Intestinal motility responses to insulin and glucagon in streptozotocin diabetic rats

1982 ◽  
Vol 60 (7) ◽  
pp. 960-967 ◽  
Author(s):  
X. Pascaud ◽  
J. P. Ferre ◽  
M. Genton ◽  
A. Roger ◽  
M. Ruckebusch ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Contractile Activity ◽  
Diabetic Rats ◽  
Progressive Decrease ◽  
Significant Stimulation ◽  
Streptozotocin Diabetic Rats ◽  
Motor Effects ◽  
Fasted Rats ◽  
Stimulation Of ◽  
Spiking Activity

Myoelectrical and mechanical activities were chronically recorded by use of nichrome electrodes and miniaturized strain-gage transducers sutured on the serosa of the antrum, the duodenum, and the jejunum, in a first experiment (n = 6 rats) the early (0–6 h) and late (> 4 days) effects of streptozotocin (65 mg/kg i.v.) was recorded. In addition, the effect of insulin (1–5 IU/kg) and glucagon (6–200 μg/kg) administered intravenously were studied separately each in groups of seven normal and streptozotocin-induced diabetic-fed and fasted rats. The results indicated that within the 30 min following streptozotocin administration there was a significant stimulation of the duodenal and jejunal motility lasting 46 ± 8 min. When diabetes was established as shown by the basal blood glucose level obtained in those rats (2.30 ± 0.84 g/L), a progressive decrease of the frequency of the migrating myoelectric complex was observed along with a disorganization of the regular spiking activity phases without disturbing the basal electrical rhythm. Comparing with the basal level, a significant increase in the gastrointestinal motility indexes (MI) appeared both in fasted (p < 0.01) and fed (p < 0.05) normal animals, 13.1 ± 1.6 min after an i.v. injection of 1 IU/kg insulin. Motor effects of glucagon were related to the dose. When used at 25 μg/kg a disorganization of the spiking activity was observed with a stimulation of the contractile activity in the jejunum. At higher dosages, i.e., 100 μg/kg, it induced an immediate and significant decrease of motility at any level tested and lasting up to 20 ± 7 min. The motility responses to both hormones were lower in diabetic than in normal rats.

Improvement in cardiac dysfunction in streptozotocin-induced diabetic rats following chronic oral administration of bis(maltolato)oxovanadium(IV)

1993 ◽  
Vol 71 (3-4) ◽  
pp. 270-276 ◽  
Author(s):  
Violet G. Yuen ◽  
Chris Orvig ◽  
Katherine H. Thompson ◽  
John H. McNeill
Keyword(s):  
Blood Glucose ◽  
Heart Function ◽  
Myocardial Dysfunction ◽  
Plasma Lipid ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Vanadium Complex ◽  
Significant Correction ◽  
Streptozotocin Diabetic Rats

Decreased cardiac function in streptozotocin-diabetic rats has been used as a model of diabetes-induced cardiomyopathy, which is a secondary complication in diabetic patients. The present study was designed to evaluate the therapeutic effect of a new organic vanadium complex, bis(maltolato)oxovanadium(IV), (BMOV), in improving heart function in streptozotocin-diabetic rats. There were four groups of male, Wistar rats: control (C), control treated (CT), diabetic (D), and diabetic treated (DT). Treatment consisted of BMOV, 0.5 mg/mL (1.8 mM) for the first 3 weeks and 0.75 mg/mL (2.4 mM) for the next 22 weeks, in the drinking water of rats allowed ad libitum access to food and water. BMOV lowered blood glucose to < 9 mM in 70% of DT animals without any increase in plasma insulin levels, and mean blood glucose and plasma lipid levels were significantly lower in DT vs. D rats. Tissue vanadium levels were measured in plasma, bone, kidney, liver, muscle, and fat of BMOV-treated rats. Plasma vanadium levels averaged 0.84 ± 0.07 μg/mL (16.8 μM) in CT rats and 0.76 ± 0.05 μg/mL (15.2 μM) in DT animals. The highest vanadium levels at termination of this chronic feeding study were in bone, 18.3 ± 3.0 μg/g (0.37 μmol/g) in CT and 26.4 ± 2.6 μg/g (0.53 μmol/g) in DT rats, with intermediate levels in kidney and liver, and low, but detectable levels in muscle and fat. There were no deaths in either the CT or DT group, and no overt signs of vanadium toxicity were present. Tissue vanadium levels were not correlated with the glucose-lowering effect. Isolated working heart parameters of left ventricular developed pressure (LVDP) and rate of pressure development (+dP/dT, and −dP/dT) indicated that BMOV treatment resulted in significant correction of the heart dysfunction associated with streptozotocin-induced diabetes in rat.Key words: bis(maltolato)oxovanadium(IV), vanadium, diabetes, streptozotocin, myocardial dysfunction.

