Effect of Cortisol on Plasma Lactate Levels following Cortisolinduced Hyperglycaemia in Common African Toad, Bufo regularis.

Previous studies in man have shown that cortisol induces hyperglycemia through gluconeogenesis. However,the metabolic substrates involved in cortisol-induced hyperglycemia and the role of adrenergic receptors in lactate productionin toads have not been well studied. This study investigated the effects of adrenergic receptor blockers in cortisol-inducedhyperglycemia and blood lactate levels in the common African toad (Bufo regularis). Each toad was fasted and anaesthetizedwith sodium thiopentone given intraperitoneally (50mg/kg/i.p). The animals (control) received 0.7% amphibian saline whileanimals (untreated) received cortisol intravenously (50µg/kg/i.v). In pre-treatment groups, animals received propanolol (0.5mg/kg/i.v), prazosin (0.2 mg/kg/i.v) and combination of propanolol (0.5mg/kg/i.v) and prazosin (0.2 mg/kg/i.v) respectivelyfollowed by administration of cortisol 50µg/kg/i.v. Thereafter, blood samples were collected for estimation of glucose andlactate using the modified glucose oxidase method and colorimetric method respectively. Cortisol caused significant increase in blood glucose level ((p<0.05) and reduction in blood lactate levels. Pre-treatment with Prazosin (0.2 mg/kg/i.v) causedsignificant (p<0.05) increase in blood glucose level and significant reduction in blood lactate levels while pre-treatment withPropanolol (0.5mg/kg/i.v) abolished cortisol-induced hyperglycemia and caused increase in blood lactate levels comparedwith the untreated group. The combination of both blockers abolished the hyperglycemic effect of cortisol and causedincrease in the blood lactate levels. The results of this study show that cortisol-induced hyperglycemia is a consequent ofgluconeogenesis and mediated through the beta-adrenergic receptors. The results also show that lactate is produced andused as a gluconeogenic substrate to induce cortisol hyperglycemia in the Common African toad bufo regularis. The betaadrenergic receptors are involved in the use of lactate to induce cortisol hyperglycemia in the Common African toad Buforegularis.

Effects of Petrol Exposure on Glucose, Liver and Muscle glycogen levels in the Common African toad Bufo regularis.

This study investigated the effects of exposure to petrol on blood glucose, liver and muscle glycogen levels in the common African toad Bufo regularis. A total of 126 adult toads of either sex weighing between 70-100g were used for this study. The experiment was divided into three phases. The phase 1 experiment the acute toxicity test consisted of animals divided into six groups of 10 toads per group and were exposed to water (H2O), H2O + Tween 80, 2ml/l, 3ml/l, 5ml/l, and 10ml/l of petrol respectively for 96 hours using the static renewal bioassay system. In the Phase 2 experiment, the animals were exposed to H2O, H2O + Tween 80, 0.14ml/l, 0.3ml/l, 0.6ml/l, and 1.13ml/l of petrol respectively for 3 days; while in phase 3 experiment they were exposed to petrol solutions for 14 days. After the various exposures, the blood glucose, liver and muscle glycogen contents were determined using standard methods. The results of the study showed that the median lethal concentration of petrol (96 hours LC50) was 4.5ml/l and sub-lethal concentration of petrol caused mortality of animals. Exposure to petrol solutions for 3 days had no significant effect on blood glucose level of the animals but caused significant decrease in the liver and muscle glycogen levels at high concentrations. In the animals exposed to petrol solutions for 14 days, there was a significant increase in glucose levels and significant reduction in liver and muscle glycogen levels at high concentrations when compared with the control. The results show that sub-lethal concentrations of petrol can cause mortality of animals, hyperglycemia and reduction in liver and muscle glycogen levels. The effects of petrol exposure on carbohydrate metabolism depend on the concentration and duration of exposure.

Effects of chronic administration of ethanolic extract of kolanut (Cola nitida) and caffeine on vascular function.

