FURTHER STUDIES ON THE EFFECT OF OCTANOATE ON GLUCOSE METABOLISM IN DOGS

1967 ◽  
Vol 45 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Shafeek S. Sanbar ◽  
John R. Evans ◽  
Boniface Lin ◽  
Geza Hetenyi Jr.
Keyword(s):  
Glucose Metabolism ◽  
Intravenous Administration ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Peripheral Blood ◽  
Plasma Insulin ◽  
Plasma Glucose Concentration ◽  
Intravenous Glucose ◽  
K Value ◽  
Healthy Dogs

Studies were carried out in anesthetized dogs to elucidate the mechanism of action of octanoate on glucose metabolism.Octanoate infusion in intact healthy dogs significantly decreased plasma glucose concentration, and in four out of seven dogs it raised plasma insulin concentration in peripheral blood. In contrast, intravenous administration of octanoate in four totally pancreatectomized dogs produced only small changes in plasma glucose concentration. These data suggest that the hypoglycemic action of octanoate may be mediated by increased secretion of insulin.The mean k value ([Formula: see text] of plasma glucose concentration) of intravenous glucose tolerance tests was significantly higher (2.38/minute) in healthy dogs that received an infusion of octanoate than in dogs that did not (1.2/minute). Octanoate also produced in healthy dogs greater increases in plasma insulin concentrations of peripheral blood during the tolerance tests. Furthermore, when delivered during a continuous intravenous administration of glucose (about 8 mg/kg per minute), octanoate infusion had no effect on either plasma glucose concentration or the rate of disappearance of glucose-U-14C from plasma to tissues. These findings indicate that octanoate does not impair glucose utilization in healthy dogs but actually improves tolerance of an intravenous glucose load, probably by stimulating greater release of insulin. These findings in vivo are discussed in the light of opposite effects of octanoate in vitro, to be described elsewhere, on glucose metabolism in the isolated heart and fat pad of rats.

scholarly journals The effect of dietary starch level on postprandial glucose and insulin concentrations in cats and dogs

2011 ◽  
Vol 106 (S1) ◽  
pp. S105-S109 ◽  
Author(s):  
Adrian K. Hewson-Hughes ◽  
Matthew S. Gilham ◽  
Sarah Upton ◽  
Alison Colyer ◽  
Richard Butterwick ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Time Course ◽  
Starch Content ◽  
Time Lag ◽  
Postprandial Glucose ◽  
Plasma Glucose Concentration ◽  
High Blood Glucose ◽  
A Charge

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.

scholarly journals Orally administered, insulin-loaded amidated pectin hydrogel beads sustain plasma concentrations of insulin in streptozotocin-diabetic rats

2000 ◽  
Vol 164 (1) ◽  
pp. 1-6 ◽  
Author(s):  
CT Musabayane ◽  
O Munjeri ◽  
P Bwititi ◽  
EE Osim
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Diabetic Rats ◽  
Plasma Glucose Concentration ◽  
Pharmacokinetic Parameters ◽  
Plasma Insulin Concentration ◽  
Hydrogel Beads ◽  
Concomitant Reduction

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.

Glucose intolerance following chronic metabolic acidosis in man.

1979 ◽  
Vol 236 (4) ◽  
pp. E328 ◽  
Author(s):  
R A DeFronzo ◽  
A D Beckles
Keyword(s):  
Metabolic Acidosis ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Chronic Metabolic Acidosis ◽  
Tissue Sensitivity

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.

scholarly journals Postprandial glucose and insulin profiles following a glucose-loaded meal in cats and dogs

2011 ◽  
Vol 106 (S1) ◽  
pp. S101-S104 ◽  
Author(s):  
Adrian K. Hewson-Hughes ◽  
Matthew S. Gilham ◽  
Sarah Upton ◽  
Alison Colyer ◽  
Richard Butterwick ◽  
...  
Keyword(s):  
Body Weight ◽  
Plasma Glucose ◽  
Test Meal ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Plasma Glucose Concentration ◽  
Insulin Concentration ◽  
Metabolic Adaptation ◽  
Plasma Insulin Concentration ◽  
High Blood Glucose

Data from intravenous (i.v.) glucose tolerance tests suggest that glucose clearance from the blood is slower in cats than in dogs. Since different physiological pathways are activated following oral administration compared with i.v. administration, we investigated the profiles of plasma glucose and insulin in cats and dogs following ingestion of a test meal with or without glucose. Adult male and female cats and dogs were fed either a high-protein (HP) test meal (15 g/kg body weight; ten cats and eleven dogs) or a HP+glucose test meal (13 g/kg body-weight HP diet+2 g/kg body-weight d-glucose; seven cats and thirteen dogs) following a 24 h fast. Marked differences in plasma glucose and insulin profiles were observed in cats and dogs following ingestion of the glucose-loaded meal. In cats, mean plasma glucose concentration reached a peak at 120 min (10·2, 95 % CI 9·7, 10·8 mmol/l) and returned to baseline by 240 min, but no statistically significant change in plasma insulin concentration was observed. In dogs, mean plasma glucose concentration reached a peak at 60 min (6·3, 95 % CI 5·9, 6·7 mmol/l) and returned to baseline by 90 min, while plasma insulin concentration was significantly higher than pre-meal values from 30 to 120 min following the glucose-loaded meal. These results indicate that cats are not as efficient as dogs at rapidly decreasing high blood glucose levels and are consistent with a known metabolic adaptation of cats, namely a lack of glucokinase, which is important for both insulin secretion and glucose uptake from the blood.