Insulin resistance of denervated rat muscle: a model for impaired receptor-function coupling

1984 ◽  
Vol 247 (5) ◽  
pp. E657-E666 ◽  
Author(s):  
C. F. Burant ◽  
S. K. Lemmon ◽  
M. K. Treutelaar ◽  
M. G. Buse
Keyword(s):  
Insulin Resistance ◽  
Glycogen Synthase ◽  
Contractile Activity ◽  
Signal Transmission ◽  
Glycogen Synthesis ◽  
Insulin Binding ◽  
Receptor Function ◽  
Modulate Signal ◽  
Fasted Rats ◽  
Stimulation Of

The effect of short-term denervation on the response to insulin was studied in isolated rat soleus and extensor digitorum longus (EDL) muscles 6 and 24 h after severing one sciatic nerve. Impaired insulin sensitivity and response occurred within 6 h postdenervation in solei. After 24 h, EDL of fed and fasted rats and solei of fed rats showed no stimulation of glycogen synthesis even with supraphysiological doses, whereas solei of fasted rats showed markedly decreased sensitivity and response to insulin. Insulin resistance of glycogen synthesis represented impaired stimulation of glucose transport and impaired glucose-independent activation of glycogen synthase by insulin. Changes in initial glycogen content of muscles did not correlate with insulin resistance. Insulin binding after denervation showed only minimum impairment and did not account for the marked insulin resistance. The response of denervated solei to epinephrine was unimpaired. Insulin resistance, which develops early after denervation in red and white muscles, represents primarily a defect in receptor-function coupling, suggesting that in muscle, nervous stimuli and/or contractile activity modulate signal transmission by the occupied insulin receptor.

Induction of control genes in intestinal gluconeogenesis is sequential during fasting and maximal in diabetes

2004 ◽  
Vol 286 (3) ◽  
pp. E370-E375 ◽  
Author(s):  
Gilles Mithieux ◽  
Isabelle Bady ◽  
Amandine Gautier ◽  
Martine Croset ◽  
Fabienne Rajas ◽  
...  
Keyword(s):  
Small Intestine ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Prolonged Fasting ◽  
Expression Of Genes ◽  
New Findings ◽  
Streptozotocin Diabetic Rats ◽  
Intestinal Gluconeogenesis ◽  
Total Glucose ◽  
Fasted Rats

We studied in rats the expression of genes involved in gluconeogenesis from glutamine and glycerol in the small intestine (SI) during fasting and diabetes. From Northern blot and enzymatic studies, we report that only phospho enolpyruvate carboxykinase (PEPCK) activity is induced at 24 h of fasting, whereas glucose-6-phosphatase (G-6-Pase) activity is induced only from 48 h. Both genes then plateau, whereas glutaminase and glycerokinase strikingly rebound between 48 and 72 h. The two latter genes are fully expressed in streptozotocin-diabetic rats. From arteriovenous balance and isotopic techniques, we show that the SI does not release glucose at 24 h of fasting and that SI gluconeogenesis contributes to 35% of total glucose production in 72-h-fasted rats. The new findings are that 1) the SI can quantitatively account for up to one-third of glucose production in prolonged fasting; 2) the induction of PEPCK is not sufficient by itself to trigger SI gluconeogenesis; 3) G-6-Pase likely plays a crucial role in this process; and 4) glutaminase and glycerokinase may play a key potentiating role in the latest times of fasting and in diabetes.

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