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H T Yang

Publications and source records attributed to H T Yang.

At least 73 records · Page 4Linked to original sources

[The application of sex pheromones and juvenile hormone analogs on cockroaches].

The sex pheromone of cockroaches is the chemical which transmits the copulation signal between female and male roaches of the same species. It is produced by virgin females in most roaches, and the chemical structures have been identified for the American, German and Japanese cockroaches. Periplanone-B (PB) and periplanone-A (PA) have been synthesized in the laboratory and tested both in lab and field, showing good biological responses. The sex pheromones of the German cockroach are 3,11-dimethyl-2-nonacosanone, 29-hydroxy-3,11-dimethyl-2-nonacosanone and 29-oxo-3,11-dimethyl-2-nonacosanone, and because of their low volatile nature, they would not be used up in a short time. Periplanone-J (PJ) is produced by the Japanese cockroach. The juvenile hormone analogs (JHA) are chemicals which mimic the juvenile hormones (JH). They have the physiological actions of JH which are maintaining the larvae and nymphs in their immature stages or making the reproductive organs differentiate incompletely, and thereby interfering with their reproduction. The JHA which have been commercialized to control roaches are hydroprene, pyriproxyfen and fenoxycarb. The first two have been proved to reduce the roach population in field tests in the USA and Japan. For some reason, if the sex pheromone and the JHA are used together, the net effect will be more than if they are used alone. In the presence of the sex pheromone, the cockroaches' movements increase, so the chance for a roach to contact the sprayed JHA is also increased. This might be the possible reason for the above observation.

Animals↗

Effect of intravenous caffeine on muscle glycogenolysis in fasted exercising rats.

Caffeine has been reported to enhance performance by increasing fat utilization and by sparing liver and muscle glycogen. The lipolytic effect of caffeine has been reported to be diminished in response to previous carbohydrate loading of the subjects. The present study was designed to investigate the effects of caffeine during submaximal exercise in rats where the influence of dietary carbohydrate was removed by fasting. Rats were fasted overnight and given injection of 25 mg.kg-1 caffeine (CAF) or 0.9% NaCl (SAL) 60 min before exercise. They were run for 15, 30, and 60 min on a rodent treadmill up a 15% grade at 21 m.min-1. Plasma free fatty acids (FFA) were significantly elevated to 0.72 +/- 0.04 mM in CAF as compared to 0.45 +/- 0.03 mM in SAL at the beginning of exercise. During exercise, however, a significant difference in FFA levels between CAF and SAL was seen only at 30 min and not at other time points. No significant decrease in muscle glycogenolysis was observed in the CAF as compared to SAL rats, and the liver cyclic AMP remained the same in both CAF and SAL. Blood lactate (mM) showed an increase due to caffeine only at 15 min of exercise (CAF = 2.4 +/- 0.2; SAL = 1.7 +/- 0.3). Intravenous caffeine during exercise did not alter plasma glucagon or blood glucose. We conclude that caffeine has no effect on muscle glycogen utilization in fasted rats during exercise even though there was an increased FFA in CAF rats at the beginning of exercise.

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Effect of caffeine on glycogenolysis during exercise in endurance trained rats.

