Nucleus ambiguus stimulation increases plasma insulin levels in the rat

1981 ◽  
Vol 241 (1) ◽  
pp. E22-E27 ◽  
Author(s):  
D. A. Bereiter ◽  
H. R. Berthoud ◽  
M. Brunsmann ◽  
B. Jeanrenaud
Keyword(s):  
Electrical Stimulation ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Inhibitory Effect ◽  
Nucleus Ambiguus ◽  
Male Rats ◽  
Insulin Levels ◽  
Adrenergic Antagonist ◽  
Cervical Vagotomy ◽  
Plasma Insulin Levels

The ventral lateral brainstem has been explored for sites that facilitate insulin release unilaterally, using electrical stimulation techniques in male rats anesthetized with alpha-chloralose/urethane. Stimulation in the region of nucleus ambiguus (amb) produced a rapid rise (by 1 min) in plasma insulin levels, whereas stimulation of brainstem regions further than 500 micrometers from amb had no consistent effect on insulin levels. The amb-induced rise in insulin was markedly exaggerated by the alpha-adrenergic antagonist, phentolamine, and was greatly diminished by bilateral cervical vagotomy or atropine pretreatment. These results strongly suggest that the amb is one source of vagal motoneurons that facilitate insulin secretion. However, amb electrical stimulation alone also activated an apparent sympathetic efferent output whose inhibitory effect on insulin release could be blocked by phentolamine.

scholarly journals Fructose feeding and intermittent hypoxia affect ventilatory responsiveness to hypoxia and hypercapnia in rats

2004 ◽  
Vol 97 (4) ◽  
pp. 1387-1394 ◽  
Author(s):  
Evelyn H. Schlenker ◽  
Yijiang Shi ◽  
Joni Wipf ◽  
Douglas S. Martin ◽  
Curtis K. Kost
Keyword(s):  
Intermittent Hypoxia ◽  
Plasma Insulin ◽  
Tap Water ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Male Rats ◽  
Control Group ◽  
Insulin Levels ◽  
Ventilatory Responses ◽  
Plasma Insulin Levels

We hypothesized that, in male rats, 10% fructose in drinking water would depress ventilatory responsiveness to acute hypoxia (10% O2 in N2) and hypercapnia (5% CO2 in O2) that would be depressed further by exposure to intermittent hypoxia. Minute ventilation (V̇e) in air and in response to acute hypoxia and hypercapnia was evaluated in 10 rats before fructose feeding (FF), during 6 wk of FF, and after FF was removed for 2 wk. During FF, five rats were exposed to intermittent air and five to intermittent hypoxia for 13 days. Six rats given tap water acted as control and were exposed to intermittent air and subsequently intermittent hypoxia. In FF rats, plasma insulin levels increased threefold in the rats exposed to intermittent hypoxia and during washout returned to levels observed in rats exposed to intermittent air. During FF, ventilatory responsiveness to acute hypoxia was depressed because of decreased tidal volume (Vt) responsiveness. During washout, V̇e decreased as a result of decreased Vt and frequency of breathing, and the ventilatory responsiveness to hypoxia in intermittent hypoxia rats did not recover. In all rats, the ventilatory responses to hypercapnia were decreased during FF and recovered after washout because of an increased Vt responsiveness. In the control group, hypoxic responsiveness was not depressed after intermittent hypoxia and was augmented after washout. Thus FF attenuated the ventilatory responsiveness of conscious rats to hypoxia and hypercapnia. Intermittent hypoxia interacted with FF to increase insulin levels and depress ventilatory responses to acute hypoxia that remained depressed during washout.

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.

scholarly journals Plasma corticosterone, insulin and glucose changes induced by brief exposure to isoflurane, diethyl ether and CO2 in male rats

2010 ◽  
Author(s):  
H Zardooz ◽  
F Rostamkhani ◽  
J Zaringhalam ◽  
F Faraji Shahrivar
Keyword(s):  
Diethyl Ether ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Insulin Levels ◽  
Short Term Exposure ◽  
Plasma Insulin Levels ◽  
The Impact ◽  
Fasted Rats

The impact of anesthetic agents on endocrine and metabolic factors is an important issue. The present study has compared the effects of a short-term exposure to diethyl ether, isoflurane, or CO2 on plasma corticosterone, insulin and glucose concentrations since the duration of anesthetic exposure may have an effect on those factors. Male rats were divided into fed and fasted groups. The experimental rats were briefly exposed to diethyl ether, isoflurane, or CO2 (the degree of anesthesia was identical), while a control group was not exposed to the anesthetics. In the fed rats, diethyl ether exposure increased the levels of plasma glucose. CO2 exposure decreased plasma corticosterone and increased plasma glucose levels. Isoflurane exposure caused no changes in plasma corticosterone, glucose, or insulin levels. In the fasted rats, diethyl ether exposure increased plasma corticosterone and reduced plasma insulin levels. The plasma corticosterone and insulin levels were significantly increased by CO2 exposure. Isoflurane exposure decreased plasma insulin levels. A brief exposure to either diethyl ether or CO2 changed the plasma corticosterone, glucose, and insulin levels in fed and/or fasted rats. However, isoflurane exposure had the least effect on the concentration of these factors in both the fed and fasted states.

