• Korean Journal of Food Science and Technology
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• v.36 no.3
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• pp.465-471
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• 2004

This study was designed to investigate the effect of a butanol (BuOH) fraction of Alisma canaliculatum (Ac) with/without vitamin E (VE) on glycogen, lipid levels and oxidative stress in streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley rats were divided into 5 groups: normal, STZ-control, and 3 diabetic experimental groups. Diabetes was induced by injection of STZ (45 mg) into the tail vein. The BuOH fraction of Ac and VE were administrated orally in rats for 21 days: Ac group (400 mg), Ac-VE group (Ac 400 mg & vitamin E 10 mg) and VE group (10 mg). Liver and muscle glycogen levels decrease in STZ-control group versus normal group and these alteration in glycogen levels were prevented Ac-VE group and VE group. Oral administration of Ac or VE resulted in reduction in liver cholesterol. Liver triglycerides were significantly higher in the VE group than in STZ-control group. Liver malondialdehyde (MDA) was increase in STZ-control group compared to normal group, but that of Ac group and Ac-VE group were similar to normal group. Meanwhile MDA in kidney, lung and pancreas were not significantly different among five groups. Ac-VE group increase lung protein that were significantly higher than diabetic control rats. These results suggest that the VE could increase glycogen and triglyceride levels and BuOH fraction of Ac decrease MDA of liver in the diabetic rats. The use of Ac together with VE did not show better control hyperglycemia-induced oxidative stress.

• Journal of Yeungnam Medical Science
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• v.14 no.1
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• pp.137-154
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• 1997

The aim of the present investigation has, been to evaluate the depletion pattern of the supercompensated glycogen of hindlimb muscles during strenous exercise in rats. The plan of the maximizing muscle glycogen stores is based on the fact that a glycogen-depleted muscle by exercise will have an increased avidity for glycogen when exposed to a high carbohydrate diet. The glycogen concentration of soleus, red gastrocnemius and plantaris muscle, and liver was measured at 0, 30 and 60 minutes during treadmill exercise. The experimental animals were divided into 5 group - Normal(N), Control(C), 1Hour(1HR:after 1hour of glucose ingestion), 2Hour(2HR:after 2hour of glucose ingestion) and Exercise-1Hour(EX-1HR:glucose ingestion after 1 hour of preloading treadmill exercise)group - for glycogen storage study. The glycogen concentration of soleus, red gastrocnemius and plantaris muscles in N group was $4.57{\pm}0.34$, 5.11+0.24 and $6.55{\pm}0.20mg/gm\;wet\;wt.$, respectively. The glycogen concentration of soleus and red gastrocnemius in EX-1HR group were about 1.9 and 1.8 times than that of N group, respectively, but the concentration of plantaris was not higher than that of N group. The glycogen concentration of liver in N group was $41.0{\pm}1.47mg/gm\;wet\;wt.$ and the concentration of the overnight fasted C group was only 2.9% of the value of N group. The level of glycogen concentration of liver in the other glucose ingested groups(1HR, 2HR, including EX-1HR) was within 19 - 32% of that of N group. The blood glucose concentration of EX-1HR group was higher than that of N group, the plasma free fatty acid concentration of C and 2HR group was higher than that of N group, and the plasma insulin concentration of EX-1HR group was higher than that of N group. The concentrations of supercompensated glycogen of soleus and red gastrocnemius were rapidly decreased during 30 minutes of exercise but there was almost no changes of the concentration during the other 30 minutes of continuing exercise. The concentration of N group during 30 minutes of exercise was decreased but more slowly than those of EX-1HR group. The remaining level of glycogen after 60 minutes of exercise in EX-1HR group was higher than that of N group. Taken together, the mobilization of endogenous muscle glycogen at the first stage of exercise was proportioned to the initial level of glycogen concentration, and later on, when exercise continued, the muscle glycogen level was stabilized. And the remaining level of supercompensated muscle glycogen after 60 minutes of exercise was higher than that of normally stored glycogen level. The mobilization of the glycogen stroed in slow and fast oxidative muscle fibers is faster than in the fast glycolytic muscle fibers during strenous exercise.

• Preventive Nutrition and Food Science
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• v.22 no.3
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• pp.172-183
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• 2017

Vitamin A and its metabolites modulate insulin resistance and regulate stearoyl-CoA desaturase 1 (SCD1), which are also known to affect insulin resistance. Here, we tested, whether vitamin A-mediated changes in insulin resistance markers are associated with SCD1 regulation or not. For this purpose, 30-week old male lean and glucose-intolerant obese rats of WNIN/GR-Ob strain were given either a stock or vitamin A-enriched diet, i.e. 2.6 mg or 129 mg vitamin A/kg diet, for 14 weeks. Compared to the stock diet, vitamin A-enriched diet feeding improved hyperglycemia and glucose-clearance rate in obese rats and no such changes were seen in lean rats receiving identical diets. These changes were corroborated with concomitant increase in circulatory insulin and glycogen levels of liver and muscle (whose insulin signaling pathway genes were up-regulated) in obese rats. Further, the observed increase in muscle glycogen content in these obese rats could be explained by increased levels of the active form of glycogen synthase, the key regulator of glycogen synthesis pathway, possibly inactivated through increased phosphorylation of its upstream inhibitor, glycogen synthase kinase. However, the unaltered hepatic SCD1 protein expression (despite decreased mRNA level) and increased muscle-SCD1 expression (both at gene and protein levels) suggest that vitamin A-mediated changes on glucose metabolism are not associated with SCD1 regulation. Chronic consumption of vitamin A-enriched diet improved hyperglycemia and glucose-intolerance, possibly, through the regulation of intracellular signaling and glycogen synthesis pathways of muscle and liver, but not associated with SCD1.