Caffeine has been reported to enhance performance by increasing lipid oxidation and sparing liver and muscle glycogen in human subjects during prolonged endurance exercise. In the present study, the effects of intravenous caffeine on the liver and muscle glycogenolysis during exercise in endurance trained rats were investigated. Male endurance trained rats (2 h.d-1 for 6-7 wk) were given injections of 5 mg.kg-1 caffeine (5 CAF), 25 mg.kg-1 caffeine (25 CAF), or 0.9% sodium chloride (SAL) and were run on the treadmill for 45 min, 90 min, or until exhaustion at 26 m.min-1 up a 15% grade. Intravenous caffeine did not enhance the endurance run time: 5 CAF = 149 +/- 14 min, 25 CAF = 152 +/- 10 min, and SAL = 176 +/- 10 min. Caffeine did not influence the rate of liver glycogenolysis during exercise [liver glycogen (mmol glucose units.g-1) after 90 min: 5 CAF = 139 +/- 26, 25 CAF = 133 +/- 25, and SAL = 120 +/- 32]. Liver cAMP, muscle glycogen, plasma free fatty acids, blood glucose, and lactate were likewise not affected by caffeine [plasma free fatty acids (mM) after 90 min: 5 CAF = 0.42 +/- 0.04, 25 CAF = 0.45 +/- 0.07, and SAL = 0.41 +/- 0.05]. These data indicate that intravenous caffeine does not enhance the endurance run time or alter the plasma free fatty acids or liver and muscle glycogen utilization in endurance trained rats.

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Adrenodemedullation affects endurance but not hepatic fructose 2,6-bisphosphate.

Sham-operated (SHAM) and saline (ADM-S)- or epinephrine (ADM-E)-infused adrenodemedullated rats were run on a treadmill (21 m/min, 15% grade) for 80 min or until exhaustion. ADM-S rats had significantly lower endurance run times (116 +/- 6 min) than ADM-E rats (136 +/- 8 min) and SHAM rats (150 +/- 6 min). Liver glycogen content dropped from 56 +/- 4 to 10 +/- 2 mg/g in SHAM and from 54 +/- 4 to 18 +/- 5 mg/g in ADM-S and to 20 +/- 8 mg/g in ADM-E rats at 80 min. Liver glycogen was depleted in all rats at exhaustion. Liver fructose 2,6-bisphosphate was decreased markedly in exercising rats, and the extent of decrease was not influenced by adrenodemedullation or by epinephrine infusion. ADM-S rats showed impaired glycogen depletion in the white vastus lateralis and soleus muscles, hypoglycemia, and low blood lactate at 80 min and at exhaustion. Infusion of epinephrine into ADM rats reversed these deficiencies. These data indicate that the adrenal medulla is unessential for normal endurance exercise as long as liver glycogen is available. After liver glycogen is depleted, epinephrine from the adrenal medulla prevents hypoglycemia and is essential for allowing continuation of exercise.

Adrenal Medulla↗

Liver fructose 2,6-bisphosphate in rats running at different treadmill speeds.

To determine the effect of work rate on liver fructose 2,6-bisphosphate (fructose 2,6-P2), rats were run for 5 min on a treadmill up a 15% grade at 16, 21, 26, 31, and 36 m/min. The liver content of fructose 2,6-P2 decreased 25, 42, 50, 62, and 71% from resting values after 5 min of running at these work rates. The time course of the decline in liver fructose 2,6-P2 was also studied in rats run at 16 m/min for times ranging from 5 to 100 min, at 23 m/min for times ranging from 5 to 60 min, and at 31 m/min for times of 5, 10, and 20 min. The hepatic content of fructose 2,6-P2 declined significantly after 5 min in all three groups of rats. The rate of decline was greatest in rats run at 31 m/min. After 100 min of running, fructose 2,6-P2 in livers of rats running at 16 m/min declined to levels seen in rats run at 31 m/min for 20 min. Changes in fructose 2,6-P2 occurred before a detectable decline in liver glycogen and in the absence of any significant change in blood glucose. Liver adenosine 3',5'-cyclic monophosphate (cAMP) was elevated after 5 min of exercise in rats running at 23 and 31 m/min but not in rats running at 16 m/min. By the end of exercise, hepatic cAMP was elevated in rats running at all speeds. The rapid decline in fructose 2,6-P2 probably plays a role in decreasing hepatic glycolysis, thereby ensuring that glucose 6-phosphate derived from glycogenolysis is diverted to blood glucose.

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Effects of glucose infusion in exercising rats.

