Enzymological and biochemical changes produced by chronic chromium exposure in a teleost fish, Channa punctatus

The chronic toxic effects of chromium (2.6 mg/1) on the carbohydrate metabolism of a teleost fish, Channa punctatus were examined after 60 and 120 days of exposure. After 60 days the lactic acid content of blood and muscles was increased but liver lactic acid content decreased. Liver glycogen was also depleted. The activity of lactate dehydrogenase was inhibited in liver and kidney. Pyruvate dehydrogenase and succinate dehydrogenase activities were also inhibited in all the tissues except muscles. Fish were hypoglycemic and hyperlactemic after 120 days of exposure to chromium. The glycogen content increased in liver but decreased in muscles. Lactate dehydrogenase activity was inhibited in all the six tissues. The activity of pyruvate dehydrogenase decreased in liver, intestine, gill and muscles. In muscles succinate dehydrogenase activity was elevated but inhibition was recorded in other tissues.     

人参糖肽降血糖机制(英文)

目的:研究人参糖肽(GGP)降血糖机制。方法:为了观察GGP对胰岛素分泌和糖酵解的影响,给予GGP后,测定血糖(BG)和肝糖元(LG)含量,及胰岛素、乳酸脱氢酶(LDH)、乳酸(LC)水平。通过测定给予GGP前后肝组织柠檬酸合成酶(CTS)、苹果酸脱氢酶(MDH)、琥珀酸脱氢酶(SDH)和细胞色素氧化酶(CCO)活性变化,推测对糖有氧氧化过程的影响。通过测定肝组织腺苷酸环化酶(AC)活性和cAMP水平,研究人参糖肽对糖代谢的影响及与第二信使cAMP的关系。通过检测肝组织磷酸化酶(PP)活性推测药物对肝糖元代谢的影响。检测药物对细胞膜受体的影响,观察了β-受体阻滞剂普萘洛尔和α-受体阻滞剂酚妥拉明对GGP作用的影响。为了证明GGP与β-受体的结合,观察了GGP与[~3H]DHA对北京鸭红细胞膜β-受体的竞争性结合。结果:GGP在降低血糖和肝糖原的剂量下(100,200mg/kg,ip或50,100mg/kg,iv),仅于给药后20分钟,小鼠血浆胰岛素水平即升高,且GGP降低血糖作用可持续16小时;同时,血中LC含量及血和肝组织LDH活性降低。而肝组织AC、CTS、MDH、SDH、COO、PP活力和cAMP水平升高,β-受体阻滞剂普萘洛尔可阻滞GP降低肝糖元作用,GGP可竞争性抑制放射配基[~3H]DHA与红细胞膜β-受体的结合,其IC_(50)为63nmol·L~(-1)。结论:GGP为β-受体激动剂,通过第二信使cAM     

Effect of tetrahydrocurcumin on blood glucose, plasma insulin and hepatic key enzymes in streptozotocin induced diabetic rats

The enzymes of glucose and lipid metabolism are markedly altered in experimental diabetes. In the present study, we investigated the effect of tetrahydrocurcumin (THC), one of the active metabolites in curcumin, on the key hepatic metabolic enzymes involved in carbohydrate metabolism in streptozotocin-induced diabetic rats. Different doses of THC (20, 40, and 80 mg\kg body weight) were orally administered to diabetic rats for 45 days. The activities of hexokinase, glucose-6-phosphate dehydrogenase (G6PD), glucose-6-phosphatase, fructose-1,6-bisphosphatase, and sorbitol dehydrogenase in liver, and glycogen content in liver and muscle were assayed. In untreated diabetic control rats, the activities of the gluconeogenic enzymes were significantly increased, whereas hexokinase and G6PD activity and glycogen levels were significantly decreased. Both THC and curcumin were able to restore the altered enzyme activities to near normal levels. Tetrahydrocurcumin was more effective than curcumin. Our results indicate that the administration of THC to diabetic animals normalizes blood glucose and causes a marked improvement of altered carbohydrate metabolic enzymes.     

Impact of Distillery Effluent on Carbohydrate Metabolism of Freshwater Fish, <Emphasis Type="Italic">Cyprinus carpio</Emphasis>

The impact of distillery effluent on carbohydrate metabolism of Cyprinus carpio was studied at different days during exposure (7, 14, and 21 days) in the ambient temperature of 28±1 °C. Oxygen consumption in fish decreased with increasing effluent concentrations as well as duration of exposure. Effluent concentrations and exposure durations (days) had a significant effect on oxygen consumption of tested fish (p<0.0005). Total carbohydrate, glycogen content and SDH enzyme activity in muscle, liver and brain tissues of C. carpio exposed to different sublethal concentrations decreased gradually and significantly. This was also the case with exposure duration. Reduction in glycogen content was greater in liver tissue i.e., 54.1% in 0.2% effluent concentration on the 21st day of exposure. However, serum glucose and lactic acid content showed an increasing trend with increase in effluent concentration and time of exposure. Unlike SDH, LDH enzyme activity of muscle, liver and brain tissues showed an increasing trend and the enhancement of enzyme activity was more in liver tissue (71.3%). From these results, it could be inferred that respiratory processes in C. carpio under distillery effluent stress was affected resulting in a shift towards anaerobiosis at organ level during sublethal intoxication.     

