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At least 883 records · Page 49Linked to original sources
PubMed1992

PNMT inhibition decreases exercise performance in the rat.

The purpose of this investigation was to examine the effect of phenylethanolamine N-methyltransferase (PNMT) inhibition on the regulation of peripheral metabolic and hormonal responses during treadmill exercise in the rat. Changes in plasma catecholamine (epinephrine, norepinephrine, and dopamine), glucagon and glucose, and the glycogen content of the liver and two skeletal muscles were studied in four groups of rats. Two groups of rats were studied at rest: one group had been treated with LY134046, an inhibitor of PNMT, and the second group was treated with physiological saline. A third group treated with LY134046 was studied after treadmill exercise (28 m.min-1 and 8% slope). In this group of rats, exhaustion came after 37.5 +/- 7.9 minutes of exercise. In order to make appropriate comparisons, a fourth group of rats treated with physiological saline was exercised for 37.5 min. Running endurance during the treadmill exercise was thus reduced in LY134046-treated rats. Plasma epinephrine and glucagon concentrations and other metabolic (plasma glucose and gastrocnemius lateralis and superficial vastus lateralis muscles and liver glycogen contents) responses were similar between LY134046- and saline-treated rats at rest and after exercise. These results suggest that PNMT inhibition in epinephrine brain neurons might be the principal factor involved in the LY134046-induced reduction of exercise endurance.

Animals↗
PubMed1983

Physiological changes in carps induced by pollution.

Several pollutants like DDT, atrazine, PCP, and others induce changes of cortisol and glucose levels in serum, variations of the amount of liver glycogen and liver function, and exert changes of the activity of gill ATPase and acetylcholinesterase in brain and serum of carps. There is always a biphasic response, an increase of concentration or enzyme activity for a short time, and a decrease or inhibition of the enzymes after a longer exposure to the pollutants. The time scale, the duration of the period of increase and that of decrease, depends on the concentration and the toxicity of the pollutants. The influence of the pollutants in normal fresh water was compared with the effects occurring in carps acclimated to 1.2% salt water. This condition enables one to show that the carps are more sensitive to the pollutants under this condition. All responses are unspecific. Advice for the use of these tests as criteria for water quality are given.

Acetylcholinesterase↗
PubMed1986

Effects of isolated zinc deficiency on the composition of skeletal muscle, liver and bone during growth in rats.

We investigated the effects of zinc deficiency on body composition by using intragastric force-feeding to obviate decreased food intake and altered eating patterns. Weanling male Sprague-Dawley rats were fed a purified zinc-deficient diet: the ad libitum-fed control group (AL; eight rats) was given powdered diet and water containing 25 ppm zinc; the zinc-replete group (ZN; nine rats) was force-fed a diet blended with water containing zinc in an amount of equal caloric intake to the AL group and allowed access to water containing zinc. The zinc intake of ZN rats was approximately twice that of AL rats based on water intake. The zinc-deficient group (ZD; 13 rats) was fed similarly to the ZN group except deionized water was used for diet preparation and drinking water. After 8 d, body and muscle weight were lower in the ZD group than in the ZN group. Femur weights were similar in the two groups. Serum, liver and femur zinc concentrations were 85, 22 and 42% lower, respectively, in the ZD group than in the ZN group. Serum glucose, relative liver weight, liver glycogen and liver lipids were higher, but muscle and liver DNA were lower in the ZD group than in control groups.

Animals↗
PubMed1987

Preexercise feedings of glucose, fructose or sucrose: effects on substrate depletion in rats.

Male Wistar rats (n = 72) trained to run on a treadmill were fasted overnight and fed by gavage 3 ml unsupplemented water or a solution containing 2 g of glucose, fructose or sucrose 30 min prior to exercise. Six rats from each dietary group were killed after 0, 1 or 2 h of exercise. Blood glucose levels decreased in all groups over the 2-h exercise period; however, the largest decline in blood glucose was exhibited by the rats fed unsupplemented water (-32.1%), followed by those fed fructose (-26.9%), sucrose (-13.9%) and glucose (-8.3%). The water-fed control rats also had the largest increase in circulating free fatty acids (+215.4%), followed by those fed fructose (+120.8%), sucrose (+69.2%) and glucose (+57.5%). The fructose-fed animals exhibited the greatest depletion of liver glycogen and the smallest decline in soleus and red vastus lateralis muscle glycogen of the rats fed the different carbohydrates. The data indicate that exercise-induced changes in substrate levels can be modified by the type of carbohydrate given prior to exercise.

