• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.3
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• pp.380-386
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• 1994

The behavior of glycogen and histological changes of hepatic tissues in the liver of rats, aged 6 to 7 weeks, fed 18% casein diet under control, gramoxone and gramoxone + vitamin C(Vt. C) diets has been investigated in a comined histropathological and histochemical studies. Cloudy swelling and fat changes of hepatic cells were observed in the gramoxone group with the duration of feeding time. Fat changes of hepatic cells were observed more obviously than cloudy welling, especially in the hepatic cells of periportal area. The number of Kupffer's cells increased signifciantly in the gramoxone group fed for 4weeks. The cloudy swelling and fat changes decreased obviously in the gramxone + Vt. C group. Glycogen content of heaptic cells tended to increase slightly in the gramoxone group as compared with the control group . moreover, glycogen depositons were higher in the hepatic cells where fat changes were obvious. It seems to be that Vt.C alleviating effects on the gramoxone toxicity in the patterns of glycogen distribution and histological structure of heaptic tissues.

• The Korean Journal of Pharmacology
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• v.17 no.1 s.28
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• pp.33-39
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• 1981

In this paper, the influences of adrenergic neuronal blockades of different mode: guanethidine and ${\alpha}$-methyl-para-tyrosine on the changes induced by carbon tetrachloride $(CCl_4)$ of hepatic total lipid, glycogen, and lipid peroxide contents and serum lactic dehydrogenase activity were investigated in male mice. The results obtained were summarized as follows: 1) The hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were markedly increased by $CCl_4$, but hepatic glycogen content were decreased. 2) The hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were not significantly changed by guanethidine(20mg/kg) or ${\alpha}$-methyl-para-tyrosine (5 mg/kg) injection. 3) The increase of hepatic total lipid induced by $CCl_4$ was inhibited by the pretreatment of guanethidine or ${\alpha}$-methyl-para-tyrosine, and the increase of hepatic lipid peroxide content induced by $CCl_4$ was slightly inhibited by them. But the decrease of hepatic glycogen content and the increase of serum lactic dehydrogenase activity induced by $CCl_4$ were not affected by them.

• The Korean Journal of Pharmacology
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• v.16 no.2 s.27
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• pp.31-38
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• 1980

Calvert et al. formulated the hypothesis that carbon tetrachloride ($CCl_4$) acted on the central nervous system to produce and intensify sympathetic discharge which resulted in anoxic necrosis of the liver. Recknagel suggested that the essential feature of $CCl_4$ hepatotoxicity depended on the cleavage of it to $CCl_3$(free radical) and the peroxidative decomposition of cytoplasmic membrane structural lipids. And there are many reports which show the increase of adrenergic activity in hyperthyroidism. In this paper, the influence of thyroxine on the hepatotexicity of carbon tetrachloride was investigated in mice. The results obtained were summarized as follows; 1) Hepatic total lipid and lipid peroxide contents were slightly decreased by L-sodium thyroxine injection(4mg/kg/day for 4days or 6days), but hepatic glycogen content was significantly decreased. 2) Hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were significantly increased by $CCl_4$ (4 ml/kg single dose or triple dose: 4ml/kg/day for 3days), but hepatic glycogen content was significantly decreased. 3) The increase of hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity induced by $CCl_4$ were significantly inhitited by the pretreatment of thyroxine. 4) The decrease of hepatic glycogen induced by $CCl_4$ was not affected by the pretreatment of thyroxine.

• Proceedings of the Ginseng society Conference
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• 1990.06a
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• pp.196-200
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• 1990

the ginseng polypeptide (GPP) isolated from the root of Panax ginseng C.A. Meyer was demonstrated to decrease the levels of blood sugar and hepatic glycogen when injected intravenously to rats at a doses of 50-200mg/kg without affecting blood total lipid. When mice were injected subcutaneously daily at a dose of 50 and 100mg/kg for 7 successive days, GPP was also found to decreased blood sugar and hepatic glycoge. In addition, GPP was found to decrease various experimenta hyperglycemias induced by injection of adrenaline, glucose and alloxan. GPP exhibited inhibiting effect on the glycogen enhancement induced by glucose, but strengthening effect on the glycogen decrease induced by adrenaline. When the levels of blood total lipid and liver glycogen were increased by alloxan, GPP was shown to inhibit these changes except its lowering blood sugar. the toxicity of GPP is very low, its LD50 was found to be 1.62$\pm$0.130 g/kg for iv.

