite an increased plasma insulin concentration (I) 23 +/- 9%, P less than 0.05). Consequently the M/I ratio, an index of tissue sensitivity to insulin, decreased by 32 +/- 5% (P less than 0.005). Euglycemic clamp. Plasma insulin concentration is acutely raised and maintained 101 +/- 3 microU/ml above basal and plasma glucose is held constant at the fasting level by a variable glucose infusion (M). Following NH4Cl both M and M/I decreased by 15 +/- 4% (P = 0.005) and 15 +/- 5% (P = 0.01), respectively. Metabolic acidosis had no effect on basal [3-3H]glucose production or the percent of decline (91 +/- 4%) following hyperinsulinemia. Both hyperglycemic and euglycemic clamp studies indicate that impaired glucose metabolism following metabolic acidosis results from impaired tissue sensitivity to insulin.


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