Swim training alters sympathoadrenal and endocrine responses to hemorrhage in borderline hypertensive rats

1995 ◽  
Vol 269 (1) ◽  
pp. R124-R130
Author(s):  
D. E. McCoy ◽  
J. E. Steele ◽  
R. H. Cox ◽  
R. L. Wiley
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Rest Period ◽  
Endocrine Function ◽  
Plasma Norepinephrine ◽  
Hypertensive Rats ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Plasma Insulin Levels ◽  
Positive Correlations

Swim training alters cardiovascular, sympathoadrenal, and endocrine responses to hemorrhage in borderline hypertensive rats (BHR). The effects of 10, 20, and 30% blood volume hemorrhages on cardiovascular, sympathoadrenal, and endocrine function in swim-trained (T; 2 h/day, 5 day/wk for 10-12 wk) and age-matched, untrained, sedentary, control (UT) borderline hypertensive rats (BHR) were assessed. Heart rate (HR) in UT BHR was significantly greater during the baseline (rest) period than T BHR. HR increased slightly from baseline in both groups after 10% hemorrhage but was significantly decreased in both groups after 20 and 30% hemorrhages. The decrease was eliminated by atropine (1 mg/kg iv). Systolic (SBP) and diastolic (DBP) blood pressures decreased significantly after 20 and 30% hemorrhages in both T and UT BHR but were not different between the groups at these times. Plasma norepinephrine levels were significantly increased above baseline after 20 and 30% hemorrhages in UT BHR and were significantly greater in UT BHR than T BHR after 30% hemorrhage. Plasma glucose levels increased significantly after 30% hemorrhage in both groups but were significantly greater in UT BHR than T BHR. Both plasma norepinephrine and plasma epinephrine levels showed strong positive correlations with plasma glucose. After 20 and 30% hemorrhages, plasma insulin levels were unchanged in T BHR but were significantly decreased in UT BHR. Plasma insulin levels were significantly less in UT than T BHR after 30% hemorrhage. These results suggest that swim training alters the effect that hemorrhage exerts on endocrine and sympathoadrenal function in BHR.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

Metformin decreases plasma insulin levels and systolic blood pressure in spontaneously hypertensive rats

1994 ◽  
Vol 267 (4) ◽  
pp. H1250-H1253 ◽  
Author(s):  
S. Verma ◽  
S. Bhanot ◽  
J. H. McNeill
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Insulin ◽  
Metformin Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Wistar Kyoto

To determine the relationship between hyperinsulinemia and hypertension in spontaneously hypertensive rats (SHR), the antihyperglycemic agent metformin was administered to SHR and their Wistar-Kyoto (WKY) controls, and its effects on plasma insulin levels and blood pressure were examined. Five-week-old rats were started on oral metformin treatment (350 mg.kg-1.day-1, which was gradually increased to 500 mg.kg-1.day-1 over a 2-wk period). Metformin treatment caused sustained decreases in plasma insulin levels in the SHR (27.1 +/- 2.3 vs. untreated SHR 53.5 +/- 2.7 microU/ml, P < 0.001) without having any effect in the WKY (30.7 +/- 2.2 vs. untreated WKY 37.8 +/- 1.6 microU/ml, P > 0.05). The treatment did not affect the plasma glucose levels in any group. Metformin treatment also attenuated the increase in systolic blood pressure in the SHR (157 +/- 6.0 vs. untreated SHR 196 +/- 9.0 mmHg, P < 0.001) but had no effect in the WKY (134 +/- 3 vs. untreated WKY 136 +/- 4 mmHg, P > 0.05). Furthermore, raising plasma insulin levels in the metformin-treated SHR to levels that existed in the untreated SHR reversed the effect of metformin on blood pressure (189 +/- 3 vs. untreated SHR 208 +/- 5.0 mmHg, P > 0.05). These findings suggest that either hyperinsulinemia may contribute toward the increase in blood pressure in the SHR or that the underlying mechanism is closely associated with the expression of both these disorders.

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.