• Journal of Ginseng Research
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• v.14 no.2
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• pp.338-342
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• 1990

The ginseng Polypeptide (GPP) Isolated from the root of Panax ginseng C.A. Meyer was domonstrated to decrease the levels of blood sugar and hepatic glycogen when injected intravenoilsly to rats at a doses of 50-200 mg/kg without affecting blood total lipid. When mice were injected slibclitaneollsly daily at a dose of 50 and 100 mg/kg for 7 successive days. GPP was also found to decrease blood sligar and hepatic glycogen. In addition, GPP was found to decrease variolls experimental hypergly cemias induced by injection of adrenaline, glilcose and alloxan. GPP exhibited inhibiting effect on the glut rogen enhancement indllced by glucose, but strenthening effect on the glycogen decrease indliced by adrenaline. When the levels of blood total lipid and lilrer glycogen were increased by T alloxan. GPP was shown to inhibit these changes except its lowering blood sugar. The toxicity of GPP is very low, LD50 was found to be 1.62 $\pm$ 0.130 g/kg for iv.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.23 no.2
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• pp.8-14
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• 2023

The hepatic glycogen storage disease type 0 (GSD type 0) is an autosomal recessive disorder caused by a deficiency of hepatic glycogen synthase encoded by the glycogen synthase 2 (GYS2) gene, leading to abnormal synthesis glycogen. The clinical findings of GSD type 0 are hyperketotic hypoglycemia at fasting state and accompanying postprandial hyperglycemia and hyperlactatemia. GSD type 0 has only been reported in a very small number so far, and the diagnosis is likely to be missed because symptoms are mild, severe hypoglycemia is rare or asymptomatic, or symptoms gradually disappear with age. Essential management strategies include feeding high-protein meals to stimulate gluconeogenesis, frequent meals to prevent hypoglycemia during the day and feeding complex carbohydrates such as uncooked cornstarch to slowly release glucose during nignt. GSD type 0 has a good prognosis, with appropriate treatment, normal growth can be achieved and no complications occur. Significant hypoglycemia occurs less common in adulthood, but ongoing dietary management may be necessary.

• Korean Journal of Veterinary Research
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• v.32 no.3
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• pp.357-364
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• 1992

Artemisia Iwayomogi Compositae) has been used clinically for jaundice, hepatitis, liver cirrhosis etc. The purposes of present study were to examine pharmacological effects of Artemisia Iwayomogi water extract(AIWE) on biochemical parameters (activities of ALP and LAP, contents of glucose, total bilirubin, total protein and albumin in serum, A/G ratio, and levels of hepatic glycogen) against hepatic injury by carbon tetrachloride($CCl_4$) in rats. The results were as follows ; 1. Increased ALP activities by $CCl_4$ were very significantly(p<0.001) decreased in AIWE posttreatment groups at 72 hours and significantly(p<0.05) decreased in AIWE pretreatment groups at 72 hours. Increased LAP activities by $CCl_4$ were significantly (p<0.05) decreased in AIWE posttreatment groups at 72 hours. A little increased total bilirubin contents by $CCl_4$ were very significantly (p<0.001) decreased in AIWE posttreatment groups at 24, 48 and 72 hours. 2. Increased glucose contents by $CCl_4$ were decreased in AIWE posttreatment groups. Decreased hepatic glycogen levels by $CCl_4$, were significantly (p<0.05) increased in AIWE posttreatment groups at 48 and 72 hours. 3. Decreased total protein contents by $CCl_4$ were significantly (p<0.05) increased in AIWE posttreatment groups at 48, 72 hours. Decreased albumin contents by $CCl_4$ were increased in proportion to numbers of AIWE treatments in AIWE pre- and posttreatement groups. Decreased A/G ratios by $CCl_4$ were significantly (p<0.05) increased in AIWE posttreatment groups at 48 hours. In conclusion, AIWE did not affect normal liver function and had hepatoprotective effects rather than direct preventive effects to $CCl_4$-induced cholestasis, damages in metabolisms of glucose, protein and bilirubin.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.17 no.4
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• pp.239-247
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• 2014