Protective effect of N-acetylcysteine against arsenic-induced depletion in vivo of carbohydrate

N-acetylcysteine (NAC), a synthetic aminothiol, possesses antioxidative and cytoprotective properties. The present study evaluates the effect of NAC supplementation on arsenic-induced depletion in vivo of carbohydrates. Arsenic (as sodium arsenite) treatment (i.p.) of male Wistar rats (120-140 g b.w.) at a dose of 5.55 mg/kg body weight (35% of LD50) per day for a period of 30 days produced a significant decrease in blood glucose level (hypoglycemia) and a fall in liver glycogen and pyruvic acid contents. The free amino acid nitrogen content of liver increased while that of kidney decreased after arsenic treatment. Arsenic also enhanced the liver lactate dehydrogenase activity whereas glucose 6-phosphatase activity in both liver and kidney decreased significantly following arsenic treatment. Transaminase activities in liver and kidney were not significantly altered except the glutamate-pyruvate transaminase activity that was reduced in kidney after arsenic treatment. Oral administration of NAC (163.2 mg/kg/day) for last 7 days of treatment prevented the arsenic-induced hypoglycemia and glycogenolytic effects to an appreciable extent. There was also recovery of liver pyruvic acid as well as liver and kidney free amino acid nitrogen content after NAC supplementation. Arsenic-induced alteration of glucose 6-phosphatase activity in both liver and kidney was also counteracted by NAC. It is suggested that carbohydrate depletion in vivo due to exposure to arsenic can be counteracted by NAC supplementation.     

Effect of praziquantel on some aspects of carbohydrate metabolism in mice infected with Schistosoma mansoni

Schistosoma mansoni infection in mice resulted in a marked decrease in blood glucose and liver glycogen accompanied by a significant increase in hepatic glucose-6-phosphatase (G-6-Pase) activity. Moreover, the results indicated that infection produced a significant increase in blood pyruvate and hepatic glucose-6-phosphate dehydrogenase (G-6-PD) activity with a significant decrease in blood lactate. Infected mice were treated with praziquantel which was given at two doses of 500 mg/kg body wt on two consecutive days. Seven and 14 days respectively after drug administration, such treatment caused a marked improvement in the previous aspects of carbohydrate metabolism. This is indicated by the tendency of the blood glucose of infected mice to be restored, the marked increase in their liver glycogen content, the normalization of their blood lactate and pyruvate as well as by the marked decrease of their hepatic G-6-Pase activity and the progressive increase in their hepatic G-6-PD activity. Praziquantel given to normal mice moderately affected the blood glucose and the previously mentioned hepatic enzymes. However, the drug markedly increased the liver glycogen content of normal mice and failed to elicit any change in their blood pyruvate and lactate. Possible explanations of these findings are discussed.     

人参多肽降血糖机制的研究

人参多肽(GP)无论sc或iv(50～200 mg/kg)对大鼠和小鼠均有明显的降低血糖和肝糖原作用,肾上腺切除并未影响其降低肝糖原作用。酚妥拉明和普萘洛尔分別抑制GP对大鼠肝糖原和血糖的影响。GP在降低血糖和肝糖原时,可使小鼠肝组织cAMP增加。由于血及肝组织LDH受到抑制,血乳酸含量降低,而血丙酮酸含量升高。实验证明,GP降血糖作用除了其促进糖原分解或抑制乳酸合成肝糖原作用外,主要由于其刺激了SDH和CCD的活性使糖的有氧氧化作用增强的缘故。     

Protective Effect of N‐Acetylcysteine Against Arsenic‐Induced Depletion In Vivo of Carbohydrate

N‐acetylcysteine (NAC), a synthetic aminothiol, possesses antioxidative and cytoprotective properties. The present study evaluates the effect of NAC supplementation on arsenic‐induced depletion in vivo of carbohydrates. Arsenic (as sodium arsenite) treatment (i.p.) of male Wistar rats (120–140 g b.w.) at a dose of 5.55 mg/kg body weight (35% of LD₅₀) per day for a period of 30 days produced a significant decrease in blood glucose level (hypoglycemia) and a fall in liver glycogen and pyruvic acid contents. The free amino acid nitrogen content of liver increased while that of kidney decreased after arsenic treatment. Arsenic also enhanced the liver lactate dehydrogenase activity whereas glucose 6‐phosphatase activity in both liver and kidney decreased significantly following arsenic treatment. Transaminase activities in liver and kidney were not significantly altered except the glutamate–pyruvate transaminase activity that was reduced in kidney after arsenic treatment. Oral administration of NAC (163.2 mg/kg/day) for last 7 days of treatment prevented the arsenic‐induced hypoglycemia and glycogenolytic effects to an appreciable extent. There was also recovery of liver pyruvic acid as well as liver and kidney free amino acid nitrogen content after NAC supplementation. Arsenic‐induced alteration of glucose 6‐phosphatase activity in both liver and kidney was also counteracted by NAC. It is suggested that carbohydrate depletion in vivo due to exposure to arsenic can be counteracted by NAC supplementation.     

Protective effect of methionine supplementation on arsenic-induced alteration of glucose homeostasis.

Short term exposure of arsenic produces carbohydrate depletion and hypoglycemia. Dietary deficiency of methionine causes impaired biotransformation of arsenic which has been attributed to the pathogenesis of different diseases induced by arsenic. Accordingly, the effects of methionine supplementation on the altered glucose homeostasis induced by arsenic were studied. Arsenic (as sodium arsenite) treatment (i.p) of male Wistar rats (weighing 80-100 g) at a dose of 5.55 mg kg(-1) body weight (equivalent to 35% LD50) per day for a period of 21 days caused a significant diminution in blood glucose level and fall in liver glycogen and pyruvic acid contents. The free amino acid nitrogen content of liver was elevated while that of kidney was decreased after arsenic treatment. Transaminase activities in liver and kidney were not significantly altered except that glutamate-pyruvate transaminase activity of kidney decreased significantly after arsenic treatment. Methionine supplementation reversed the above changes except decreased liver glycogen due to arsenic treatment. It may be suggested that hypoglycemia with associated decreased glycolytic activity induced by arsenic treatment at the present dose and duration can be partially counteracted by dietary methionine supplementation.