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Distribution and function of hepatic - and -adrenoceptors were examined in rainbow trout (Oncorhynchus mykiss) injected with slow release hydrogenated coconut oil implants alone (sham) or containing cortisol. - and -Adrenoceptors were assayed on purified hepatic membranes 10–14 days post-implantation using 3H-prazosin () and 3H-CGP (). At 10–14 days, plasma cortisol values were significantly elevated to approximately 220 compared with 35.0 ng ml-1 in cortisol implanted vs. sham trout. No significant differences were found between any of the experimental groups for either the affinity (Kd) or maximal number of binding sites (Bmax) for either receptor type. Epinephrine significantly stimulated glucose release from hepatocytes isolated from sham injected trout, but not from cortisol-treated fish. Epinephrine-induced glucose release was blocked by both - and -antagonists. These studies do not support the hypothesis that rainbow trout exposed to chronic cortisol alter properties of hepatic adrenoceptors.  相似文献   
2.
Short-term exposure of isolated toadfish hepatocytes to high concentrations (100 nM) of glucagon, glucagon-like peptide (GLP) or epinephrine significantly increases the rate of lactate gluconeogenesis (1.3-fold) and glycogenolysis (5- to 7-fold). Half-maximal responsiveness to GLP is reached at about 2 nM for gluconeogenesis and 6 nM for glycogenolysis, while the value for glycogenolysis activated by catfish glucagon is 28 nM. Cells do not to respond to 5 nM epinephrine. Norepinephrine, urotensin II and leucine-enkephalin, each applied at 100 nM, increase the rate of glycogenolysis by 1.3 to 1.5-fold. All other hormones tested (vasotocin, isotocin, VIP, methionine-enkephalin, ovine prolactin, -endorphin, APY, salmon insulin) failed to affect metabolic flux through glycogenolysis or gluconeogenesis. None of the hormones altered the rate of urea synthesis or the rate of lactate oxidation by hepatocytes. Although toadfish hepatocytes are responsive to hormonal stimuli, they do not appear to be a useful model to study evolutionary trends in short-term hormonal regulation of urea synthesis. However, the obvious differences in mechanisms of control of urea synthesis in this species compared with ureogenic amphibians and mammals open an intriguing avenue for research.  相似文献   
3.
Metabolic actions of glucagon-family hormones in liver   总被引:1,自引:0,他引:1  
This review addresses direct and indirect metabolic actions of hormones co-encoded in the preproglucagon gene of fishes. Emphasis is placed on a critical analysis of the effects of glucagon and glucagon-like peptide (GLP) and the current knowledge of the respective modes of action is reviewed. In mammals GLPs exert no direct metabolic actions. In fish liver, GLP and glucagon act on similar targets of intermediary metabolism by enhancing flux through glycogenolysis, lipolysis and gluconeogenesis. Increases in substrate oxidation are not uniform. Hormonal activation of glycogen phosphorylase and triglyceride lipase and inhibition of pyruvate kinase are implicated in these actions. Hormone-dependent hyperglycemia, depletion of hepatic glycogen and increases in free fatty acids are noticeablein vivo. Glucagon also activates hepatic amino acid uptake and ammonia excretion. Glucagon actions are accompanied by large increases in hepatic cAMP and increased phosphorylation of pyruvate kinase. Metabolic effects measured after GLP administration are associated with minor, if any, increases in cAMP and effects on pyruvate kinase are variable. We hypothesize that different hepatic receptors with differing modes of intracellular message transduction are involved in glucagon and GLP actions while targetting identical metabolic routes. Responses of different species of fish cover a wide spectrum, and variation of response with the circannual cycle of experimental animals makes comparisons of results, even within one species, difficult.  相似文献   
4.