Animals↗
PubMed1991

Catecholamine stimulation of hepatic glycogenolysis during anoxia in the turtle Chrysemys picta.

The remarkable tolerance of some species of turtles to anoxia is well documented. The role that hormones play in this anoxia tolerance, however, is poorly understood. This study examined the role of catecholamines in the mobilization of liver glycogen during anoxic submergence in painted turtles (Chrysemys picta). Turtles were subjected to 4 h of submergence anoxia or air (normoxic controls) and received injections of propranolol, a beta-adrenergic receptor antagonist, or saline. The results indicated that the catecholamines function during anoxia to increase blood glucose levels by stimulating hepatic glycogenolysis through an increase in both the total activity of glycogen phosphorylase and the percent a form. Anoxic turtles given propranolol showed a decrease in the percent a form of glycogen phosphorylase compared with control turtles given propranolol, indicating that anoxia per se or a correlate of anoxia may depress hepatic glycogenolysis. Catecholamines may counteract this depressant effect. Hepatic glycogen mobilization during anoxia appeared to be stimulated via beta-adrenergic receptors, as propranolol was effective in blocking the stimulation, whereas phentolamine, an alpha-receptor antagonist, was not.

Animals↗
PubMed1981

Effect of supplemental dietary chromium or nicotinic acid on carbohydrate metabolism during basal, starvation, and refeeding periods in poults.

A series of experiments were conducted with turkey poults to ascertain the effects of supplemental chromium or excess of nicotinic acid on growth and carbohydrate metabolism. A 23% protein starter diet was selected to emphasize the effect of chromium under basal, starvation for 48 hr, and refeeding periods. Thirty percent protein diets were also used to determine if the effects were compounded by protein levels. Supplemental chromium (20 ppm) significantly increased (P less than .05) weight at 3 weeks of age of poults consuming 23% protein diets, while an additional 250 ppm of nicotinic acid had little effect on poult weight at 3 weeks (P greater than .05). Supplemental chromium did not increase (P greater than .05) feed consumption of poults consuming both 23 and 30% protein diets. Supplemental chromium increased liver glycogen at 3 weeks of age and following refeeding after the 48 hr fast (P less than .05). Blood glucose was significantly affected by starvation-refeeding (P less than .05) but was not affected by either chromium or nicotinic acid. Supplemental chromium increased (P less than .01) active glycogen synthetase, while nicotinic acid increased (P less than .01) active phosphorylase at both protein levels. Synthetase was not decreased by starvation but was increased (P less than .01) by refeeding regardless of protein level fed. Phosphorylase was not affected by a starvation-refeeding regimen. Chromium supplementation increased in the vitro incorporation of (14C) glucose into glycogen during basal, starvation and refeeding periods (P less than .01), again, regardless of protein level.

Animal Feed↗
PubMed1975

[Pharmacological study of 9 alpha-fluoro-11 beta, 17, 21-trihydroxy-16 beta-methylpregna-1, 4-diene-3,20-dione-17-benzoate (betamethasone-17-benzoate, MS-1112), a local anti-inflammatory agent. (1). Its anti-inflammatory and other pharmacological properties].