• Journal of Yeungnam Medical Science
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• v.23 no.2
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• pp.252-257
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• 2006

Glycogen storage diseases are a heterogeneous group of metabolic disorder affecting multiple organ system: liver, skeletal muscle, heart and brain. Clinical features include: short status, hepatomegaly, hypoglycemia, dyslipidemia and rare involvement of the myocardium except in the case of type III, glycogen storage diseases with hypertrophic cardiomyopathy in adult, which is extremely rare. We treated a case of hypertrophic cardiomyopathy with hepatomegaly that was unknown etiology. The patient was diagnosed as having glycogen storage disease. This 46-year old women was transferred with dyspnea on exertion and abnormal LFTs. She was diagnosed with hypertrophic cardiomyopathy by echocardiography but there was no specific cause for hypertrophic cardiomyopathy. A liver biopsy was performed. The result showed glycogen storage disease possible type III, IV or IX. In conclusion, patients with hypertrophic cardiomyopathy of unknown etiology and abnormal LFTs should be evaluated for glycogen storage disease.

• Nutritional Sciences
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• v.8 no.3
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• pp.181-188
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• 2005

We investigated the effects of diet manipulation on pro- and macro-glycogen accumulation and mobilization during exercise in different kinds of muscle fiber and tissue. Thirty-two Sprague-Dawley rats were divided into groups representing one of two dietary conditions: high fat (HF, n=16) or standard chow (CHOW, n=16). Each dietary group was fm1her divided into control (REST, n=8) and exercise (EXE, n=8). After an eight-week dietary intervention period, the animals in EXE swam for 3 hours while the animals in REST remained at rest Skeletal muscle (soleus, red gastrocnemius and white gastrocnemius) and liver samples were then dissected out and used for analyses. 1here was no statistical difference in body weight between the animals in the HF and mow groups (p>.05). Three hours of exercise significantly increased plasma free fatty acid (FFA) concentration in the animals in the CHOW group but not in the animals in the HF group. Both citrate. synthase (CS) and $\beta$-hydroxyacyl dehydrogenase ($\beta$-HAD) activities in skeletal muscles were higher in the HF group than in the mow group. CS and $\beta$-HAD activities were also the highest in red gastrocnemius and the lowest in white gastrocnemius. At both time points (i.e., rest and immediately after exercise) intramuscular triglyceride (IMTG) and liver TG concentrations were significantly higher in the HF compared to the CHOW. IMTG and liver TG changed selectively in the CHOW. Except in white gastrocnemius muscle, there was no significant difference in total glycogen content between HF and mow at rest. Although exercise significantly lowered total glycogen content in all groups and tissues (p<.05), the degree of reduction was markedly greater in the mow than in the HF. Whereas changes in proglycogen concentration showed a trend similar to those of total glycogen, alterations in macroglycogen concentrations clearly differed from those of total glycogen. Specifically, the degree of reduction of macroglycogen following three hours of exercise was substantially greater in the CHOW than in the HF. These results suggest that metabolic alterations induced by a long-term high fat diet may be caused by macro-glycogen rather than pro-glycogen.

• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.6
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• pp.981-985
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• 1996

To study the effect of toluene administration on the liver damage, rats were previously fed a low (casein 7%, LP) or standard(casein 20%, SP) protein diet and for four days toluene(50% in olive oil) was given at 0.2ml/100g body weight/day to the male rats, and then the degree of liver damage in toluenetreated animals fed LP were compared with those fed SP. The increasing rate of liver weight/body weight and the serum levels of xanthine oxidase to the control group were higher in rats fed SP than those fed LP. The decreasing rate of protein contents in cytosol, mitochondria and glycogen, glutathione contents of liver to the control group were higher in rats fed SP than those fed LP. In histopathological findings, the swelling of hepatic cell around the central vein was demonstrated in all the two groups toluene-treated rats. But the degree of swelling severity in hepatocytes was somewhat higher in rats fed SP than those fed LP. Therefore it is assumed that the degree of liver damage severity in toluenetreated animals was higher in rats fed SP than those fed LP.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.12 no.2
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• pp.108-112
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• 2012

