Glucose tolerance and insulin secretion after adrenalectomy in mice made obese with gold thioglucose

1996 ◽  
Vol 148 (3) ◽  
pp. 391-398 ◽  
Author(s):  
S C Blair ◽  
I D Caterson ◽  
G J Cooney
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
The Body ◽  
Obese Mice ◽  
Glucose Load ◽  
Intravenous Glucose ◽  
Gold Thioglucose

Abstract The effect of adrenalectomy (ADX) on glucose tolerance and insulin secretion was examined in conscious mice made obese by a single injection of gold thioglucose (GTG). To facilitate such a study a chronic jugular catheter was implanted into the mice at the time of performing the ADX or sham-ADX. One week after ADX, the body weight (GTG-obese+sham-ADX, 35·6 ± 0·6 g; GTG-obese+ADX, 33·1 ± 0·6 g; P<0·05) and glycogen content of the liver (GTG-obese+sham-ADX, 2·4 ± 0·2 μmol/liver; GTG-obese+ADX, 1·6 ± 0·1 μmol/liver; P<0·05) of GTG-injected mice were reduced. Plasma glucose concentrations, in both the overnight fasted state and in response to an intravenous glucose load were also reduced following ADX of GTG-obese mice, but not to the level of the sham-ADX control mice. However, ADX completely normalized plasma insulin concentrations in both the basal state and also in response to a glucose load, as indicated by the finding that the integrated insulin secretory response of the ADX GTG-obese mice was not different from that of sham-ADX control mice (control+sham-ADX, 192 ± 5 min.μU/ml; GTG-obese+ADX, 196 ± 10 min.μU/ml). The effects of ADX on carbohydrate metabolism were not restricted to GTG-injected mice, as ADX of control mice decreased fasting plasma glucose levels and reduced liver glycogen and plasma insulin concentrations. The normalization of insulin release in ADX GTG-obese mice occurred while these mice were still obese and glucose intolerant. This suggests that the decreased insulin release was not due solely to an ADX-induced improvement in insulin sensitivity and/or weight loss. Removal of central glucocorticoid effects on the parasympathetic stimulation of insulin release may play a role in the reduced insulin release observed after ADX of obese and control mice, although peripheral effects of glucocorticoid deficiency on glycogen synthesis in the liver may also influence whole animal glucose homeostasis. Journal of Endocrinology (1996) 148, 391–398

Effects of hyperprolactinaemia on glucose tolerance and insulin release in male and female rats

1997 ◽  
Vol 153 (3) ◽  
pp. 423-428 ◽  
Author(s):  
F M Reis ◽  
A M Reis ◽  
C C Coimbra
Keyword(s):  
Glucose Tolerance ◽  
Insulin Release ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Female Rats ◽  
Insulin Concentration ◽  
Glucose Load ◽  
Plasma Insulin Concentration ◽  
Male And Female ◽  
Male And Female Rats

Abstract It has been shown that prolactin (PRL) induces glucose intolerance, hyperinsulinaemia and insulin resistance in several animal species, including rats. However, the sex differences regarding glucose homeostasis and insulin release in hyperprolactinaemic subjects have not been assessed to date. In the present study, hyperprolactinaemic (pituitary-grafted) or control (sham-operated) male and female rats were submitted to an i.v. glucose tolerance test (30 mg/100 g body weight, 30% glucose). Grafted female rats had fasting plasma glucose concentrations 26% above control (P<0·01). After the glucose load there was a rapid and pronounced increase in plasma glucose levels in all animal groups, followed by a return to basal values within 30 min. However, the glucose concentrations in hyperprolactinaemic rats were significantly greater than those in controls at 5 min (males, P<0·05) and 30 min (females, P<0·05). The glucose disappearance rate was significantly increased in the grafted females compared with control (P<0·01) and slightly increased in the grafted males. Plasma insulin concentration increased just after glucose load and returned to basal values within 5 min in all groups except for the grafted females, which had recovered their basal insulin levels at 15 min. The grafted male rats had insulin concentrations higher than those of sham-operated controls at 2 min (28·9 ± 3·6 vs 17·3 ± 2·1 μU/ml, P<0·01), whereas females had plasma insulin concentrations greater than those in sham-operated controls 10 min after the glucose load (15·9 ± 1·9 vs 10·1 ± 1·4 μU/ml, P<0·05). The areas under the plasma insulin concentration–time curves were also significantly increased in the hyperprolactinaemic rats and were positively correlated with plasma PRL concentrations (r=0·613, P<0·01). These results demonstrate that moderate chronic hyperprolactinaemia is associated with increased glucose-induced insulin release, which was altered at different times after the glucose load in grafted male and female rats, whereas fasting hyperglycaemia was observed only in grafted females, indicating a sexual dimorphism in the diabetogenic effects of PRL in rats. Journal of Endocrinology (1997) 153, 423–428

