scholarly journals Effects of Cold Exposure and Intravenous Glucose Infusion on Feed Intake and Plasma Insulin Response to Feeding in Sheep

1994 ◽  
Vol 65 (1) ◽  
pp. 1-8
Author(s):  
Hiroaki SANO ◽  
Hiroki TAKAYA ◽  
Naoko HASEMI ◽  
Yoshiaki TERASHIMA
Keyword(s):  
Cold Exposure ◽  
Feed Intake ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Glucose Infusion ◽  
Intravenous Glucose ◽  
Plasma Insulin Response

Interactions of cold exposure and starvation on glucose tolerance and insulin response

1983 ◽  
Vol 245 (6) ◽  
pp. E575-E581 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Lupien ◽  
L. J. Bukowiecki
Keyword(s):  
Glucose Tolerance ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Insulinogenic Index ◽  
Intravenous Glucose ◽  
Peripheral Tissues ◽  
Insulin Levels ◽  
Plasma Insulin Levels

The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. “Accelerated starvation” induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15–18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.

FURTHER STUDIES ON HEALTHY SUBJECTS WITH LOW AND HIGH INSULIN RESPONSE TO GLUCOSE INFUSION

1967 ◽  
Vol 55 (2) ◽  
pp. 305-329 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft
Keyword(s):  
Healthy Subjects ◽  
Insulin Response ◽  
Glucose Infusion ◽  
Oral Glucose ◽  
Intravenous Glucose ◽  
The Family ◽  
High Insulin ◽  
History Of ◽  
Insulin Response To Glucose ◽  
Plasma Insulin Response

ABSTRACT In a previous paper it was shown that 15 out of 85 healthy subjects with a normal intravenous glucose tolerance demonstrated a low plasma insulin response to glucose infusion which was similar to that obtained in diabetic subjects. In the present paper it has been shown that the type of insulin response to glucose infusion was the same when the test was repeated. Low insulin responders to glucose infusion, as a group, also showed low insulin response to intravenous tolbutamide and oral glucose. This indicates that the type of insulin response is characteristic for a given subject irrespective of the stimulation used. There seemed to be no difference in the occurrence of diabetes in the family history of the groups of low and high insulin responders.

STUDIES ON THE PATHOGENESIS OF DIABETES IN ACROMEGALY

1967 ◽  
Vol 56 (4) ◽  
pp. 593-607 ◽  
Author(s):  
Rolf Luft ◽  
Erol Cerasi ◽  
Carl Axel Hamberger
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Glucose Infusion ◽  
Intravenous Glucose ◽  
Highly Active ◽  
Normal Glucose ◽  
Insulin Response To Glucose ◽  
Active Acromegaly ◽  
Plasma Insulin Response

ABSTRACT Plasma insulin response to glucose infusion was found to be markedly increased in 20 patients with active acromegaly and with normal intravenous glucose tolerance. The insulin response was more pronounced in patients with highly active acromegaly than in those showing moderately active disease. In five patients with active acromegaly and with decreased glucose tolerance the insulin response was delayed and smaller than normal, i. e. similar to that seen in diabetic subjects without acromegaly. After successful treatment of the acromegaly insulin response to glucose infusion was normalized in the patients with normal glucose tolerance. In those with decreased glucose tolerance the diabetic type of insulin response remained unchanged even when the glucose tolerance was normalized. It is suggested that diabetes in connection with acromegaly develops only in prediabetic individuals, i.e. subjects with decreased insulin response to hyperglycaemia, who are unable to overcome the diabetogenic effect of growth hormone by compensatory hyperinsulinism.

OBESITY AS AN ADDITIONAL FACTOR IN THE PATHOGENESIS OF DIABETES

1968 ◽  
Vol 59 (2) ◽  
pp. 344-352 ◽  
Author(s):  
Rolf Luft ◽  
Erol Cerasi ◽  
Bo Andersson
Keyword(s):  
Glucose Tolerance ◽  
Plasma Insulin ◽  
Peripheral Resistance ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Endogenous Insulin ◽  
Intravenous Glucose Tolerance ◽  
Obese Subjects ◽  
Insulin Response To Glucose ◽  
Plasma Insulin Response

ABSTRACT Plasma insulin response to glucose infusion was measured in obese subjects with normal and decreased intravenous glucose tolerance. In obese non-diabetic subjects there was insulin hyperresponsiveness to glucose accompanied by peripheral resistance to endogenous insulin. In the obese diabetic subjects insulin response was of the type seen in non-obese diabetics; in no such instance could insulin hyperresponsiveness to glucose be obtained. It is suggested that obesity precipitates diabetes only in subjects with preexisting impairment of insulin response, i. e. in prediabetics. Subjects with unimpaired insulin secreting capacity would overcome the diabetogenic effect of obesity by compensatory hyperinsulinism.

Insulin response in rats acutely exposed to cold

1984 ◽  
Vol 62 (8) ◽  
pp. 924-927 ◽  
Author(s):  
Ora L. K. Smith
Keyword(s):  
Cold Exposure ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Blocking Agent ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Challenge ◽  
Plasma Insulin Levels ◽  
Adrenergic Blocking

To examine the role of insulin during shivering thermogenesis, rats (unacclimatized) were exposed to 4 °C for 24 h and compared with control rats kept at 25 °C. Cold exposure lowered plasma insulin levels by one half, despite unchanged plasma glucose concentrations. Adrenodemedullation 2 weeks prior to cold exposure partially restored the ability of cold rats' plasma insulin levels to respond to a glucose load, unless it was accompanied by a subcutaneous injection of epinephrine. When additional normal rats were cold stressed and injected immediately after exposure with an α-adrenergic blocking agent (phentolamine), an intravenous glucose challenge caused a mean peak insulin value that was 50% higher than that of untreated controls, while the glucose level was less elevated. The results suggest that cold depresses blood insulin levels through activation of the sympathetic adrenal system, an effect most likely mediated by α-adrenergic inhibition of the pancreatic insulin response.

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