BACKGROUND: Kolanut (Cola nitida) is consumed in virtually every part of the world. The caffeine content of kolanut is scarce and the number of investigations studying the health benefits of kolanut is negligible compared to coffee. OBJECTIVE: The present study was designed to identify the caffeine content of kolanut and evaluate the effect of its chronic consumption on cardiovascular functions in rats. METHODS: The caffeine content of kolanut was determined by Gas chromatography-mass spectrometry (GC-MS). Wistar albino rats were divided into four groups (10 Rats/group). Kolanut extract (11.9 mg/kg), caffeine extracted from kolanut (7.5 mg/kg), decaffeinated of kolanut extract (6 mg/kg) and distilled water (control) was administered orally to each group for six-weeks. Effect of treatment on body weight, blood pressure and relaxation response to acetylcholine (ACh) and sodium nitroprusside (SNP) of the aortic rings was assessed. RESULTS: The total caffeine content of kolanut extract was found to be 51% and it was 96% pure from GC-MS analysis. Chronic consumption of kolanut and caffeine significantly (p < 0.05) decreased body weight. Similarly, kolanut extract decaffeinated kolanut and caffeine significantly (p < 0.05) reduced the contractile response to noradrenaline and higher potassium solution. Kolanut extract and caffeine also significantly (p < 0.05) increased the mean arterial blood pressure. Caffeine and kolanut consumption reduced the relaxation response to both acetylcholine and sodium nitroprusside. Atropine and L-NAME considerably inhibit the ACh-induced relaxation of the rat aortic ring suggesting the involvement of cholinergic mechanism. However, indomethacin (10(-4)M) also attenuated the ACh response indicating involvement of protanoids. CONCLUSION: The results suggest that treatment with both kolanut extract and caffeine had similar characteristics between the two groups with no significant differences in the ACh-induced relaxation of thering suggesting that the action of kolanut extract is due to its caffeine content.

Effect of adrenaline on glucose uptake in the rabbit small intestine.

OBJECTIVES: Previous study had shown that nicotine acts on blood glucose through release of adrenaline. While there are reports on the hyperglyceic effect of adrenaline in rabbits, there is no information on the effect of adrenaline on intestinal glucose uptake of rabbits. The present study was carried out to find out if adrenaline has any effect on glucose uptake in the rabbit small intestine. MATERIALS AND METHODS: Experiments were carried out on fasted anaesthetized male rabbits. Five groups of rabbits (6 rabbits per group) were studied. A vein draining a segment of the upper jejunum was cannulated for blood flow and venous glucose measurements. The left femoral artery and vein were cannulated for arterial blood sampling and drug infusion respectively. Glucose uptake was calculated as a product of jejunal blood flow and the glucose difference between arterial (A) and venous (V) blood. RESULTS: The fasting venous blood glucose levels were 151.8 +/- 4.4mg/dl and 164.0 + 2.3mg/dl in Groups I and V that were not given adrenoceptor blockers. The upper jejunum had a resting (or basal) glucose uptake of 38.3 +/- 1.6mg/min in the control group. When adrenaline (2ug/kg) was injected intravenously, arterial blood glucose rose from a basal value of 245.5 +/- 4.6mg/dl to 307.5+4.7mg/dl at the peak of response while venous glucose rose from 151.8+4.4mg/dl to 275.8 +/- 4.2mg/dl at the peak of response. Glucose uptake increased to 107.4 +/- 2.5mg/ min at the peak of response. The hyperglycaemic response to adrenaline injection was abolished by propranolol but not by prazosin indicating that this effect of adrenaline is mediated through beta adrenoceptor. Both prazosin and propranolol reduced considerably adrenaline-induced increase in blood flow and glucose uptake, prazosin being more potent in flow reduction. CONCLUSION: This study showed that the resting small intestine of rabbits took up large amounts of glucose. The intestinal glucose uptake was markedly increased by adrenaline injection. The response to adrenaline was mediated through alpha and beta adrenoceptors. The responses to adrenaline are different in many respects from those induced by nicotine in rabbits in our earlier study. The reason for the differences is obscure.

Effect of nicotine on glucose uptake in the rabbit small intestine.

A technique for measuring glucose uptake in the small intestine of rabbits was developed. Using this technique, the glucose uptake in the resting jejunum of rabbits and the effect of nicotine infusion on glucose uptake were studied. Experiments were carried out on fasted anaesthetized male rabbits. Four groups of rabbits (6 per group) were studied. A vein draining segment of the upper jejunum was cannulated for blood flow and venous glucose measurements. The left femoral artery and vein were cannulated for arterial blood sampling and drug infusion respectively. Glucose uptake was calculated as a product of jejunal blood flow and the (A-V) glucose difference. The fasting blood glucose levels were 101.0 +/- 8.4 mg/dl and 127.0 +/- 11.3 mg/dl before and after anaesthesia respectively. Basal blood glucose was much higher than this following surgery. The upper jejunum had a resting glucose uptake of 24.1 +/- 7.0 mg/min. When nicotine (50 ug/kg) was infused intravenously, blood glucose rose from a basal value of 253.8 +/- 9.5 mg/dl to 379.8 +/- 20.3 mg/dl at the peak of response. Glucose uptake increased to 73.1 +/- 11.3 mg/min at the peak of response. These effects of nicotine are mediated through both beta and alpha adrenoceptors. Comparison with previous studies in dogs and rats showed that different adrenoceptors are involved in nicotine hyperglycaemia in fasted dogs, rats and rabbits.