The effects of porcine, scombroid, and salmon insulins, and bovine and anglerfish glucagons on glycogen depletion and glycogen phosphorylase (GPase) activities were examined in freshly isolated American eel (Anguilla rostrata) hepatocytes. Eel liver GPase in crude homogenates was activated (increase in % GPase a) by phosphorylating conditions and was rapidly inactivated (less than 1 h) when a phosphatase inhibitor (fluoride) was absent. Caffeine inhibits, and AMP activates, the b form of GPase consistent with their effects on rat liver GPase. Both mammalian and fish glucagons increased glucose production in eel hepatocytes, but had more ambiguous effects on glycogen levels and GPase activities. The magnitude of bovine glucagon effects were dependent on the initial glycogen content of the cells; only at glycogen concentrations less than approximately 70 μmoles.g−1 did glucagon significantly increase % GPase a. Anglerfish glucagon significantly increased cyclic AMP (cAMP) concentrations by 90% at 10−7 M, but had no effects at 10−9 M and 10−8 M. Scombroid and salmon insulins maintained hepatocyte glycogen concentrations and decreased glucose production, with these effects more pronounced at low (10−9 to 10−8 M) rather than high (10−7 M) hormone concentrations. Porcine and salmon insulins decreased total GPase and % GPase a activities, and salmon insulin decreased CAMP levels, but only at 10−8 M (by 44%). Glycogen is, therefore, depleted by glucagon and maintained by insulin in freshly isolated American eel hepatocytes, and these changes are accomplished, at least in part, by changes in the activities of GPase. Changes in cAMP do not explain all of the observed hormone effects.  相似文献   
5.
The sea raven, Hemitripterus americanus, is a sit-and-wait, low metabolic rate, marine teleost. The objective of this study was to determine i) whether cortisol implantation (50 mg. kg-1) for 7 days altered hepatocyte metabolism, and hepatocyte responsiveness to epinephrine, glucagon and insulin, and ii) whether 8 weeks of food-deprivation modified the above response. Cortisol implantation significantly increased hepatocyte total glucose production and oxidation from alanine compared to the sham group. There was no cortisol effect on glycogen breakdown, suggesting that the activation of other pathways, including gluconeogenesis, are required to account for the increased glucose production. Epinephrine-mediated (10-5M) glycogen breakdown and insulin-mediated (10-8M) total glucose production were enhanced in hepatocytes of cortisol implanted sea ravens, but there were no change in any glucagon (10-7M) effects. The enhanced glycogen breakdown in the absence of similar increases in total glucose production with epinephrine indicates mobilization of carbohydrate reserves for endogenous use by the liver. Food-deprivation for 8 weeks significantly decreased condition factor, plasma cortisol concentration and liver glycogen content in the sea raven, but had no effect on plasma glucose concentration. Hepatocyte total glucose production and flux rates from alanine increased significantly with food-deprivation. Moreover, food-deprivation increased responsiveness of total hepatocyte glucose production to the actions of glucagon and insulin, but not to epinephrine; none of these effects were modified by cortisol implantation. Our results indicate that cortisol in the sea raven exerts both a direct and an indirect or permissive effect on hepatocyte metabolism by modifying hepatocyte responsiveness to epinephrine and insulin stimulation. Cortisol implantation did not modify the effects of glucagon or food-deprivation in this species.  相似文献   
6.
SUMMARY: Common carp Cyprinus carpio were administered intraperitoneally with 10 μmol epinephrine per 100 g bodyweight, and enzyme activities and metabolic intermediate concentrations were determined in the hepatopancreas and muscle. Glycogen phosphorylase a (GPase a) activity together with cyclic AMP (cAMP) concentration was increased, and glycogen content was decreased in the hepatopancreas and muscle at 2 h after the administration. The epinephrine administration also increased hepatopancreatic glucose-6-phosphatase and fructose-1,6-biphosphatase activities as well as serum glucose, lactate, and free amino acid concentrations. Furthermore, its administration increased phosphofructokinase activity together with lactate, fructose-6-phosphate, adenosine-5'-monophosphate, and adenosine-5'-diphosphate concentrations and decreased citrate concentration in the muscle. Thereafter, almost all parameter concentrations in the hepatopancreas and muscle recovered to the pre-administered levels during 24 h after the administration. These results suggest that epinephrine administration enhanced glycogenolysis and gluconeogenesis in the hepatopancreas, and released glucose into the bloodstream to supply it to the muscle. The blood glucose together with muscle glycogen seems to be metabolized through enhanced glycolysis in the muscle.  相似文献   
7.
杨叶金  黄凤钦 《水产学报》1991,15(2):165-168
甲壳类高血糖激素(Crustacean hyperglycemic hormone,CHH)于1944年在眼柄抽提液发现,当时称致糖尿因子(diabetogenic factor),此后大量报告相继出现。现已清楚,CHH由眼柄内或脑下的窦腺(sinus gland)所分泌,是一类热敏(heat-labile)、大分子(约7000MW)肽类激素,其靶器官(target organ)为肌肉,系经腺苷环酶而起作用,使肌肉中醣原分解而增加血淋巴中葡萄糖浓度。为了探讨无脊椎动物的激素对脊椎动物的效应。作者等从克氏螯虾(Procambarus clarkii)的眼柄  相似文献   
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