• Journal of Microbiology and Biotechnology
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• v.29 no.3
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• pp.357-366
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• 2019

We first confirmed the involvement of MalQ (4-${\alpha}$-glucanotransferase) in Escherichia coli glycogen breakdown by both in vitro and in vivo assays. In vivo tests of the knock-out mutant, ${\Delta}malQ$, showed that glycogen slowly decreased after the stationary phase compared to the wild-type strain, indicating the involvement of MalQ in glycogen degradation. In vitro assays incubated glycogen-mimic substrate, branched cyclodextrin (maltotetraosyl-${\beta}$-CD: G4-${\beta}$-CD) and glycogen phosphorylase (GlgP)-limit dextrin with a set of variable combinations of E. coli enzymes, including GlgX (debranching enzyme), MalP (maltodextrin phosphorylase), GlgP and MalQ. In the absence of GlgP, the reaction of MalP, GlgX and MalQ on substrates produced glucose-1-P (glc-1-P) 3-fold faster than without MalQ. The results revealed that MalQ led to disproportionate G4 released from GlgP-limit dextrin to another acceptor, G4, which is phosphorylated by MalP. In contrast, in the absence of MalP, the reaction of GlgX, GlgP and MalQ resulted in a 1.6-fold increased production of glc-1-P than without MalQ. The result indicated that the G4-branch chains of GlgP-limit dextrin are released by GlgX hydrolysis, and then MalQ transfers the resultant G4 either to another branch chain or another G4 that can immediately be phosphorylated into glc-1-P by GlgP. Thus, we propose a model of two possible MalQ-involved pathways in glycogen degradation. The operon structure of MalP-defecting enterobacteria strongly supports the involvement of MalQ and GlgP as alternative pathways in glycogen degradation.

• Journal of Nutrition and Health
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• v.34 no.7
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• pp.748-753
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• 2001

This study is to investigate the effects of capsaicin with high-fat diet on tissue glycogen contents in exercise-trained rats. Forty male Sprague-Dawley rats were offered a high-fat diet for 2 wks in individual cages and were exercise-trained by a animal treadmill running throughout the experimental period. After 2 wks of the prefeeding with high-fat diet, the rats were divided into two group: high-fat diet group(CON)and high-fat diet + capsaicin(0.014%) group(CAP). The rats were killed by decapitation at 10 hr(rest), 1 hr and 2 hr after treadmill running(27m/min, 6$^{\circ}$). Body weight and epididymal adipose tissure weight were significantly lower in CAP than in CON, but soleus muscle weight was not different between the two groups. Glycogen contents in liver, soleus and gastrocnemius white muscles were significantly lower in CAP than in CON at rest, 1 hr and 2 hr (p<0.05). However, glycogen content in gastrocnemius red muscle was significantly higher in CAP compared with CON at 2 hr after the exercise(p<0.05). These results indicate that capsaicin intake with high-fat diet would decrease glycogen contents in liver and muscle, however, this effect on glycogen metabolism could be changed by muscle type.

• Journal of Yeungnam Medical Science
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• v.7 no.1
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• pp.19-27
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• 1990

This investigation was undertaken to clarify the in vitro effect of the various stimulations, such as exercise(E), insulin(I), direct electrical stimulation(EST) and the combinations of the above, on the glucose incorporation into glycogen molecules (glycogen synthesis) of the normal slow(soleus) and fast twitch(plantaris) muscles, and the different responses of slow and fast twitch muscles to persistent overloads causing compensatory muscle hypertrophy. In resting state, slow twitch muscle has greater capacity for glycogen synthesis than fast twitch muscle, and responses of different muscle to various stimuli were differ as follows : In slow twitch muscle, the glycogen synthesis was increased by insulin, and electrical stimulation but not increased by exercise ; exercise increased insulin sensitivity and the effect of electrical stimulation. Whereas the glycogen synthesis in fast twitch muscle was increased only by the stimuli combined with E and EST, and E, I, and EST. As the result of removal of synergistic muscle, both muscles were hypertropied, and the degree of hypertrophy in response to persistent overload was higher in fast twitch muscle(182%) than slow twitch muscle(151%). In hypertrophied muscles, glycogen synthesis of soleus in any groups was lower than that of the control, but similar in plantaris. In conclusions, there were marked heterogeneity in defferent muscle fiber in the effects of exercise and insulin addition and electrical stimulation on muscle glycogen synthesis, and fast twitch muscle may be adapted more easily to that kind of persistent overload than slow twitch muscle.