Glucose Disposal of Low Birth Weight Infants: Steady State Hyperglycemia Produced by Constant Intravenous Glucose Infusion

PEDIATRICS ◽  
1979 ◽  
Vol 63 (3) ◽  
pp. 389-396 ◽  
Author(s):  
Richard M. Cowett ◽  
William Oh ◽  
Arnold Pollak ◽  
Robert Schwartz ◽  
Barbara S. Stonestreet
Keyword(s):  
Steady State ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Gestational Age ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Plasma Glucose Concentration ◽  
Glucose Disposal ◽  
Osmotic Diuresis

Tolerance for glucose was studied in 35 well, appropriate for gestational age, low birth weight (LBW) infants (mean birth weight, 1,216 gm; mean gestational age, 30 weeks) between 3 and 38 days of age. Infants were given a graded dose of glucose at 8.1, 11.2, or 14.0 mg/kg/min for three hours by continuous peripheral intravenous infusion. Plasma glucose and insulin, and timed urine glucose and volume were measured. A steady state of plasma glucose concentration was noted by one hour at all infusion rates. In the nine infants receiving 8.1 mg/kg/min, plasma glucose and insulin were similar to the baseline values during the steady state, and none of these infants evidenced glucosuria. In the 16 infants receiving 11.2 mg/kg/min, the plasma glucose concentration significantly increased (140 to 166 mg/dl) during the steady state but the plasma insulin levels were not significantly different compared to baseline. Half of these infants developed hyperglycemia (plasma glucose 150 mg/dl) and glucosuria. Ten infants receiving 14.0 mg/kg/min developed a significantly higher plasma glucose and plasma insulin response in colmparison to those infants who received 8.1 and 11.2 mg/kg/min, and all evidenced hyperglycemia and glucosuria. Glucosuria did not exceed 6.4 mg/kg/hr (0.1 mg/kg/min) so that glucose disposal (retention) exceeded 99% of intake, and an osmotic diuresis was not noted in those infants who had glucosuria. Our data suggested that in well LBW infants, a three-hour infusion of glucose up to 14.0 mg/kg/min (approximately 80 kcal/kg/day) did not produce an osmotic diuresis, but in the highest infusion group (14 mg/kg/min), hyperglycemia did occur. The effect of hyperglycemia in the neonate is unknown and needs to be investigated.

scholarly journals Enhanced insulin sensitivity of gene-targeted mice lacking functional KCNQ1

2009 ◽  
Vol 296 (6) ◽  
pp. R1695-R1701 ◽  
Author(s):  
Krishna M. Boini ◽  
Dirk Graf ◽  
Anita M. Hennige ◽  
Saisudha Koka ◽  
Daniela S. Kempe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Peak Plasma ◽  
Plasma Glucose Concentration ◽  
Α Subunit ◽  
Glucose Injection ◽  
Regulation Of Metabolism

The pore-forming K+-channel α-subunit KCNQ1 is expressed in a wide variety of tissues including heart, skeletal muscle, liver, and epithelia. Most recent evidence revealed an association of the KCNQ1 gene with the susceptibility to type 2 diabetes. KCNQ1 participates in the regulation of cell volume, which is, in turn, critically important for the regulation of metabolism by insulin. The present study explored the influence of KCNQ1 on insulin-induced cellular K+ uptake and glucose metabolism. Insulin (100 nM)-induced K+ uptake was determined in isolated perfused livers from KCNQ1-deficient mice ( kcnq1−/−) and their wild-type littermates ( kcnq1+/+). Moreover, plasma glucose and insulin levels, intraperitoneal glucose (3 g/kg) tolerance, insulin (0.15 U/kg)-induced hypoglycemia, and peripheral uptake of radiolabeled 3H-deoxy-glucose were determined in both genotypes. Insulin-stimulated hepatocellular K+ uptake was significantly more sustained in isolated perfused livers from kcnq1−/− mice than from kcnq1+/+mice. The decline of plasma glucose concentration following an intraperitoneal injection of insulin was again significantly more sustained in kcnq1−/− than in kcnq1+/+ mice. Both fasted and nonfasted plasma glucose and insulin concentrations were significantly lower in kcnq1−/− than in kcnq1+/+mice. Following an intraperitoneal glucose injection, the peak plasma glucose concentration was significantly lower in kcnq1−/− than in kcnq1+/+mice. Uptake of 3H-deoxy-glucose into skeletal muscle, liver, kidney and lung tissue was significantly higher in kcnq1−/− than in kcnq1+/+mice. In conclusion, KCNQ1 counteracts the stimulation of cellular K+ uptake by insulin and thereby influences K+-dependent insulin signaling on glucose metabolism. The observations indicate that KCNQ1 is a novel molecule affecting insulin sensitivity of glucose metabolism.

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
Keyword(s):  
Growth Hormone ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Secretory Response ◽  
Glucose Infusion ◽  
Plasma Glucose Concentration ◽  
Plasma Growth Hormone

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.

Insulin does not mediate the attenuation of fatigue associated with glucose infusion in rat plantaris muscle

2003 ◽  
Vol 95 (1) ◽  
pp. 330-335 ◽  
Author(s):  
Antony D. Karelis ◽  
François Péronnet ◽  
Phillip F. Gardiner
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Plasma Glucose Concentration ◽  
Muscle Performance ◽  
Insulin Concentration ◽  
Dynamic Force ◽  
Plantaris Muscle ◽  
Plasma Insulin Concentration

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.

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