Studies on the Mechanism of Pentobarbital-Induced Glucose Intolerance

Mb, Davidson

doi:10.1055/s-0028-1094141

Cited by 27 publications

(10 citation statements)

References 2 publications

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“…There was no statistically significant difference between the results obtained for the treated obese and control lean animals although the values obtained for the former tended to be slightly higher. The removal of glucose from the blood was slower than is normally observed and we ascribe this to the fact that for these tests the animals were kept under pentobarbital anaesthesia (Davidson, 1971).…”

Section: Resultsmentioning

confidence: 94%

The effect of oxytetracycline on insulin resistance in obese mice

Bégin–Heick

Bourassa

Heick

1974

Biochemical Journal

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1. Chronic oxytetracycline treatment was found to improve the insulin resistance of the obese-hyperglycaemic mouse. 2. The improved response to insulin was accompanied by decreased concentrations of circulating insulin and glucose, by a decrease in the lipid content of the liver and by an increase in the insulin-receptor sites of the liver and adipose tissue. 3. The increase in insulin-receptor sites preceded the fall in blood glucose. 4. Comparable studies done on food-restricted animals indicated that although chronic food restriction corrected the hyperinsulinaemia it did not restore the insulin-receptor sites or the hyperglycaemia.The obese-hyperglycaemic mouse is characterized by obesity, non-ketotic hyperglycaemia, hyperinsulinism, islet-cell hyperplasia and resistance to exogenous insulin. Insulin resistance in the obesehyperglycaemic mouse has been attributed to several factors.(1) The number of insulin-binding sites on

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Section: Resultsmentioning

confidence: 94%

The effect of oxytetracycline on insulin resistance in obese mice

Bégin–Heick

Bourassa

Heick

1974

Biochemical Journal

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“…anesthesia, since pentobarbital was shown not to alter the metabolic parameters tested herein (constant rate for glucose disappearance [ K ITT ], fasting glycemia, insulinemia, and free fatty acids) in comparison with conscious animals (20) or insulin responses to glucose (21). At the end of the experiments, the rats were killed by an intracardiac overdose of pentobarbital, except when heart puncture was performed to collect blood.…”

Section: Methodsmentioning

confidence: 99%

Carotid Body Denervation Prevents the Development of Insulin Resistance and Hypertension Induced by Hypercaloric Diets

et al. 2013

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Increased sympathetic activity is a well-known pathophysiological mechanism in insulin resistance (IR) and hypertension (HT). The carotid bodies (CB) are peripheral chemoreceptors that classically respond to hypoxia by increasing chemosensory activity in the carotid sinus nerve (CSN), causing hyperventilation and activation of the sympathoadrenal system. Besides its role in the control of ventilation, the CB has been proposed as a glucose sensor implicated in the control of energy homeostasis. However, to date no studies have anticipated its role in the development of IR. Herein, we propose that CB overstimulation is involved in the etiology of IR and HT, core metabolic and hemodynamic disturbances of highly prevalent diseases like the metabolic syndrome, type 2 diabetes, and obstructive sleep apnoea. We demonstrate that CB activity is increased in IR animal models and that CSN resection prevents CB overactivation and diet-induced IR and HT. Moreover, we show that insulin triggers CB, highlighting a new role for hyperinsulinemia as a stimulus for CB overactivation. We propose that CB is implicated in the pathogenesis of metabolic and hemodynamic disturbances through sympathoadrenal overactivation and may represent a novel therapeutic target in these diseases.

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“…We found that the arginine-stimulated IRG "secretion" from A cells in the STZ-treated dogs did not differ from the The secretion of IRG stimulated by insulin-induced hypoglycemia is considered to be influenced by several factors including the degree of hypoglycemia and the rate of decrease in blood glucose (Gerich et al, 1974). We found that the rate of the fall and the nadirs of blood glucose levels in the It is well known that anaesthesia may affect pancreatic hormonal secretion and glucose metabolism (Davidson, 1971;Bailey and Flatt, 1980). We evaluated the hormonal secretions in the STZ-treated dogs under the same conditions as the control dogs which showed significant insulin and glucagon secretion in response to stimuli.…”

Section: Discussionmentioning

confidence: 66%

Glucagon secretory responses to insulin-induced hypoglycemia and arginine in streptozotocin-induced diabetic dogs.

et al. 1983

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To clarify whether the reactivity of A cells is regulated by B cell function in the pancreas, plasma glucagon (IRG) responses to insulin-induced hypoglycemia and to arginine infusion were evaluated in streptozotocin (STZ; total 40 mg/kg) treated and control dogs. There was no significant rise in plasma IRG levels during the insulin-induced hypoglycemia in the STZ-treated dogs. In contrast, arginine enhanced the IRG secretion from the pancreas to a similar extent in the two groups. This was deduced from the difference between IRG levels in the pancreaticoduodenal and peripheral veins. Neither intravenous glucose nor arginine infusion resulted in a significant rise in plasma insulin (IRI) levels in the STZ-treated dogs. IRI content in the pancreas of STZ-treated dogs was significantly reduced to 5 percent below the levels in the control dogs. The IRG content for control and STZ-treated dogs did not differ. These results indicate that while the responsiveness of A cells to hypoglycemia may depend on the secretory capacity of B cells, such is not the case with arginine.

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Studies on the Mechanism of Pentobarbital-Induced Glucose Intolerance

Cited by 27 publications

References 2 publications

The effect of oxytetracycline on insulin resistance in obese mice

The effect of oxytetracycline on insulin resistance in obese mice

Carotid Body Denervation Prevents the Development of Insulin Resistance and Hypertension Induced by Hypercaloric Diets

Glucagon secretory responses to insulin-induced hypoglycemia and arginine in streptozotocin-induced diabetic dogs.

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