• The Korean Journal of Physiology and Pharmacology
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• v.24 no.4
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• pp.319-328
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• 2020

High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague-Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

• Journal of Microbiology and Biotechnology
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• v.24 no.4
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• pp.483-488
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• 2014

In order to improve the expression of heat-resistant xylanase XYNB from Aspergillus niger SCTCC 400264, XynB has been cloned into Pichia pastoris secretary vector pPIC9K. The XynB production of recombinant P. pastoris was four times that of E. coli, and the $V_{max}$ and specific activity of XynB reached $2,547.7{\mu}mol/mg$ and 4,757 U/mg, respectively. XynB still had 74% residual enzyme activity after 30 min of heat treatment at $80^{\circ}C$. From the van der Waals force analysis of XYNB (ACN89393 and AAS67299), there is one more oxygen radical in AAS67299 in their catalytic site, indicating that the local cavity is much more free, and it is more optimal for substrate binding, affinity reaction, and proton transfer, etc, and eventually increasing enzyme activity. The H-bonds analysis of XYNB indicated that there are two more H-bonds in the 33rd Ser of XYNB (AAS67299) than in the 33rd Ala(ACN89393 ), and two H-bonds between Ser70 and Asp67.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.24 no.3
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• pp.306-315
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• 2021

Purpose: Obesity is defined as the abnormal or excessive accumulation of fat over acceptable limits. Leptin is a metabolic hormone present in the circulation in amounts proportional to fat mass. Leptin reduces food intake and increases energy expenditure, thus regulating body weight and homeostasis. Various polymorphisms are present in the leptin gene and its receptor. These polymorphisms may be associated with obesity. This study aimed to show the association of leptin (+19) AG, leptin (2548) GA, and Gln223Arg leptin receptor polymorphisms with obesity and metabolic syndrome in Turkish children aged 6-17 years, and to conduct further investigations regarding the genetic etiology of obesity. Methods: A total of 174 patients diagnosed with obesity and 150 healthy children who were treated at Tokat Gaziosmanpasa Medical School Hospital between September 2014 and March 2015 were included in this study. The ages of the children were between 6 and 17 years, and anthropometric and laboratory results were recorded. Genotyping of leptin (+19) AG, leptin (2548) GA, and leptin receptor Gln223Arg polymorphisms was performed by polymerase chain reaction. Results: An association between leptin receptor Gln223Arg gene polymorphism and obesity was detected. Conclusion: Further studies are needed to determine the role of genetic etiologies and to indicate the role of leptin signal transmission impairment in the pathogenesis of obesity. We hope that gene therapy can soon provide a solution for obesity.

• Journal of Microbiology and Biotechnology
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• v.11 no.3
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• pp.384-388
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• 2001

The metabolic pathway synthesis algorithm was applied to estimate the maximum ethanol yield from xylose in a model recombinant Saccharomyces cerevisiae strain containing the genes involved in xylose metabolism. The stoichiometrically independent pathways were identified by constructing a biochemical reaction network for conversion of xylose to ethanol in the recombinant S. cerevisiae. Two independent pathways were obtained in xylose-assimilating recombinant S. cerevisiae as opposed to six independent pathways for conversion of glucose to ethanol. The maximum ethanol yield from xylose was estimated to be 0.46 g/g, which was lower than the known value of 0.51 g/g for glucose-fermenting and wild-type xylose-fermenting yeasts.

• Journal of Industrial and Engineering Chemistry
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• v.67
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• pp.231-235
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• 2018

In this study, we demonstrate the conversion of starch to (R,R)-2,3-butanediol (2,3-BD) in a hybrid cell-free synthesis system containing a mixture of lysates derived from Escherichia coli (E. coli) and cyanobacteria. A sufficient pool of pyruvate required for the synthesis of 2,3-BD was generated by combining metabolic pathways of cyanobacteria and E. coli. Successful synthesis of 2,3-BD was achieved by additional modifications of the hybrid cell-free system with the enzymes required to convert pyruvate to 2,3-BD. The results demonstrate a new approach to harness biological pathways to expand the scope of cell-free metabolic engineering by cross-species combinations of cell lysates.