Glycogen storage disease type III (GSD type III, OMIM #232400) is a rare autosomal recessive disease caused by a deficiency of the glycogen-debranching enzyme (GDE) with a mutation in the AGL gene (OMIM *610860). It is known to be bifunctional enzyme, that is, having two independent catalytic activities; 1,4-${\alpha}$-D-glucan 4-${\alpha}$-D-glycosyltransferase (EC 2.4.1.25) and amylo-1,6-glucosidase (EC 3.2.1.33) that occur at separate active sites on a single polypeptide chain. Most patients with GSD type III usually have symptoms related to decreased glycogenolysis in liver and muscles, such as hepatomegaly, hypoglycemia, failure to thrive, hyperlipidemia, muscle weakness and cardiomyopathy (type IIIa), however some patients show symptoms restricted to liver (type IIIb). GSD type III is diagnosed by enzyme test through liver or muscle biopsy or mutation analysis of the AGL gene. We report the case of GSD type III proven by gene study after liver biopsy, which revealed c.476delA, c.3444_3445insA in exon 6, 27 of AGL gene in Korean patient.

• Korean Journal of Veterinary Research
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• v.18 no.2
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• pp.87-95
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• 1978

Election microscopic investigation were conducted on the mature mouse (B.W. about 25g) liver which was treated with Ginseng water extract during three, six and nine days respectivelly after carbon tetracholride injection into abdominal cavity. The results obtained were as follows: The liver cells of control group treated with carbon tetrachloride alone were restored slowly. The liver cells of experimental group treated with Ginseng water extract after carbon tetrachloride injection, however, were shown the appearance of well-developed ${\gamma}-ER$ and Golgi complex, marked aggregation of glycogen particles, and a number of large lipid droplets which are attached markedly with glycogen particles as compared to the control group. As these findings, it could be suggested that Ginseng gives an activation to restore the damaged liver cells.

• The Korea Journal of Herbology
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• v.37 no.6
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• pp.9-17
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• 2022

Objective : In modern society, liver diseases such as liver fibrosis are on the rise as inflammation and wound healing processes of the liver are repeated due to factors such as drinking, smoking, and stress. This study was conducted to evaluate the effect of Saenggangeonbi-tang (SGGBT) on thioacetamide (TAA)-induced liver fibrosis. Methods : The mice were divided into 4 groups for examination (n=6): Normal group (Nor), distilled water-treated liver fibrosis mice (Con), silymarin 50 mg/kg-treated liver fibrosis mice (Sily), SGGBT 200 mg/kg-treated liver fibrosis mice (S200). Liver fibrosis was established in the mice via TAA for 8 weeks (1 week 100 mg/kg, 2,3 weeks 200 mg/kg, 4-8 weeks 400 mg/kg, three times a week, intraperitoneal injection) and they were administered silymarin and SGGBT (every day, oral administration) with the TAA. Results : SGGBT significantly decreased the levels of aspartate aminotransferase, alanine aminotransferanse, ammonia, and myeloperoxidase in serum increased by liver fibrosis. As a result of confirming H&E and MT staining, it was confirmed that SGGBT reduced damage and inflammatory cell infiltration in liver tissue, and alleviated changes in collagen fiber deposition and histological fibrosis. Also, it was confirmed through PAS staining that it reduced glycogen deposition in liver tissue. In addition, SGGBT significantly decreased the NADPH oxidases as well as significantly modulated the expression of MMP-2 and TIMP-2. Conclusions : These results suggest that SGGBT regulates the expression of MMP/TIMP protein through inhibition of oxidative stress and alleviates liver fibrosis by reducing collagen and glycogen deposition in liver tissue.

• Advances in Traditional Medicine
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• v.10 no.3
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• pp.165-172
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• 2010

The present study investigated the effect of silymarin, a flavonoid, on streptozotocin (STZ) - induced diabetic dyslipidaemia in rats. Experimental diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg). Silymarin (25 mg/kg and 50 mg/kg) was orally administered to diabetic rats for a period of 15 days. Blood glucose levels, serum lipid profile and liver glycogen levels were estimated following the established procedures. Biochemical observations were supplemented with histological examination of liver sections. Oral administration of silymarin to diabetic rats significantly (P < 0.001) decreased the blood glucose levels ($259.99{\pm}23.64$ vs. $99.90{\pm}2.62$ [25 mg] & $89.17{\pm}3.32$ [50 mg]). The most interesting finding was the significant (p < 0.001) increase in HDL-cholesterol levels ($26.99{\pm}0.61$ vs. $40.55{\pm}0.52$ [25 mg] & $41.12{\pm}0.37$ [50 mg]) whereas, there was a significant decrease in serum total cholesterol (TCh), triglycerides (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL) cholesterol levels observed in silymarin treated diabetic rats. STZ treatment caused significant degeneration of liver parenchyma, which was normalized to near normal morphology by administration of silymarin. The findings indicate that silymarin effectively improved the overall lipid profile and restored the glycogen stores in the liver of STZ-induced diabetic rats, in a dose dependent manner. The results indicate existence of abnormalities in lipid metabolism in STZ-induced diabetic rats and suggest a protective effect of silymarin in this animal model.