To determine whether feedforward control of liver glycogenolysis during exercise is subject to negative feedback by elevated blood glucose, glucose was infused into exercising rats at a rate that elevated blood glucose greater than 10 mM. Liver glycogen content decreased 22.4 mg/g in saline-infused rats compared with 13.6 mg/g in glucose-infused rats during the first 40 min of treadmill running (21 m/min, 15% grade). Liver adenosine 3',5'-cyclic monophosphate (cAMP) concentration was significantly lower in the glucose-infused rats during the exercise bout. The concentration of hepatic fructose 2,6-bisphosphate remained elevated throughout the exercise bout in glucose-infused rats but decreased markedly in saline-infused rats. Plasma insulin concentration was higher and plasma glucagon concentration lower in glucose-infused rats than in saline-infused rats during exercise. Early in exercise, liver glycogenolysis proceeds in the glucose-infused rats despite the fact that glucose and insulin concentrations are markedly elevated and liver cAMP is unchanged from resting values. These observations suggest the existence of a cAMP-independent feedforward system for activation of liver glycogenolysis that can override classical negative feedback mechanisms during exercise.

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Effect of the exercise-induced increase in glucocorticoids on endurance in the rat.

To investigate the effect of the increase in glucocorticoids during exercise on endurance, rats were either sham operated (SO) or adrenalectomized. All adrenalectomized rats were given a subcutaneously implanted corticosterone pellet at the time of adrenalectomy. Adrenalectomized rats were injected with corticosterone (ADX Cort) or corn oil (ADX) 5 min before exercise. Rats were killed at rest or after running on a treadmill (21 m/min, 15% grade) until exhaustion. SO rats ran 138 +/- 6 min compared with 114 +/- 9 min for ADX Cort and 89 +/- 8 min for ADX. All differences in run times were significant (P less than 0.05). Corticosterone levels were similar in exhausted SO and ADX Cort groups. ADX exhausted rats had corticosterone levels similar to resting values in SO and ADX rats. Inhibition of the rise in glucocorticoids during exercise had no effect on liver glycogen, liver adenosine 3',5'-cyclic monophosphate, plasma insulin, blood glucose, lactate, glycerol, or 3-hydroxybutyrate, plasma norepinephrine, or red quadriceps and soleus glycogen. Plasma free fatty acids were significantly depressed at exhaustion in ADX rats compared with SO. These data show that glucocorticoids exert effects within the time frame of a prolonged exercise bout and play a role in increasing endurance.

Adrenalectomy↗

Insulin does not influence muscle glycogenolysis in adrenodemedullated exercising rats.

Previous reports have indicated that adrenodemedullated (ADM) rats exhibit an impairment in muscle glycogenolysis and elevated plasma insulin during exercise. This study was designed to determine whether the impaired muscle glycogenolysis in ADM rats is due to absence of epinephrine or to the inappropriately elevated plasma insulin. Fasted ADM rats were infused with saline, with epinephrine (0.045 micrograms . 100 g-1 . min-1), or with epinephrine + insulin (1.6, 3.3, 6.6, and 8.3 ng . 100 g-1 . min-1) during a 30-min run on the treadmill (21 m/min, 10% grade). Soleus muscle glycogen decreased from 5.1 +/- 0.2 mg/g in resting ADM rats to 4.0 +/- 0.2, 0.8 +/- 0.1, and 0.8 +/- 0.1 mg/g in the exercising saline-, epinephrine-, and epinephrine + insulin (8.3 ng . 100 g-1 . min-1)-infused rats, respectively. Glycogen utilization in gastrocnemius and red and white quadriceps muscles during exercise was likewise unaffected by insulin infusion. Blood glucose concentrations were 3.75 +/- 0.08, 2.65 +/- 0.14, 3.93 +/- 0.20, and 2.03 +/- 0.09 mM in the same groups at the end of exercise. Blood lactate was 50% lower and the blood 3-hydroxybutyrate and plasma free fatty acid concentrations were significantly higher in the ADM + saline rats than the other exercising rats. We conclude that inappropriately elevated plasma insulin does not impair epinephrine-stimulated muscle glycogenolysis in fasted ADM rats during exercise.

