• Clinical and Experimental Pediatrics
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• v.52 no.11
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• pp.1279-1282
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• 2009

Hepatomegaly and liver dysfunction might develop in patients with diabetes mellitus due to glycogen deposition or nonalcoholic steatohepatitis. We experienced a case of hepatic glycogenosis in a patient with type 1 diabetes mellitus who presented with recurrent hypoglycemia, suggesting impairment of glycogenolysis and gluconeogenesis. A 10-year-old girl with a 4-year history of type 1 diabetes mellitus was admitted because of recurrent hypoglycemia and abdominal pain in the right upper quadrant. She had Cushingoid features and hepatomegaly that extended 6 cm below the right costal margin. Laboratory data and radiologic examination revealed elevated liver enzyme levels due to fatty liver. Periodic acid-Schiff (PAS) staining revealed intense glycogen deposition in the cytoplasm of the hepatocytes and PAS reactivity was lost with diastase treatment. At 2 months after administration of glucagon injection and uncooked cornstarch between meals and at bedtime, the hypoglycemic episodes and liver dysfunction improved. It is important to distinguish hepatic glycogenosis from steatohepatitis, because it is possible to prevent excessive hepatic glycogen storage in hepatic glycogenosis cases by strictly controlling blood glucose level and by glucagon administration. To prevent severe hypoglycemic symptoms accompanied by hepatic glycogenosis, we suggest that uncooked cornstarch, which is effective in maintaining blood glucose level, can also be administered.

• Journal of Dairy Science and Biotechnology
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• v.39 no.2
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• pp.78-85
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• 2021

Previously, we showed that oral administration of probiotics, Lactobacillus acidophilus NS1 (LNS1), improved insulin sensitivity in high-fat-diet-fed mice (HFD mice). Furthermore, LNS1-conditioned media (LNS1-CM) reduced HNF4α transcription activity and the expression of phosphoenol pyruvate carboxykinase (PEPCK), a key enzyme in gluconeogenesis in HepG2 cells. In this study, we demonstrated that LNS1 administration increased the expression of glycosyltransferase 2 (GYS2) and glucose transporter 2 (GLUT2), while reduced the expression of glucose-6-phosphatase (G6PC) expression in liver of HFD mice. Furthermore, LNS1 suppressed hepatic expression of glucokinase regulatory unit (GCKR) in HFD mice without changing the mRNA levels of glucokinase (GCK), suggesting that LNS1 may inhibit nuclear GCK activity. Consistently, addition of LNS1-CM to HepG2 cells increased the mRNA levels of GYS2 and GLUT2 with reduced mRNA levels of G6PC and GCKR. Moreover, hepatic glycogen contents were increased in HFD mice upon administration of LNS1. Together, these results suggest that LNS1 facilitates glycogen accumulation in liver by regulating the expression of genes involved in glycogen metabolism, contributing to improved insulin sensitivity in the HFD mice.

• Korean Journal of Veterinary Research
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• v.22 no.2
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• pp.187-195
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• 1982

This paper dealt with the light microscopical and electron microscopical findings on the morphological changes of the liver of Korean native goat injected with toxin (culture filtrate) of Clostridium perfringens which was isolated from Korean native cattle died of acute Clostridium perfringens enterotoxemia. The results observed are summarized as follows. In the microscopical findings, hyperemia and minute hemorrhage of the liver parenchyma, dilatation of hepatic central vein and centrilobular necrosis of liver, cloudy swelling and hydropic degeneration of hepatic cells, and appearance of light eosinophilic granular bodies in the vacuoles were recognized. In the electron microscopical findings, appearance of pinocytotic vesicle (coated vesicle), fusion of these vesicles, formation of vacuole and accumulation of minute granular proteinous materials in the vacuole were observed in the hepatic cells. Decreased number of glycogen granules, swelling and destruction of mitochondria, proliferation of smooth-surfaced endoplasmic reticulum, enlargement of rough-surfaced endoplasmic reticulum, dispersal of thready agranular membranous structure and appearance of secondary lysosome were recognized in the hepatic cell cytoplasm.

• 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.

• Korean Journal of Environmental Agriculture
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• v.20 no.3
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• pp.155-161
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• 2001

This study was carried out to investigate cytotoxicity of paraquat or bentazone on NIH 3T3 fibroblasts, toxicity of paraquat or bentazone, and compensatory effects of 3-Methylcholanthrene(3-MC) on the rat liver. In order to MTT assay, the $5.0{\times}10^4$ cell/mL of NIH 3T3 fibroblast in each well of 24 multidish were cultured. After 24 hours, the cells were treated with solution of paraquat or bentazone(1, 25, 50, 100 ${\mu}M$ respectively). After the NIH 3T3 fibroblast of all groups were cultured in same condition for 48 hours. MTT assay were performed to evaluate the cytotoxicity of cell organelles. Paraquat or bentazone $MTT_{50}$ were 1668.97 ${\mu}M$ and 1506.97 ${\mu}M$, respectively. These $IC_{50}$ of paraquat or bentazone were decided low cytotoxicity by Borenfreund. In order to observe the toxicity and compensatory effects of paraquat or bentazone on the rat liver, Sprague-Dawley male rats were used as experimental animals and divided into paraquat or bentazone only treated group and simultaneous application group of paraquat or bentazone and 3-MC. At 30 min and 1, 3, 6, 12, 24, 48 and 96 hrs interval after each treatment, the animals were sacrificed by decapitation and liver were immediately removed, immersed in fixatives, and processed with routine method for light microscopic study. Paraffin sections were stained with H-E, PAM and Best Carmine. Under the light microscope, degenerative changes of hepatic lobules were frequently observed in portal area from 3 hrs after paraquat or bentazone treatment. All hepatic cells were induced degenerative change at 12 hrs and more severe degenerative change at 48 hrs after paraquat or bentazone treatment. Especially, hepatic cells of bentazone only treated group were distinctly showed pyknotic. Glycogen granules were increased in portal area at 3 hrs, all hepatic cells at 12 hrs and remarkably increased at 48 hrs after paraquat or bentazone treated group. But hepatic cells of bentazone only treated group were regeneration at 48 hrs from portal area and glycogen granules of hepatic cells of paraquat or bentazone and 3-MC combination treated group showed in central area only at 48 hrs. The results indicate that 3-MC may be decrease paraquat or bentazone cytotoxicity on the rat liver.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.6 no.2
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• pp.129-139
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• 2003