Plasma glucose and insulin responses in growing rats fed a total parenteral nutrition diet either intravenously or intragastrically

1984 ◽  
Vol 62 (7) ◽  
pp. 775-780 ◽  
Author(s):  
Norman S. Track ◽  
Ernest Cutz ◽  
Barbara H. Witt
Keyword(s):  
Amino Acid ◽  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glucose Levels ◽  
Group I ◽  
Plasma Insulin Levels ◽  
Group Ii ◽  
Insulin Responses

The effect of administering either intravenously (group I) or intragastrically (group II) a glucose – amino acid total parenteral nutrition diet over a 12-day period upon plasma glucose and insulin responses was examined in adolescent rats. Infusion of the 25% glucose – 12.2% amino acid diet at a rate of 300 kCal∙kg body weight−1∙24 h−1 supported normal weight gain over the 12-day study period in both intravenously (group I) and intragastrically (group II) alimented rats. Mean plasma glucose levels rose dramatically in both groups by the end of day 1; group I had significantly higher mean plasma insulin levels. By day 3, the group I mean plasma glucose value decreased significantly while the group II mean glucose value remained virtually unchanged. Mean plasma insulin values more than doubled in both groups with the group I level still remaining significantly above the group II level. At days 6 and 12, group I mean plasma glucose levels were significantly below group II while both groups had similar plasma insulin levels. Data from this 12-day intravenous–intragastric alimentation study reveals quite different metabolic responses compared with acute (120–180 min) studies of the enteroinsular axis.

Adrenergic control of plasma magnesium in man

1987 ◽  
Vol 72 (1) ◽  
pp. 135-138 ◽  
Author(s):  
Kenneth F. Whyte ◽  
George J. Addis ◽  
Robert Whitesmith ◽  
John L. Reid
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Stress Tests ◽  
Adrenergic Stimulation ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Adrenaline Infusion ◽  
Plasma Magnesium

1. Regulation of magnesium balance is poorly understood. However, hypomagnesaemia has been reported in patients in clinical situations where circulating catecholamines are raised including myocardial infarction, cardiac surgery and insulin-induced hypoglycaemia stress tests. 2. The effects of l-adrenaline infusions, sufficient to achieve pathophysiological levels of adrenaline, and of therapeutic intravenous infusions of salbutamol, a β2-agonist, on plasma magnesium, plasma potassium, plasma glucose and plasma insulin levels were studied in a placebo-controlled design in eight normal subjects. 3. Plasma magnesium levels fell significantly during the adrenaline infusion and also during the salbutamol infusion, though more slowly. In a 1 h period of observation after cessation of the infusions no recovery of plasma magnesium levels was seen. Significant falls in plasma potassium levels were also observed during both infusions with spontaneous recovery within 30 min after the infusions. 4. No significant changes in plasma insulin levels occurred with either salbutamol or l-adrenaline compared with control. Plasma glucose levels rose significantly during the adrenaline infusion. 5. The study suggests that both l-adrenaline and salbutamol cause shifts in plasma magnesium which are not mediated by insulin. We propose that intracellular shifts of magnesium occur as a result of β-adrenergic stimulation.

Insulin modulates glucose-dependent insulinotropic polypeptide (GIP) secretion from enteroendocrine K cells in rats

2011 ◽  
Vol 392 (10) ◽  
pp. 909-918 ◽  
Author(s):  
Nigel Irwin ◽  
Jacqueline M.E. Francis ◽  
Peter R. Flatt
Keyword(s):  
Plasma Glucose ◽  
Oral Glucose ◽  
Glucose Lowering ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Elevated Glucose ◽  
Plasma Insulin Levels ◽  
Glucose Plasma ◽  
And Control ◽  
Intestinal Weight

Abstract Effects of insulin excess and deficiency on glucose-dependent insulinotropic polypeptide (GIP) was examined in rats following insulinoma transplantation or streptozotocin (STZ) administration. Over 14 days, food intake was increased (p<0.001) in both groups of rats, with decreased body weight (p<0.01) in STZ rats. Non-fasting plasma glucose levels were decreased (p<0.01) and plasma insulin levels increased (p<0.001) in insulinoma-bearing rats, whereas STZ treatment elevated glucose (p<0.001) and decreased insulin (p<0.01). Circulating GIP concentrations were elevated (p<0.01) in both animal models. At 14 days, oral glucose resulted in a decreased glycaemic excursion (p<0.05) with concomitant elevations in insulin release (p<0.001) in insulinoma-bearing rats, whereas STZ-treated rats displayed similar glucose-lowering effects but reduced insulin levels (p<0.01). GIP concentrations were augmented in STZ rats (p<0.05) following oral glucose. Plasma glucose and insulin concentrations were not affected by oral fat, but fat-induced GIP secretion was particularly (p<0.05) increased in insulinoma-bearing rats. Exogenous GIP enhanced (p<0.05) glucose-lowering in all groups of rats accompanied by insulin releasing (p<0.001) effects in insulinoma-bearing and control rats. Both rat models exhibited increased (p<0.001) intestinal weight but decreased intestinal GIP concentrations. These data suggest that circulating insulin has direct and indirect effects on the synthesis and secretion of GIP.