• The Korean Journal of Physiology
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• v.21 no.2
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• pp.323-325
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• 1987

The concentrations of glucose and glycogen in the normal gastrocnemius muscles of Uromastix hardwickii were $88.82{\pm}4.52\;mg/100\;gm$ and $158.98{\pm}23.19\;mg/100gm$ of wet weight of the muscle, respectively. 14-days denervation period has no any effect on glucose contents while the glycogen concentration was decreased to 1/3 of the normal control innervated muscles.

• The Korean Journal of Physiology
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• v.22 no.1
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• pp.63-77
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• 1988

This study was carried out to investigate relationships between maximal running time (MRT) and glycogen supercompensation in fast twitch white fibers (white vastus, WV), fast twitch red fibers (red vastus, RV) and slow twitch red fibers (soleus muscle, SM) of endurance-trained rats. Male rats of a Sprague-Dawley strain were divided into the trained groups and untrained groups. Untrained groups were acquired to run on the treadmill 10 minutes for 3 days and remained rest and maintained with mixed diet for 4 weeks. For last 10 days of resting period, the untrained rats were divided into 3 groups i.e. mixed diet (untrained control), high and low carbohydrate (CHO) diet groups. And each group was subdivided into 2 groups, one group was tested for the MRT and the other was sacrificed to measure the blood glucose, blood lactate, glycogen contents of liver and muscles. The experimental groups were trained on treadmill by a modified method of Constable et al. (1984) maintained with mixed diet for 4 weeks. After measurement of MRT of this group, they were also divided into high and low CHO groups and fed with these diet for 2 days and MRT of each group was measured again to see the effect of high or low CHO feeding on the MRT. Each group was maintained with the same diet for next 2 days during which some of the rats were sacrificed at given time intervals for the measurements of blood glucose and lactate, liver and the muscles glycogen. The results were summarized as follows; 1) In the untrained group, there were no significant differences between subgroups in MRT, glycogen conent of SM, RV and WV. But blood glucose concentration and glycogen content of liver of low CHO group were significantly lower than those of mixed diet group. 2) The MRT and glycogen content of SM, RV and WV of trained mixed diet group were significantly increased compared to those of untrained mixed diet group, but there was no significant difference in glycogen content of liver. 3) MRT of trained mixed, high CHO and low CHO groups were $137{\pm}9.8,\;176{\pm}9.8\;and\;129{\pm}7.3\;min$ respectively with the significant difference between them. 4) There were no differences in blood lactate concentrations between the trained high and low CHO groups immediately after maximal running and during recovery period. 5) Glycogen contents in RV and SM of trained high CHO group were significantly increased, and glycogen contents in RV, WV and liver of trained low CHO group were significantly decreased compared to those of trained mixed diet group. 6) Immediately after maximal running, the blood glucose concentrations of trained high CHO and low CHO groups were $73{\pm}4.0\;and\;67{\pm}6.9mg%$ respecitively. The blood glucose of the trained high CHO group was fully recovered within one hour by feeding. But blood glucose concentration of low CHO group was slowly recovered up to $114{\pm}4.1mg%$ after two hours of feeding and maintained. Those values were still significantly lower than that of trained mixed diet group. The synthetic rates of glycogen in liver and muscles during the recovery period followed the similar time course of the blood glucose recoveries in each group. These results suggest that an increase in MRT of trained high CHO group was attributed to the glycogen supercompensation in slow twitch muscle fibers. And a decrease in MRT of trained low CHO may be due to decreased glycogen contents of liver and muscles. The results also suggest that glycogen supercompensation was more evident in slow twitch red fibers of endurance-trained rats and blood glucose is one of the limiting factors of glycogen synthesis.

