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.

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.

The Disposition of Intravenous Potassium in Normal Man: The Role of Insulin

1981 ◽  
Vol 61 (1) ◽  
pp. 23-28 ◽  
Author(s):  
R. H. Sterns ◽  
J. Guzzo ◽  
P. U. Feig
Keyword(s):  
Plasma Insulin ◽  
Normal Volunteer ◽  
Immunoreactive Insulin ◽  
K Uptake ◽  
Insulin Levels ◽  
Urinary Potassium ◽  
Plasma Insulin Levels ◽  
Normal Man ◽  
K Concentration

1. Potassium infusion causes an increase in immunoreactive insulin levels in dogs, but either a small (30%) or no increase in humans. Since insulin stimulates the uptake of K+ by cells, a regulatory role for K+-induced insulin release has been postulated. To study the role of insulin in regulating cellular K+ uptake, six fasting normal volunteer subjects underwent two K+ infusions on separate days. Both infusions delivered 0.6 mmol h−1 kg−1 for 3 h. In one subject glucose was simultaneously infused at 0.67 mmol h−1 kg−1 (a rate known to increase peripheral insulin levels by 40–100%); the other infusion contained no glucose. 2. Plasma insulin levels did not increase during the glucose-free infusions. During glucose-containing infusions, insulin levels were 40% higher than those during glucose-free infusions. Despite this, neither urinary potassium excretion nor the increment in plasma K+ concentration or the calculated cellular K+ uptake differed significantly during the 3 h of glucose-free and glucose-containing infusions respectively. 3. These data do not support the view that potassium-induced insulin secretion regulates cellular potassium uptake within the physiological range of plasma K+ concentration.

scholarly journals Evaluation of Antidiabetic Effects of the Traditional Medicinal PlantGynostemma pentaphyllumand the Possible Mechanisms of Insulin Release

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Ezarul Faradianna Lokman ◽  
Harvest F. Gu ◽  
Wan Nazaimoon Wan Mohamud ◽  
Claes-Göran Östenson
Keyword(s):  
Glucose Tolerance ◽  
Insulin Release ◽  
Pertussis Toxin ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Gk Rat ◽  
Insulin Levels ◽  
Gk Rats ◽  
Plasma Insulin Levels ◽  
Antidiabetic Effects

Aims. To evaluate the antidiabetic effects ofGynostemma pentaphyllum(GP) in Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, and to investigate the mechanisms of insulin release.Methods. Oral glucose tolerance test was performed and plasma insulin levels were measured.Results. An oral treatment withGP(0.3 g/kg of body weight daily) for two weeks in GK rats improved glucose tolerance versus placebo group (P<0.01). Plasma insulin levels were significantly increased in theGP-treated group. The insulin release fromGP-treated GK rats was 1.9-fold higher as compared to the control group (P<0.001).GPstimulated insulin release in isolated GK rat islets at high glucose. Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response toGP. Furthermore, the protein kinase A (PKA) inhibitor H89 decreased the insulin response toGP(P<0.05). In addition,GP-induced insulin secretion was decreased after preincubation of GK islets with pertussis toxin to inhibit exocytoticGeproteins (P<0.05).Conclusion.The antidiabetic effect ofGPis associated with the stimulation of insulin release from the islets.GP-induced insulin release is partly mediated via K-ATP and L-type Ca2+channels, the PKA system and also dependent on pertussis toxin sensitiveGe-protein.

Effect of adrenaline on insulin secretion in rats treated chronically with adrenaline

1976 ◽  
Vol 54 (6) ◽  
pp. 870-875 ◽  
Author(s):  
Suzanne Rousseau-Migneron ◽  
André Nadeau ◽  
Jacques LeBlanc
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Basal Insulin ◽  
Plasma Insulin ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Plasma Insulin Levels ◽  
Adrenaline Infusion

To determine whether rats could adapt to a chronic exogenous supply of adrenaline by a decrease in the well-known inhibitory effect of adrenaline on insulin secretion, plasma glucose and insulin levels were measured in unanesthetized control and adrenaline-treated rats (300 μg/kg twice a day for 28 days) during an adrenaline infusion (0.75 μg kg−1 min−1), after an acute glucose load (0.5 g/kg), and during the simultaneous administration of both agents. Chronic treatment with adrenaline did not modify the initial glucose levels but it greatly diminished the basal insulin values (21.57 ± 2.48 vs. 44.69 ± 3.3 μU/ml, p < 0.01). In the control rats, despite the elevated glucose concentrations, a significant drop in plasma insulin levels was observed within the first 15 min of adrenaline infusion, followed by a period of recovery. In the adrenaline-treated group, in which plasma glucose levels were lower than in control animals, plasma insulin levels did not drop as in control rats, but a significant increase was found after 30 min of infusion. During the intravenous glucose tolerance test, the plasma glucose and insulin responses showed similar patterns; however, during the concomitant adrenaline infusion, the treated rats showed a better glucose tolerance than their controls. These results indicate that rats chronically treated with adrenaline adapt to the diabetogenic effect of an infusion of adrenaline by having a lower inhibition of insulin release, although the lower basal insulin levels may indicate a greater sensitivity to endogenous insulin.