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.

scholarly journals Glucose Tolerance and Insulin Release in Malnourished Rats

1976 ◽  
Vol 50 (3) ◽  
pp. 153-163 ◽  
Author(s):  
C. Weinkove ◽  
E. A. Weinkove ◽  
B. L. Pimstone
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Protein Energy

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.

ENHANCEMENT OF INSULIN RELEASE TO ACUTE GLYCAEMIC STIMULATION WITH DEPRESSION OF BASAL INSULIN PRODUCTION RATES IN INSULINOMA FOLLOWING DIAZOXIDE ADMINISTRATION

1970 ◽  
Vol 63 (3) ◽  
pp. 392-404 ◽  
Author(s):  
Richard E. Bailey ◽  
Albert Castro ◽  
Rosanne M. Kramer ◽  
Dorothy Macfarlane
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Insulin Biosynthesis ◽  
Oral Glucose ◽  
Glucose Tolerance Tests ◽  
Tolerance Curve ◽  
Insulinoma Cells ◽  
Secretion Rates

ABSTRACT Single and double load oral glucose tolerance tests were performed repetitively both before and during administration of diazoxide to a 15-year old girl who had an insulin secreting islet cell tumour. Plasma insulin concentrations increased above baseline values by a greater magnitude in response to a single acute oral glycaemic stimulus following diazoxide treatment, compared to the increases resulting from comparable prediazoxide glucose tolerance tests, and plasma insulin either attained higher values or sustained elevations for a longer duration during the early part (first hour) of the single load tests. This provides evidence that diazoxide does not prevent the normal insulin release response to a glycaemic stimulus, and that enhanced insulin secretion rates may occur with insulinomas under the study conditions employed. Fasting plasma insulin concentrations were lower during the period of diazoxide administration which indicates that insulin biosynthesis was depressed under fasting steady-state conditions. Considering that the first part of the glucose tolerance curve reflects primarily insulin release, our data is consistent with the view that insulin storage within the insulinoma cells is preserved under the study conditions employed and may even be enhanced by diazoxide. Consequently, depression of insulin biosynthesis is considered to be a resultant effect and not a primary action of diazoxide. These results suggest a possible basis for »distinguishing« types of insulinomas should additional perspective reveal that glycaemic-induced enhancement of insulin secretion rates cannot be made to occur uniformly in diazoxide treated patients having insulinomas.

Low Vitamin K Intake Effects on Glucose Tolerance in Rats

1999 ◽  
Vol 69 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Sakamoto ◽  
Wakabayashi ◽  
Sakamoto
Keyword(s):  
Glucose Tolerance ◽  
Vitamin K ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Glucose Load ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance ◽  
Glucose Tolerance Tests ◽  
Early Insulin Response ◽  
Intravenous Glucose Tolerance Tests

