Glucose Ingestion during Recovery

2015 ◽  
pp. 161-168
Author(s):  
F. Pirnay ◽  
G. Krzentowski ◽  
A. Luyckx ◽  
N. Pallikarakis ◽  
F. Mosora ◽  
...  
Keyword(s):  
Glucose Ingestion

THE EFFECT OF FASTING AND SELECTIVE RE-FEEDING ON INSULIN RELEASE IN THE RAT

1973 ◽  
Vol 72 (1) ◽  
pp. 46-53 ◽  
Author(s):  
D. S. Turner ◽  
D. A. B. Young
Keyword(s):  
Insulin Release ◽  
Acute Effect ◽  
Secretory Response ◽  
Release Mechanism ◽  
Β Cell ◽  
Intestinal Hormones ◽  
Intravenous Glucose ◽  
Glucose Ingestion ◽  
Glucose Test ◽  
Insulin Secretory Response

ABSTRACT The insulin secretory response in the rat to intravenous glucose was found to be greatly impaired by fasting for three days, whereas that to orally administered glucose was not significantly affected. Rats fasted for two days were given either protein or starch pellets for six hours, and then fasted for a further eighteen hours before the intravenous glucose test. The protein pre-feeding failed to affect significantly the subsequent insulin secretory response to intravenous glucose, whereas starch prefeeding greatly enhanced it. It is suggested that intestinal hormones released by glucose ingestion may exert not only an acute effect on insulin release, but also a 'priming' effect on the insulin release mechanism of the β cell, which enables it to respond to the subsequent stimulus of glucose alone.

Effect of stress hormones on splanchnic substrate and insulin disposal after glucose ingestion in healthy humans

Diabetes ◽  
1987 ◽  
Vol 36 (2) ◽  
pp. 127-135 ◽  
Author(s):  
W. K. Waldhausl ◽  
S. Gasic ◽  
P. Bratusch-Marrain ◽  
M. Komjati ◽  
A. Korn
Keyword(s):  
Stress Hormones ◽  
Healthy Humans ◽  
Glucose Ingestion

Effects of nonesterified fatty acids on glucose metabolism after glucose ingestion

Diabetes ◽  
1997 ◽  
Vol 46 (10) ◽  
pp. 1586-1593 ◽  
Author(s):  
Y. T. Kruszynska ◽  
M. I. Mulford ◽  
J. G. Yu ◽  
D. A. Armstrong ◽  
J. M. Olefsky
Keyword(s):  
Fatty Acids ◽  
Glucose Metabolism ◽  
Nonesterified Fatty Acids ◽  
Glucose Ingestion

scholarly journals EFFECTS OF FASTING AND GLUCOSE INGESTION ON THE RETENTION OF AMMONIA

1950 ◽  
Vol 186 (1) ◽  
pp. 373-375
Author(s):  
Henry D. Hoberman ◽  
Jack. Graff
Keyword(s):  
Glucose Ingestion

scholarly journals BLOOD PYRUVATE CURVES FOLLOWING GLUCOSE INGESTION IN NORMAL AND THIAMINE-DEFICIENT SUBJECTS

1941 ◽  
Vol 140 (3) ◽  
pp. 697-703
Author(s):  
Ernest Bueding ◽  
Martin H. Stein ◽  
Herman Wortis
Keyword(s):  
Glucose Ingestion ◽  
Blood Pyruvate

Abnormal Regulation of Venous Alanine after Glucose Ingestion in Myotonic Dystrophy

1985 ◽  
Vol 68 (2) ◽  
pp. 151-157 ◽  
Author(s):  
Richard T. Moxley ◽  
William Kingston ◽  
Robert C. Griggs
Keyword(s):  
Amino Acids ◽  
Glucose Tolerance ◽  
Myotonic Dystrophy ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Oral Glucose Tolerance Testing ◽  
Glucose Ingestion ◽  
Normal Glucose ◽  
Normal Males ◽  
Slight Rise

1. The concentration of amino acids in whole blood was measured before and during standard 5 h oral glucose tolerance testing in six male patients with myotonic dystrophy and five normal males. The plasma levels of insulin and glucose were also determined. 2. From 90 to 240 min after glucose ingestion there was a striking decline in venous alanine concentration in the patients with myotonic dystrophy in contrast to a slight rise in alanine in the normal group. 3. The patients displayed normal glucose tolerance, and there was a sustained fall in the venous concentration of the insulin-sensitive amino acids comparable with that seen in the normal controls. However, the patients showed a threefold increase of plasma insulin after glucose. 4. These data indicate an abnormal regulation of alanine in myotonic dystrophy which may be the result of an alteration in muscle synthesis of this amino acid. This defect in alanine synthesis may be due to a decreased availability of intracellular pyruvate caused by the insulin resistance that exists in these patients.

Rapid translocation of hepatic glucokinase in response to intraduodenal glucose infusion and changes in plasma glucose and insulin in conscious rats

2004 ◽  
Vol 286 (4) ◽  
pp. G627-G634 ◽  
Author(s):  
Chang An Chu ◽  
Yuka Fujimoto ◽  
Kayano Igawa ◽  
Joseph Grimsby ◽  
Joseph F. Grippo ◽  
...  
Keyword(s):  
Portal Vein ◽  
Plasma Glucose ◽  
Regulatory Protein ◽  
Glucose Infusion ◽  
Insulin Levels ◽  
Conscious Rats ◽  
Glucose Levels ◽  
Glucose Ingestion ◽  
Plasma Insulin Levels

The rate of liver glucokinase (GK) translocation from the nucleus to the cytoplasm in response to intraduodenal glucose infusion and the effect of physiological rises of plasma glucose and/or insulin on GK translocation were examined in 6-h-fasted conscious rats. Intraduodenal glucose infusion (28 mg·kg-1·min-1 after a priming dose at 500 mg/kg) elevated blood glucose levels (mg/dl) in the artery and portal vein from 90 ± 3 and 87 ± 3 to 154 ± 4 and 185 ± 4, respectively, at 10 min. At 120 min, the levels had decreased to 133 ± 6 and 156 ± 5, respectively. Plasma insulin levels (ng/ml) in the artery and the portal vein rose from 0.7 ± 0.1 and 1.8 ± 0.3 to 11.8 ± 1.5 and 20.2 ± 2.0 at 10 min, respectively, and 12.4 ± 3.1 and 18.0 ± 4.8 at 30 min, respectively. GK was rapidly exported from the nucleus as determined by measuring the ratio of the nuclear to the cytoplasmic immunofluorescence (N/C) of GK (2.9 ± 0.3 at 0 min to 1.7 ± 0.2 at 10 min, 1.5 ± 0.1 at 20 min, 1.3 ± 0.1 at 30 min, and 1.3 ± 0.1 at 120 min). When plasma glucose (arterial; mg/dl) and insulin (arterial; ng/ml) levels were clamped for 30 min at 93 ± 7 and 0.7 ± 0.1, 81 ± 5 and 8.9 ± 1.3, 175 ± 5 and 0.7 ± 0.1, or 162 ± 5 and 9.2 ± 1.5, the N/C of GK was 3.0 ± 0.5, 1.8 ± 0.1, 1.5 ± 0.1, and 1.2 ± 0.1, respectively. The N/C of GK regulatory protein (GKRP) did not change in response to the intraduodenal glucose infusion or the rise in plasma glucose and/or insulin levels. The results suggest that GK but not GKRP translocates rapidly in a manner that corresponds with changes in the hepatic glucose balance in response to glucose ingestion in vivo. Additionally, the translocation of GK is induced by the postprandial rise in plasma glucose and insulin.

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