The Effects of Electroconvulsive Therapy on Plasma Insulin and Glucose in Depression

1992 ◽  
Vol 161 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Karen Williams ◽  
Jeanette Smith ◽  
Paul Glue ◽  
David Nutt
Keyword(s):  
Blood Glucose ◽  
Clinical Outcome ◽  
Electroconvulsive Therapy ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Significant Rise ◽  
Insulin Levels ◽  
Depressed Patients ◽  
Plasma Insulin Levels ◽  
Insulin Responses

The effects of ECT on plasma insulin and glucose were assessed in 20 depressed patients, during the first, third and fifth session of ECT. After each administration of ECT there was a significant rise in blood glucose and plasma insulin levels, both of which peaked at 15 minutes. Insulin responses tended to attenuate over the course of ECT, whereas the glucose responses were similar for all three treatments. ECT was effective in all patients, although two months after the last treatment nine patients had partially relapsed (Hamilton score > 15). Those who relapsed had a more attenuated insulin response at the fifth treatment than those who had remained well, which suggests that insulin response to ECT may be predictive of clinical outcome.

scholarly journals miR-467 regulates inflammation and blood insulin and glucose

2019 ◽  
Author(s):  
Jasmine Gajeton ◽  
Irene Krukovets ◽  
Revanth Yendamuri ◽  
Dmitriy Verbovetskiy ◽  
Amit Vasanji ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Plasma Insulin ◽  
Western Diet ◽  
Insulin Levels ◽  
Glucose Clearance ◽  
Physiological Feedback ◽  
Plasma Insulin Levels ◽  
Antagonist Effect

AbstractObesity is associated with inflammation and insulin resistance (IR), but the regulation of insulin sensitivity (IS) and connections between IS and inflammation remain unclear. We investigated the role of miR-467a-5p, a miRNA induced by hyperglycemia, in regulating inflammation and blood glucose handling.We previously demonstrated that miR-467a-5p is induced by hyperglycemia and inhibits the production of thrombospondin-1 (TSP-1), a protein implicated in regulating inflammation. To investigate the role of miR-467 in blood glucose handling and tissue inflammation, WT C57/BL6 mice were fed chow or Western diet from 5 to 32 weeks of age and injected weekly with miR-467a-5p antagonist. Inhibiting miR-467a-5p resulted in 47% increase in macrophage infiltration and increased Il6 levels in adipose tissue, higher plasma insulin levels (98 vs 63 ng/mL), and 17% decrease in glucose clearance without increase in weight or HDL/LDL. The antagonist effect was lost in mice on Western diet. Mice lacking TSP-1 lost some but not all of the miR-467 effects, suggesting Thbs1−/− (and other unknown transcripts) are targeted by miR-467 to regulate inflammation.miR-467a-5p provides a physiological feedback when blood glucose is elevated to avoid inflammation and increased blood glucose and insulin levels, which may prevent IR.

Plasma Insulin Studies in the Diagnosis of Insulinoma

1969 ◽  
Vol 14 (6) ◽  
pp. 200-208 ◽  
Author(s):  
M. T. McKiddie ◽  
K. D. Buchanan ◽  
R. J. Abernethy
Keyword(s):  
Plasma Insulin ◽  
Insulin Response ◽  
Insulin Level ◽  
Oral Glucose ◽  
False Negatives ◽  
Insulin Levels ◽  
Repeated Sampling ◽  
High Insulin ◽  
Plasma Insulin Levels ◽  
Fasting Plasma Insulin

Plasma insulin levels were measured in 8 patients of whom 5 were surgically proven to have, and 3 had strongly suggestive evidence of, a functioning islet cell tumour. The fasting plasma insulin level was elevated in only 3 patients, despite repeated sampling. The administration of tolbutamide produced an excessive insulin response in 5 of the 8 patients, glucagon produced an excessive insulin response in 4 of 6 patients tested, 1-leucine produced a rise in plasma insulin in 1 of 2 subjects tested and the only subject studied after 50g. oral glucose had a high insulin response. The insulin response was highest after tolbutamide in all but one patient and this would appear to be the single most valuable test. However false negatives may occur and therefore the whole range of tests may have to be performed to establish the diagnosis. Two patients were studied during surgery and in one the insulin content of the tumour was assayed after extraction with acid alcohol. Four patients were studied again after treatment by surgery (2) and diazoxide (2) when normal insulin levels were found.