Purpose: There are no studies of hepatic glycogen storage diseases (GSDs) other than type I and III in Korea. We aimed on investigating the characteristics of hepatic GSDs in Korea diagnosed and followed at a single center. Methods: We retrospectively analyzed patients who were diagnosed as GSD and followed at Samsung Medical Center from January, 1997 to December, 2013. Clinical manifestations, laboratory results, treatment, and prognosis were investigated. Results: Twenty-one patients were included in the study. The types of 17 patients were confirmed by enzyme activity tests and/or gene analysis. GSD Ia was diagnosed in 7 patients (33.3%), Ib in 1 patient (4.8%), III in 2 patients (9.5%), IV in 1 patient (4.8%), and IX in 6 patients (28.6%). Types other than GSD I constituted 52.9% (9/17) of the patients diagnosed with a specific type of hepatic GSD. The median age at presentation was 2 years. Hepatomegaly was observed in 95.2%, elevated liver transaminases in 90.5%, and hyperlactacidemia in 81.0% of the patients. The duration for follow-up was $77{\pm}62.0$ months. Uncooked corn starch was initiated in all the patients. No mortality was observed during the follow-up period, and liver transplantation was performed in 14.3%. Conclusion: Types other than GSD I comprised more than half of the patients diagnosed with a specific type of hepatic GSD. Clinical suspicion and thorough evaluation of hepatic GSDs in Korea should be focused not only on GSD I, but also on other types.

• The Korean Journal of Pharmacology
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• v.18 no.1
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• pp.33-41
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• 1982

In this paper, the influences of adrenergic blockades; propranolol and phenoxybenzamine on the changes of hyperglycemic action, hepatic glycogen content, and brain norepinephrine (NE) content induced by clonidine were investigated in the male mice. The results obtained were summarized as follows: 1) Blood glucose level was significantly increased by clonidine $(30{\mu}g/kg)$. The increase of blood glucose level induced by clonidine was not affect by the propranolol (10mg/kg) pretreatment, but significantly inhibited by the phenoxybenzamine (10mg/kg) pretreatment. 2) Hepatic glycogen content was moderately inhibited by clonidine. The decrease of hepatic glycogen content induced by clonidine was not affected by the propranolol and phenoxybenzamine pretreatment. 3) Brain NE content was significantly increased in 30 minutes and 60 minutes after clonidine treatment. The increase of brain NE content induced by clonidine was significantly inhibited by the phenoxybenzamine pretreatment. The increase of train NE content induced in 90 minutes and 120 minutes after clonidine treatment was more markedly increased by the propranolol pretreatment.

• Korean Journal of Veterinary Research
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• v.16 no.1
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• pp.97-103
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• 1976

In order to clarify the histopathological changes resulting from nitrate poisoning, rabbits were experimentally poisoned by the oral administration of $KNO_3$ or $NaNO_2$ and examined clinically and histopathologically. In addition, the quantitative changes of glycogen level in hepatic cells were histochemically observed. The results obtained were summarized as follows: 1. Clinical symptoms observed from the acute cases which died within 2 hours after the administration were severe cyanosis of visible mucosa, frequent urination, and dyspnea. However, in chronic cases administrated daily with $KNO_3$ for 43, 50 and 74 days respectively, no marked symptoms were observed. 2. Macroscopic changes observed in acute cases were severe methemoglobinemia, cloudy swelling of hepatic cells, hemorrhage and hyperemia of gastric mucosa, and hyperemia of other organs. In chronic cases there were marked hyperemia, dark-red coloring and increasing of consistency in liver and kidney, and swelling of spleen. 3. Microscopic changes observed in acute cases were hemorrhage and hyperemia of various organs, cloudy swelling and centrilobular necrosis of hepatic cells and necrosis of convoluted tubular epithelium in kidney. In chronic cases there were round cell infiltration of the interlobular connective tissue and epithelial proliferation of interlobular bile ducts in the liver, and necrosis of the convoluted tubular epithelium and proliferation of interstitial connective tissue in kidney, thickening of alveolar septa of lungs, activated hemopoiesis of bone marrow, and myeloid metaplasia of sqlenic pulp. 4. Glycogen storage in liver cells was decreased in acute cases, on the contrary, increased in chronic cases.