• The Korean Journal of Cytopathology
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• v.9 no.2
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• pp.213-219
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• 1998

Glycogen-rich clear ceil carcinoma of the breast is an unusual variant of carcinoma with a recorded incidence of $1.4{\sim}3%$ of breast carcinomas. The cytologic characteristics have not been well described. We report two cases of glycogen-rich clear cell carcinoma with corresponding fine needle aspiration(FNA) cytologic findings and compare them to infiltrating ductal carcinoma and other clear ceil malignancies with a review of literature. One was a 62-year-old woman exhibiting a palpable mass of the right breast. The smears showed atypical tight cell clusters and individually scattered single cells containing leanly or clear abundant cytoplasm with well defined cytoplasmic margins. Mild to moderate nuclear pleomorphism and a prominent nucleolus were present. The other was a 42-year-old woman who was admitted with a right breast mass. The smears showed moderately cellular, tightly cohesive tumor cells. The cytoplasmic outline was generally well demarcated. The tumor cells Contained foamy to clear abundant cytoplasm with large and small vacuoles. The nuclear pleomorphism was marked. Both tumors resected by modified radical mastectomy, were diagnosed as glycogen-rich clear cell carcinoma. Histologically, the clear cell nature of tumor cells were not characteristic enough to predict this type of the tumor. Some cytologic features can be distinguished other clear cell breast cancer from glycogen-rich carcinoma. Recognition of these unusual patterns in a breast FNAC should raise the suspicion of a clear cell carcinoma including glycogen-rich subtype. Cytological localization of glycogen using PAS and D-PAS staining may permit the correct Identification and differential diagnosis of this tumor.

• Archives of Pharmacal Research
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• v.12 no.2
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• pp.125-127
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• 1989

Effects of three types of dietary fibres on blood glucose and liver glycogen were studied in male rats. The fibres were used as 10% of the diet supplemented from dietary sources, white beans, peas and carrots. The experiment continued for 5 weeks. At the end of the experiment, fasting blood glucose and liver glycogen were determined. The results showed that replacing carrot fibres and pea fibres by white bean fibres produced significant reduction of blood glucose by 28% and 43%, respectively, while exchanging pea fibres by carrot fibres produced no significant reduction of blood glucose gy 20%. Liver glycogen level (mg/100 g liver) was not affected by altering the fibre type in the diet.

• Toxicological Research
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• v.8 no.1
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• pp.9-15
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• 1992

Hydroxybrazilin was examined for its effects on glycogen synthesis in primary cultured rat hepatocytes. At 10-6 M hydroxybrazilin, glycogen synthesis was increased in basal state, but not in insulin stimulated state. However, any signiFicant changes were nor observed at 10-5 M hydroxybrazilin in both states. The glycogen synthesis was rather suppressed at 10-5M hydroxybrazilin. It was also observed that hydroxybrazilin increased insulin sensitivity but not insulin responsiveness at 10-5M concentration. These results suggest that hydroxybrazilin might exert hypoglycemic action through its effects on insulin receptor and post receptor events.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.21 no.4
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• pp.365-368
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• 2018

Glycogen storage disease (GSD) IV is a rare autosomal recessive inherited disorder caused by mutations in the gene coding for glycogen branching enzyme leading to progressive liver disease. GSD IV is associated with mutations in GBE1, which encodes the glycogen branching enzyme. We report a case of GSD IV with rare homozygous mutations in the GBE1 gene (c.791G>A (p.Gly264Glu), which was successfully treated by liver transplantation.

• 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.