Pre- and postabsorptive insulin secretion in chronic decerebrate rats

1986 ◽  
Vol 250 (4) ◽  
pp. R539-R548 ◽  
Author(s):  
F. W. Flynn ◽  
K. C. Berridge ◽  
H. J. Grill
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Oral Glucose ◽  
Base Line ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Percent Change ◽  
Plasma Insulin Levels

Basal, taste-stimulated (preabsorptive), and postabsorptive insulin secretion and plasma glucose responses were studied in chronic decerebrate rats and their pair-fed neurologically intact controls. In experiment 1, preabsorptive insulin responses (PIR) elicited by oral infusions of glucose solution was measured in chronic decerebrate rats. Oral glucose was ingested and led to a significant short-latency elevation in plasma insulin levels. Plasma glucose levels remained constant during this time. These data show that caudal brain stem mechanisms, in isolation of the forebrain, are sufficient for the neurally mediated PIR elicited by oral glucose stimulation. In experiment 2, effects of decerebration on postabsorptive insulin secretion were measured. During the 3 h immediately after transection there was no effect of decerebration on peripheral plasma insulin or glucose levels. Thereafter, however, basal plasma insulin levels of decerebrate rats were at least twice that of control rats. Plasma glucose levels of both groups remained identical despite the hyperinsulinemia in decerebrate rats. Atropine treatment decreased, and phentolamine administration elicited a greater absolute and percent change increase in insulin levels of decerebrate rats. These data indicate that altered autonomic tone contributes to maintaining the basal hyperinsulinemia in the decerebrate rat. In response to intragastric meals and glucose and intravenous glucose administration, insulin secretion was greater in decerebrate than in control rats. Percent change in insulin levels from base line was similar in both groups after intragastric meals and intravenous glucose. In response to intragastric glucose, however, percent increase in insulin levels was greater in decerebrate rats. Decerebrate rats demonstrated mild glucose intolerance after intragastric and intravenous treatments. These results are contrasted with the known effects of ventromedial hypothalamic lesions on insulin secretion and glucose homeostasis.

Effect of adrenal demedullation and (or) physical training on glucose tolerance in the rat

1993 ◽  
Vol 71 (12) ◽  
pp. 931-937 ◽  
Author(s):  
Christine Jean ◽  
Gilles Tancrède ◽  
André Nadeau
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Physical Training ◽  
Plasma Insulin ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Basal Plasma ◽  
Plasma Insulin Levels

Physical training increases insulin sensitivity by mechanisms not yet fully understood. Because exercise also modulates adrenergic system activity, the present study was designed to ascertain whether the improved glucose homeostasis observed in trained rats is influenced by epinephrine secretion from the adrenal medullae. Male Wistar rats previously submitted to adrenal demedullation or sham operated were kept sedentary or trained on a treadmill over a 10-week period. An intravenous glucose tolerance test (IVGTT) was done 64 h after the last bout of exercise. Basal plasma glucose levels were reduced by physical training (p < 0.005) and by adrenal demedullation (p < 0.001). Adrenodemedullated rats had lower (p < 0.005) plasma glucose levels than sham-operated animals over the whole glucose tolerance curve. Trained animals had lower (p < 0.01) plasma glucose levels than sedentary rats throughout the IVGTT, except at 45 min. The glucose disappearance rate measured after the glucose bolus injection was increased by training (p < 0.05), whereas it was not modified by adrenal demedullation. Basal plasma insulin levels were reduced (p < 0.001) by physical training but unaffected by adrenal demedullation. During the IVGTT, adrenodemedullated rats had higher (p < 0.01) plasma insulin levels at 2, 4, and 6 min, whereas trained animals had lower (p < 0.05) plasma insulin levels throughout the test. Moreover, insulin in adrenodemedullated and trained rats had returned to basal levels at 30 min. The area under the curve for insulin was diminished by physical training (p < 0.001) but was not modified by adrenal demedullation. In the basal state and during the IVGTT, the sedentary adrenodemedullated rats had higher (p < 0.05) plasma glucagon levels compared with the other groups of animals. Pancreatic insulin content was not modified by adrenal demedullation but was diminished (p < 0.01) by physical training. The pancreatic glucagon content was not altered by adrenal demedullation or physical training. Because adrenal demedullation abolished the exercise-induced increase in epinephrine secretion, the results of the present study suggest that the enhanced insulin sensitivity induced by physical training is not caused by an increase in epinephrine secretion from the adrenal medullae.Key words: adrenal demedullation, physical training, glucose tolerance, insulin sensitivity, catecholamines.

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