To investigate the effects of vitamin K (VK) on pancreatic function, intravenous glucose tolerance tests were performed in rats fed with and without low VK diet (inclucing less than 20% required vitamin K1). Plasma glucose and immuno-reactive insulin (IRI) were determined. It was found that at 0 min., plasma glucose and IRI levels in low VK group were slightly less than in the control (glucose, 204.5 ± 21.7 vs. 229 ± 19.6 mg/dl, IRI, 6.6 ± 1.3 vs. 9.3 ± 1.8 ng/ml mean ± SEM). At 3 min. after glucose administration, plasma glucose was higher (391.8 ± 25.6 vs. 371.8 ± 18.7 mg/dl) and IRI, lower (11.8 ± 2.1 vs. 18.2 ± 3.6 ng/ml) in the low VK group. The disappearance rate of plasma glucose in the low VK group at 5–10 min. was significantly less than in the control (6.7 ± 2.2 vs. 11.9 ± 1.8 mg/ dl/min.). Incremental IRI area at 0 to 5 min. in the low VK group is less than in the control (15.2 ± 4.4 vs. 25.0 ± 9.1 ng/ml/min.), but at 5–60 min. and 0–60 min., it was found to be significantly higher compared to the control (210.3 ± 55.2 vs. 32.5 ± 47.1 ng/ml/min. at 5–60 min.). Dietary low VK intake would thus appear to induce a tendency of poor early insulin response, and late hyperinsulinemia to the glucose load in rats.

Glutamate stimulates insulin secretion and improves glucose tolerance in rats

1995 ◽  
Vol 269 (3) ◽  
pp. E551-E556 ◽  
Author(s):  
G. Bertrand ◽  
R. Puech ◽  
M. M. Loubatieres-Mariani ◽  
J. Bockaert
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Dependent Manner ◽  
Intravenous Glucose ◽  
Acid Receptor ◽  
Fasted Rats

We previously showed in vitro that glutamate stimulates insulin release via an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Here we address a more physiological question concerning the in vivo effect of intravenously or orally administered glutamate on insulinemia and glycemia in fed and fasted rats. In anesthetized fed rats, the intravenous administration of glutamate at 9 and 30 mg/kg transiently increased insulinemia in a dose-dependent manner. The insulin-secretory effect of glutamate (9 mg/kg) was blocked by an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. In anesthetized fasted rats, glutamate at 9 mg/kg was ineffective, but during an intravenous glucose tolerance test (0.5 g/kg), glutamate markedly potentiated insulin release and increased the glucose disappearance rate. In conscious rats, the intragastric administration of glutamate at 200 mg/kg elicited a transient insulin response in fed animals and had no effect in fasted animals but, during an oral glucose tolerance test (1 g/kg), enhanced insulin secretion and reduced the hyperglycemia. Glutamate was effective at plasma concentrations of 200-300 microM. In conclusion, intravenously and orally administered glutamate stimulates insulin secretion in vivo via an excitatory amino acid receptor and improves glucose tolerance.

Glycogenesis and glucose oxidation during an intravenous glucose tolerance test in man

2004 ◽  
Vol 106 (6) ◽  
pp. 645-652 ◽  
Author(s):  
Leslie J. C. BLUCK ◽  
Allan T. CLAPPERTON ◽  
Cheryl V. KIDNEY ◽  
W. Andy COWARD
Keyword(s):  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Glycogen Synthesis ◽  
Body Water ◽  
The Body ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance ◽  
Fasting Plasma

The quantity of deuterated glucose customarily given in labelled IVGTTs (intravenous glucose tolerance tests) changes the isotopic composition of the subject's body water enough to be detected by mass spectrometric techniques. Glucose undergoing direct glycogenesis does not contribute label to the body water pool, and isotope incorporated into it must have come from glucose that has either been oxidized or undergone indirect glycogenesis. By subtracting the amount of label found in body water from the total amount of glucose utilized, as calculated from the minimal model of glucose disappearance, it should be possible to study the partitioning of the dose given between direct glycogenesis in skeletal muscle and other metabolic pathways. To establish these principles, we used isotope ratio MS to determine body water composition in groups of healthy (n=7; mean weight, 76 kg; fasting plasma glucose and insulin, 5.1 mmol and 40 pmol respectively) and Type II diabetic (n=5; mean weight, 84 kg; fasting plasma glucose and insulin, 6.2 mmol and 75 pmol respectively) subjects undergoing IVGTTs. It was found that, for healthy subjects, 31% of the dose given was utilized in direct glycogenesis and this was decreased to 15% in diabetes. Defects in muscle glycogen synthesis in diabetes of the same order are well known from magnetic resonance studies. We conclude that measurement of label incorporation into body water is potentially useful for investigation of the metabolism of a glucose load in vivo during an IVGTT.

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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