Endocrine pancreatic morphology and function in exocrine insufficiency in rats

1987 ◽  
Vol 253 (2) ◽  
pp. G139-G145
Author(s):  
B. Goke ◽  
K. Elsebach ◽  
W. Hausmann ◽  
M. Schaar ◽  
R. Arnold ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Serum Glucose ◽  
Relative Distribution ◽  
Perfused Pancreas ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Exocrine pancreatic insufficiency was induced in rats by injection of oleic acid into the pancreatic duct. Six weeks after a single injection of 50 microliters oleic acid, the exocrine tissue was reduced by 98%. The islets of Langerhans remained intact and showed no changes in the relative distribution of beta-, alpha-, D-, and PP-cells. In rats fed ad libitum, plasma insulin levels and pancreatic insulin content did not differ between oleic acid-treated animals and controls. The dynamic insulin response was evaluated in the isolated perfused pancreas. The biphasic pattern of insulin release after stimulation by glucose was preserved. The half-maximal (10 mM) glucose-induced insulin release was reduced to 49% after onset of exocrine atrophy. After stimulation of insulin secretion by a maximal glucose load (20 mM), the insulin output from the perfused pancreas was reduced to 56%. A reduction in insulin release to 24% occurred with respect to the arginine (15 + 10 mM glucose)-stimulated secretion. To evaluate the significance of these findings in intact animals, glucose tolerance tests were performed. There were no differences between oleic acid-, saline-, or untreated animals with respect to serum glucose or plasma insulin levels during the oral glucose tolerance test. The insulin response after intravenous glucose in oleic acid-treated rats was not statistically different from controls. Nevertheless, the serum glucose levels in rats with exocrine atrophy were above controls, indicating a slight impairment of glucose tolerance.

scholarly journals Lower plasma insulin levels during overnight closed-loop in school children with type 1 diabetes: Potential advantage? A randomized cross-over trial

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0212013 ◽  
Author(s):  
Ulrike Schierloh ◽  
Malgorzata E. Wilinska ◽  
Ineke M. Pit-ten Cate ◽  
Petra Baumann ◽  
Roman Hovorka ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
School Children ◽  
Plasma Insulin ◽  
Closed Loop ◽  
Lower Plasma ◽  
Insulin Levels ◽  
Plasma Insulin Levels

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.

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.

ANF inhibits glucose-stimulated insulin secretion in mouse and rat

1988 ◽  
Vol 255 (5) ◽  
pp. E579-E582 ◽  
Author(s):  
B. Ahren
Keyword(s):  
Insulin Secretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Insulin ◽  
Glucagon Secretion ◽  
Insulin Levels ◽  
Atrial Cells ◽  
Insulin And Glucagon Secretion ◽  
Plasma Insulin Levels ◽  
Glucose Stimulated Insulin Secretion ◽  
Dose Levels

Atrial natriuretic factor (ANF) is synthesized in atrial cells and was recently demonstrated to also occur within islet glucagon cells. Therefore, we investigated the possible effects of synthetic rat ANF-(1-28) on basal and stimulated insulin and glucagon secretion in the mouse and on glucose-induced insulin secretion in the rat. We found that ANF did not affect basal levels of insulin, glucagon, or glucose when injected intravenously at dose levels between 0.25 and 4.0 nmol/kg in mice. However, when injected together with glucose (2.8 mmol/kg), ANF (4.0 nmol/kg) inhibited the increase in plasma insulin levels by 40%, from 114 +/- 8 microU/ml in controls to 81 +/- 8 microU/ml (P less than 0.01). Likewise, the increase in plasma insulin levels during an intravenous infusion of glucose in rats (10 mg/min) was significantly reduced by ANF (100 pmol.kg-1.min-1; P less than 0.001). In contrast, the increase in plasma levels of insulin and glucagon after the intravenous injection of the cholinergic agonist carbachol in mice (0.16 mumol/kg) was not significantly affected by ANF. We conclude that ANF inhibits glucose-stimulated insulin secretion in the mouse and the rat. The peptide may therefore be a modulator of insulin secretion.

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