Purpose: The aim of the study was to evaluate the long-term outcome of glycogen storage disease (GSD) type 1 with particular reference to hepatic adenoma and hepatocellular carcinoma, and to analyze risk factors affecting the development of hepatic adenoma in GSD type 1. Methods: Forty-three GSD type 1 patients (31 males and 12 females, mean age $13.9{\pm}6.4$ years) were analyzed retrospectively. Hepatic adenoma was detected on abdominal USG and diagnosed on histologic examination. Clinical profiles were compared between patients with hepatic adenoma (n=16) and age-matched controls without hepatic adenoma (n=16). Results: 1) Of 43 GSD type 1 patients, 16 (37.2%) had hepatic adeoma. Hepatic adenoma was detected at the age of mean $14.2{\pm}4.1$ years (range: 7.9~25.7 years). Fourteen (87.5%) adenomas were multiple at detection. 2) Comparison of the clinical profiles between adenoma group and non-adenoma group revealed that age at first introduction of uncooked cornstarch treatment was significantly late in adenoma group compared with non-adenoma group ($9.1{\pm}5.2$ years vs. $3.0{\pm}1.8$ years, p=0.003). Portocaval shunt surgery was performed in 11 (68.8%) patients in adenoma group and 3 (18.8%) in non-adenoma group (p=0.004). Hepatic adenoma developed mean $5.8{\pm}4.2$ years after shunt operation. 3) One patient was diagnosed as hepatocellular carcinoma at the age of 25.7 years. Conclusion: Hepatic adenoma is an important late complication of GSD type 1 with the risk of malignant transformation. Early introduction of cornstarch therapy with strict metabolic control is needed to prevent the development of hepatic adenoma in GSD type 1.

• Food Science and Biotechnology
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• v.18 no.3
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• pp.739-744
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• 2009

This study aims to evaluate the therapeutic action of administration of Nigella sativa (NS) and Peganum harmala (PH) oils in diabetes and hepatic toxicity. Results show that treatment of diabetic rats with NS oil or PH oil ameliorate hyperglycaemia induced stress oxidative and hepatic dysfunction in diabetic rats. Administration of NS or PH oil to diabetic rats caused an anti-diabetic and antioxidant activities by the decrease in plasmatic glucose level and increase in hepatic superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities, reduced glutathione (GSH) and glycogen contents compared to untreated diabetic rats. Besides, NS and PH oils protect the hepatic function observed by decrease of triglyceride (TG), total cholesterol (TCh), and increase of high density lipoprotein-cholesterol (HDL-Ch) levels in serum and hepatic tissues. Moreover, a diminution in the bilirubin, transaminase glutanic pyruvic (TGP), and transaminase pyruvic oxaloacetic (TPO) contents in serum and the thiobarbituric acid-reactive substances levels (TBARs) in hepatic tissues are also detected.

• 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 Environmental Science International
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• v.6 no.1
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• pp.53-60
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• 1997

The toxicity of purified ricln from Ricinus communis to rats was examined by histological and histochemical methods. Sprague-Dawley rats were injected intraperitoneally with 75$\mu\textrm{g}$/kg body weight of ricin and were sacrified at itntervals of 6, 24, 48 and 120 hours after injectoon. The major morphological changes, such as cloudy swelling, hydropic degeneration, necrosis, fatty change, blood congestion, increase of Kupffer cells in number and extension of sinusoids, were obvious in the liver of experimental group. These morphological changes of hepatic cells were mainly observed in both the periportal and midlobular region of hepatic lobule. The extension of sinusoids was obvious in the controlobular region. And glycogen dlstrlbution of hepatic cells tended to decrease in the same region showing morphlogical changes as compared with the control group.

• Journal of Microbiology and Biotechnology
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• v.17 no.12
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• pp.1983-1990
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• 2007

Antidiabetic effects of a novel microbial biopolymer (PGB) 1 excreted from new Enterobacter sp. BL-2 were tested in the db/db mice. The animals were divided into normal control, rosiglitazone (0.005%, wt/wt), low PGB1 (0.1%, wt/wt), and high PGB1 (0.25%, wt/wt) groups. After 5 weeks, the blood glucose levels of high PGB1 and rosiglitazone supplemented groups were significantly lower than those of the control group. In hepatic glucose metabolic enzyme activities, the glucokinase activities of PGB1 supplemented groups were significantly higher than the control group, whereas the PEPCK activities were significantly lower. The plasma insulin and hepatic glycogen levels of the low and high PGB1 supplemented groups were significantly higher compared with the control group. Specifically, the insulin and glycogen increases were dose-responsive to PGB1 supplement. PGB1 supplement did not affect the IPGTT and IPITT compared with the control group; however, rosiglitazone significantly improved IPITT. High PGB1 and rosiglitazone supplementation preserved the appearance of islets and insulin-positive cells in immunohistochemical photographs of the pancreas compared with the control group. These results demonstrated that high PGB1 (0.25% in the diet) supplementation seemingly contributes to preventing the onset and progression of type 2 diabetes by stimulating insulin secretion and enhancing the hepatic glucose metabolic enzyme activities.