• Biomolecules & Therapeutics
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• v.5 no.2
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• pp.107-109
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• 1997

For metabolic study of pinusolide, a naturally occurring platelet activating factor antagonist, a synthetic method for preparation of radiolabeled pinusolide was studied. Pinusolide was first oxidized with $OsO_4/NaIO_4 $to 17-nor-8-oxo compound (2), which was subsequently converted to pinusolide by treatment with the Lombardo reagent $(Zn/CH_2Br_2/TiCI_4)$. The Wittily reaction was unsuccessful in the latter carbonyl methylenation of 2.

• Food Science and Industry
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• v.50 no.3
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• pp.60-69
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• 2017

Kimchi is a traditional fermented food of Korea and made by salting and fermenting vegetables. A negative impression on kimchi as a great source of sodium intake has grown in Korea since 1980 as people argue that sodium is a major cause of high blood pressure and metabolic syndrome. While people are more interested in healthy living in Korea, the negative impression is stronger now. This study analyzes the sensitive and negative reaction to sodium intake from kimchi, and suggests an alternative in the viewpoint that the sensitive reaction is one of food faddism which is a very popular topic currently in Korea.

• Korean Journal of Animal Reproduction
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• v.24 no.4
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• pp.339-341
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• 2000

In mammals, fatty acid utilization is initiated by activation of fatty acid, catalyzed by acyl-CoA synthetase(ACS, EC6.2.1.3). This enzyme reaction is essential in fatty acid metabolism, since mammalian fatty acid synthetase contains a specific thioesterase to produce fatty acid as th $\varepsilon$ final reaction product. Acyl-CoA, the product of ACS, is utilized in various metabolic pathways including membrane biogenesis, energy production and fat deposition. (omitted)

• Toxicological Research
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• v.11 no.2
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• pp.273-277
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• 1995

Several metabolic modulators on the generation of carbon monoxide (CO)from dichloromethane (DCM) was examined in adult female rats. It has been known that DCM is converted to CO by cytochrome P-450 or to carbon dioxide $(CO_2)$ by glutathione-dependent metabolic reaction. In rats treated with DCM (3 mmol/kg, ip) only, the carboxyhemoglobin (COHb) level reached a peak of approximately 10% 2 or 3 hr following the treatment. Disulfiram (300 mg/kg, ip) or allylsulfide (200 mg/kg, po), both known as a selective inhibitior for cytochrome P-450 2E1, blocked the increase in COHb concentratlons almost completely suggesting that the metabolic conversion of DCM to CO is mediated by the activity of this specific type of isozyme. YH439 (125 or 250 mg/kg, po), a potential hepatoprotective agent, decreased the COHb elevation as well indicating that this chemical is a potent inhibitor for 2E1. In rats treated with pyrazine (200 mg/kg, ip) 18 hr prior to DCM the peak COHb concentration was decreased by approximately 3 or 4%. However, pretreatment of rats with pyrazine either 24 or 48 hr before DCM increased the peak COHb concentration significantly compared to the rats treated with DCM only. The results in the present study strongly suggest that the generation of CO from DCM depends on the 2E1 activity and that the pharmacological and/or toxicological action of YH439 or pyrazine in animals or human is associated with its effect on this isozyme.

• BMB Reports
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• v.41 no.8
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• pp.609-614
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• 2008

The concentrations and catalytic activities of enzymes control metabolic rates. Previous studies have focused on enzyme concentrations because there are no genome-wide techniques used for the measurement of enzyme activity. We propose a method for evaluating the significance of enzyme activity by integrating metabolic network topologies and genome-wide microarray gene expression profiles. We quantified the enzymatic activity of reactions and report the 388 significant reactions in five perturbation datasets. For the 388 enzymatic reactions, we identified 70 that were significantly regulated (P-value < 0.001). Thirty-one of these reactions were part of anaerobic metabolism, 23 were part of low-pH aerobic metabolism, 8 were part of high-pH anaerobic metabolism, 3 were part of low-pH aerobic reactions, and 5 were part of high-pH anaerobic metabolism.