Adrenal Medulla↗

Epinephrine, glucose, and lactate infusion in exercising adrenodemedullated rats.

The purpose of this study was to determine the metabolic function of the marked increase in plasma epinephrine which occurs in fasted rats during treadmill exercise. Fasted adrenodemedullated (ADM) and sham-operated (SHAM) rats were run on a rodent treadmill (21 m/min, 15% grade) for 30 min or until exhaustion. ADM rats were infused with saline, epinephrine, glucose, or lactate during the exercise bouts. ADM saline-infused rats showed markedly reduced endurance, hypoglycemia, elevated plasma insulin, reduced blood lactate, and reduced muscle glycogenolysis compared with exercising SHAM's. Epinephrine infusion corrected all deficiencies. Glucose infusion restored endurance run times and blood glucose to normal without correcting the deficiencies in blood lactate and muscle glycogenolysis. Infusion of lactate partially corrected the hypoglycemia at 30 min of exercise, but endurance was not restored to normal and rats were hypoglycemic at exhaustion. We conclude that in the fasted exercising rat, actions of epinephrine in addition to provision of gluconeogenic substrate are essential for preventing hypoglycemia and allowing the rat to run for long periods of time.

Adrenal Medulla↗

Blood collection and processing for measurement of catecholamines in exercising rats.

We have studied the time course of the decline in plasma catecholamines in the postexercise period in rats. Male Sprague-Dawley rats were run on the treadmill for 5 min at 31 m/min up a 15% grade. At the end of the exercise the rats were quickly anesthetized by intravenous injection of pentobarbital. Blood samples were collected as soon as possible (average of 43 s), at 2 and 7 min postexercise. Plasma epinephrine decreased from 0.79 +/- 0.09 ng/ml to 0.51 +/- 0.05 after 2 min and to 0.35 +/- 0.09 after 7 min. Plasma norepinephrine decreased from 0.89 +/- 0.16 ng/ml to 0.61 +/- 0.05 after 2 min and to 0.50 +/- 0.07 after 7 min. We also studied the effect of time of centrifugation with respect to time of blood collection on plasma catecholamines. If blood samples were kept on ice no significant change in plasma epinephrine occurred over a period of 1 h. A small (14%) but significant decrease in norepinephrine was observed after 15 and 60 min. These studies emphasize the importance of collecting rat blood samples as quickly as possible after the end of exercise. Catecholamines decline very quickly in the rat after intravenous pentobarbital anesthesia.

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Effect of maternal exercise on fetal liver glycogen late in gestation in the rat.

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22-60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.

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Epinephrine is unessential for stimulation of liver glycogenolysis during exercise.

To determine the role of adrenal medullary hormones in controlling the rate of liver glycogenolysis during exercise, adrenodemedullated (ADM) and sham-operated (SO) rats were run on a rodent treadmill at 21 m/min up a 15% grade for 0, 30, or 60 min. Rats were anesthetized by intravenous injection of pentobarbital sodium, and liver, muscle, and blood were collected and frozen. Liver glycogen decreased at similar rates in ADM and SO rats. Hepatic adenosine 3',5'-cyclic monophosphate (cAMP), plasma glucagon, and plasma free fatty acids increased to the same extent in both ADM and SO rats. The adrenodemedullation caused a reduction in glycogenolysis in the fast-twitch white region of the quadriceps, soleus, and lateral gastrocnemius during exercise. The normal exercise-induced increase in blood glucose and lactate and the decline in plasma insulin were not observed in the demedullated rats. During submaximal exercise the principal targets for epinephrine released from the adrenal medulla appear to be pancreatic beta-cells and skeletal muscle and not the liver.

Adrenal Medulla↗