The anti-inflammatory activity and the other pharmacological properties of MS-1112, a new steroid compound, were examined and compared with other glucocorticoid analogues such as hydrocortisone acetate (Hydr), betamethasone 17-valerate (Val) and dexamethasone (Dexa). Systemically administered MS-1112 and glucocorticoids had a significant effect in inhibiting rat paw edema induced by various phlogistic stimulations and increasing vascular permeabilities and granuloma formation by cotton pellet or granuloma pouch. The order of those inhibiting activity was, in general, Dexa greater than MS-1112 greater than Val greater than Hydr. Concomitantly, Xthymolysis and adrenal weight suppression and reduced rate of body weight gain after multiple systemical administration were also observed. Locally administered MS-1112 caused an inhibiting activity, without systemic side-effects. This activity was approximately 3 to 5 times more potent than that of Dexa in rat carrageenin paw edema and cotton pellet granuloma. MS-1112 was less active than Dexa in glycogen liver deposition activity and in the depression of plasma level of corticosterone but more active than Val and Hydr. In the dose administered, MS-1112 had neither androgenic and anabolic nor estrogenic and anti-estrogenic activity. From this data, it concluded that MS-1112 is a very potent agent applicable regarding permeability and retention of steroids in a local site.

Administration, Topical↗
PubMed1992

Circadian features of carbohydrate metabolism in domestic fowls exposed to weekly 120 degree-shifts of synchronizer schedule.

Effects of weekly 8 hr advance- or delay-shifts on the circadian rhythm of plasma glucose, liver glycogen and muscle glycogen in male domestic fowls, beginning at about 3 days of age, were examined. Circadian rhythm in the aforesaid indices of carbohydrate metabolism in control birds was also studied. Blood and tissue samples were collected from birds in all the three groups at 4 hr intervals over a single 24 hr time scale both at 6th and 12th week of age. Plasma glucose and glycogen content in the tissues were determined by employing standard techniques. Cosinor rhythmometry was used for analyzing time series data. In general, a statistically significant circadian rhythm was documented for all the three indices in control and advance-schedule birds, irrespective of age. In contrast, in delay-schedule birds, statistically significant circadian rhythm could not be detected, excluding in muscle glycogen at 12th week of age. The poor growth rate in the delay-schedule birds could be imputed to the disappearance of circadian rhythm in the indices of carbohydrate metabolism.

Animals↗
PubMed1987

[Participation of leu-enkephalin in regulating carbohydrate metabolism].

The experiments have been performed on 166 white male rats with a mass of 180-220 g. It has been revealed that leucine-enkephalin and its synthetic analogs prevent an increase in glucose blood levels and a decrease in glycogen liver levels caused by adrenaline and parathyroid hormone. At the same time the enkephalins inhibit the secretory activity of pancreatic beta-cells. The mechanisms of opioid peptide effect on carbohydrate metabolism are discussed.

Animals↗
PubMed1986

[Characteristics of the early recovery period and the level of carbohydrate-lipid metabolic substrates after 24-hour immobilization hypothermia].

The peculiarities of 24-hour hypothermia were studied in rats during immobilization and a 5-hour recovery period. The levels of glucose in blood and liver, glycogen in liver, skeletal muscles and heart, total lipids in liver and blood, nonesterified fatty acids in blood have shown that the speed of rewarming is limited both by the level of carbohydrate and lipid energy substrates.

Animals↗
PubMed1988

Electrical stimulation of the suprachiasmatic nucleus of the hypothalamus causes hyperglycemia.

We have presented evidence suggesting that the suprachiasmatic nucleus (SCN) is involved in central regulation of glucose homeostasis. To elucidate this role of the SCN, we examined the effects of its electrical stimulation on glucose metabolism in male Wistar rats. During and shortly after this stimulation, we observed hyperglycemia associated with enhanced hyperglucagonemia but no immediate hyperinsulinemia. In addition, we detected significant increase in liver glycogen phosphorylase alpha activity and significant decrease in the liver glycogen content. These findings suggest that the SCN is important in control of glucose homeostasis through effects on glucagon and insulin secretions and liver glycogen metabolism.

Animals↗
PubMed1992

Mechanism of delayed hepatic glycogen synthesis after an oral galactose load vs. an oral glucose load in adult rats.