Strength training increases insulin action in healthy 50- to 65-yr-old men

1994 ◽  
Vol 77 (3) ◽  
pp. 1122-1127 ◽  
Author(s):  
J. P. Miller ◽  
R. E. Pratley ◽  
A. P. Goldberg ◽  
P. Gordon ◽  
M. Rubin ◽  
...  
Keyword(s):  
Strength Training ◽  
Insulin Action ◽  
Plasma Insulin ◽  
Insulin Infusion ◽  
Glucose Clamp ◽  
Oral Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Fasting Plasma ◽  
Plasma Insulin Levels

The insulin resistance associated with aging may be due, in part, to reduced levels of physical activity in the elderly. We hypothesized that strength training increases insulin action in older individuals. To test this hypothesis, 11 healthy men 50–63 yr old [mean 58 +/- 1 (SE) yr] underwent a two-step hyperinsulinemic-euglycemic glucose clamp with concurrent indirect calorimetry and an oral glucose tolerance test (OGTT) before and after 16 wk of strength training. The training program increased overall strength by 47% (P < 0.001). Fat-free mass (FFM; measured by hydrodensitometry) increased (62.4 +/- 2.1 vs. 63.6 +/- 2.1 kg; P < 0.05) and body fat decreased (27.2 +/- 1.8 vs. 25.6 +/- 1.9%; P < 0.001) with training. Fasting plasma glucose levels and glucose levels during the OGTT were not significantly lower after training. In contrast, fasting plasma insulin levels decreased (85 +/- 25 vs. 55 +/- 10 pmol/l; P < 0.05) and insulin levels decreased (P < 0.05, analysis of variance) during the OGTT. Glucose infusion rates during the hyperinsulinemic-euglycemic glucose clamp increased 24% (13.5 +/- 1.7 vs. 16.7 +/- 2.2 mumol.kg FFM-1.min-1; P < 0.05) during the low (20 mU.m-2.min-1) insulin infusion and increased 22% (55.7 +/- 3.3 vs. 67.7 +/- 3.9 mumol.kg FFM-1.min-1; P < 0.05) during the high (100 mU.m-2.min-1) insulin infusion. These increases were accompanied by a 40% increase (n = 7; P < 0.08) in nonoxidative glucose metabolism during the high insulin infusion. These results demonstrate that strength training increases insulin action and lowers plasma insulin levels in middle-aged and older men.

Alterations in body fat stores and plasma insulin levels with daily intervals of heat exposure in Holtzman rats

1993 ◽  
Vol 265 (5) ◽  
pp. R1109-R1114 ◽  
Author(s):  
C. J. De Souza ◽  
A. H. Meier
Keyword(s):  
Glucose Tolerance ◽  
Ambient Temperature ◽  
Body Fat ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Time Of Day ◽  
Light Onset ◽  
Insulin Levels ◽  
Fat Stores ◽  
Plasma Insulin Levels

The ability of timed daily increases in ambient temperature (from 22 +/- 1 degree C to 40 +/- 1 degree C for 2 h) to alter body fat stores, blood lipid levels, and insulin resistance were tested in male Holtzman rats. Of the six times of day tested only temperature pulses administered 16 h after light onset consistently decreased body weights, retroperitoneal fat stores, and plasma insulin levels. Subsequently, temperature pulses were administered either 0 (TP0) or 16 (TP16) h after light onset (light-dark 12:12 h). While no differences were observed between the TP0 group and the constant temperature (22 degrees C) controls, decreases in body weight gain, food consumption, retroperitoneal fat stores, and plasma concentrations of insulin, cholesterol, and triglycerides were consistently observed in the TP16 group. Although changes in plasma glucose during an oral glucose tolerance test were similar when the two treatment groups were compared with their respective controls, glucose tolerance was achieved with less insulin in the TP16 animals than in their respective controls. Insulin effectiveness was greater in the TP16 group as indicated by a decrease in plasma glucose, after insulin injection, that was of greater magnitude and longer duration than in controls. Hence, timed daily increases in ambient temperature may decrease obesity in part by decreasing plasma insulin levels apparently as a consequence of increased tissue sensitivity to insulin (greater glucose tolerance and less insulin intolerance). Because the treatment is effective only at a particular time of day the findings support a role for circadian neuroendocrine interactions in the regulation of these metabolic states.

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