We have compared the effects of administration of oral galactose or glucose (1 g/kg) to 24-h fasted rats to examine the mechanism by which galactose regulates its own incorporation into liver glycogen in vivo. Liver glycogen increased to a maximum more slowly after galactose than after glucose administration (0.14 vs. 0.29 mumol.g liver-1.min-1). Glycogen accumulation after the galactose load was 70% of that after the glucose load (149 vs. 214 mumol), and the net increase in liver glycogen represented the same proportion (24 vs. 22%) of added carbohydrate after urinary loss of galactose was accounted for. Slower glycogen accumulation after galactose vs. glucose loading could not be explained by galactosuria, by differences in the active forms of synthase or phosphorylase, by end product (glycogen) inhibition of synthase phosphatase, or by different concentrations of the known allosteric effectors of synthase R plus I and phosphorylase a. Similar increases in glucose 6-phosphate were observed after both hexoses. AMP and ADP increased only transiently after galactose administration, and ATP, UTP, and Pi concentrations were unchanged. The UDP-glucose concentration decreased, whereas the UDP-galactose concentration increased two- to threefold after galactose but not glucose administration. The UDP-glucose pyrophosphorylase reaction is inhibited competitively by UDP-galactose. This could explain the decreased UDP-glucose concentration and the reduced rate of glycogen synthesis after galactose was given.

Absorption↗
PubMed1986

[Effect of chronic CCl4 poisoning in the rat and of partial hepatectomy of the pathologically altered organ on glycogen levels of hepatocytes].

A cytofluorometric study was made of total glycogen in rat liver cells in the norm and upon the chronic intoxication with CCl4. The liver cells were obtained from rats by means of intravital needle aspiration biopsy at the beginning of the experiment, after 3, and 6 months, and 1 month after partial hepatectomy of control and cirrhotic livers. Glycogen contents in liver cells were attributed to dry weight measured interferometrically. Upon the long-term chronic intoxication of rats with the hepatotropic poison the glycogen content increased by 1.4-2.5 times, and in some cells of cirrhotic livers even by 5-5.5 times compared to the normal level. 1 month after the resection both glycogen content and rat liver cell morphology were seen almost close to the normal. The data are discussed in terms of results earlier reported elsewhere on the increase of glycogen content in liver cells of patients with chronic hepatitis.

Animals↗
PubMed1978

Glycogen depletion and repletion in the chick.

Carcass glycogen was degraded by chicks at a faster rate than liver glycogen during the first 72 hr of a 120 hr fast. Degradation of both sources of glycogen proceeded at a slower rate during the final 48 hr. Carcass glycogen was repleted at a greater rate than liver glycogen.

Animals↗
PubMed1994

Effect of the sulfonylurea glyburide on glycogen synthesis in alloxan-induced diabetic rat hepatocytes.

1. The effect of glyburide (glibenclamide) treatment on the liver glycogen levels of diabetic rats have been studied. 2. 3 weeks treatment with glyburide (5 mg/kg, orally) increased liver glycogen and decreased blood glucose levels. 3. The results of this study demonstrated that the sulfonylurea, glyburide is capable of exerting direct insulin-like effects on liver glycogen values in vivo.

Animals↗
PubMed1998

Insulin increases liver protein phosphatase-1 and protein phosphatase-2C activities in lean, young adult rhesus monkeys.

Liver glycogen synthase activity is increased, and glycogen phosphorylase activity and glucose 6-phosphate content reduced by in vivo insulin during a euglycemic hyperinsulinemic clamp in lean young adult rhesus monkeys. To examine the mechanism of dephosphorylation of liver glycogen synthase and glycogen phosphorylase, the enzyme activities of protein phosphatase-1, protein phosphatase-2C, cAMP-dependent protein kinase, glycogen synthase kinase-3, protein kinase C and protein tyrosine kinase were determined before and after three hours of in vivo insulin in these same monkeys. The bioactivity of an inositol phosphoglycan insulin mediator (pH 2.0) and cAMP concentrations were also measured in the liver before and after insulin administration. Insulin caused significant increases in protein phosphatase-1 (p = 0.005) and in protein phosphatase-2C activities (p = 0.001). Insulin-stimulated minus basal bioactivity of the pH 2.0 insulin mediator was strongly inversely related to the insulin-stimulated minus basal glucose 6-phosphate content (r = -0.93, p < 0.0001). These findings suggest that protein phosphatase-1 and protein phosphatase-2C may be involved in the mechanism of in vivo insulin activation of liver glycogen synthase and inactivation of liver glycogen phosphorylase.

Animals↗