• Journal of Nutrition and Health
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• v.31 no.6
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• pp.1039-1048
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• 1998

It has been reported that boron may be beneficial for optimal calcium metabolism and, thus, optimal bone metabolism. Therefore, we designed a study to determine the effect of boron supplementation on Ca and bone metabolism in rats. The rats of 80-l40g body weight were given a control(0ug), 5$\mu\textrm{g}$, 10$\mu\textrm{g}$, 20$\mu\textrm{g}$, 40$\mu\textrm{g}$, or 80$\mu\textrm{g}$ boron supplement per Is diet for 4-weeks. The results are summarized as follows. There were no differences in total food intake and weight gain among the experimental groups. fecal Ca excretion, urinary Ca excretion, apparent Ca absorption, Ca retention, serum alkaline phosphatase activity, and urinary hydroxyproline were not affected by boron supplementation. There was no difference in serum creatinine. Whereas, urinary creatinine excretion was increased with increasing boron supplementation, and conse-quently creatinine clearance was increased with boron supplementation. No differences were found in length, weight, density, Ca content of femur and scapular. The findings suggest that boron supplementation was not effective in Ca and bone metabolism in growing rats fed normal Ca diet. (Korean J Nutrition 31(6) : 1039-1048, 1998)

• Journal of Plant Biotechnology
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• v.2 no.1
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• pp.13-19
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• 2000

Carbohydrates serve three different principal functions in the metabolism of plants. They are the primary products of energy fixation, they are important transport metabolites, and they are deposited as structural or storage compounds. Modification of carbohydrate metabolism therefore covers approaches to modify yield, to change sink/source relationships and thereby alter the ratio of harvestable material, and to improve the quality of crop plants. The scope of this article is to summarize research done at the Max-Planck-Institute related to the first two fields and to present in some detail what we learned, when we established a new carbohydrate storage form in potato.

• BMB Reports
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• v.43 no.9
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• pp.579-583
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• 2010

The adipocyte-derived hormone leptin regulates appetite and bone mass. Recent research demonstrates that reciprocally, osteoblasts have a role in controlling energy metabolism. Several genes expressed in osteoblasts are involved in this process, and one of them is the Esp gene. The remaining genes regulate Esp gene expression. OST-PTP, the protein name of Esp, regulates the carboxylation of osteocalcin secreted from osteoblasts, thus affecting insulin sensitivity and insulin secretion. This review provides evidence for a novel interpretation of the connection between bone and energy metabolism and expands our understanding of the novel physiology of bone beyond its classical functions.

• 한국약용작물학회:학술대회논문집
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• 2009.05a
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• pp.261-262
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• 2009

• Journal of Applied Biological Chemistry
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• v.50 no.4
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• pp.304-307
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• 2007

• Journal of Sasang Constitutional Medicine
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• v.15 no.1
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• pp.129-132
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• 2003

This case was designed to evaluate the improving effect of hepatitis on drug metabolism. Gleditsiae Spina(?甬刺) was included Taeumin' herb. but it maybe induced hepatitis on drug metabolism, if Taeumin take this herb long time. We use Taeyeumin Chungsimyeunjatang to the hepatitis on drug metabolism, and we improved it. so we report it.

• Journal of Crop Science and Biotechnology
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• v.10 no.2
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• pp.64-72
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• 2007

Iron is an important micronutrient for plants. Iron metabolism is a complex mechanism under a delicate balance. Iron metabolism represents two major problems for plants: deficiency as a consequence of solubility problems and toxicity due to excess solubility in anaerobic conditions. In the last few years, new genes have been discovered that influence iron uptake, transport and storage. Irrigated rice is exposed to high levels of $Fe^{II}$, normally rare in aerobic soil conditions. The implications of altering iron uptake rates and the effects of newly discovered genes are discussed.

• Journal of Ginseng Research
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• v.44 no.1
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• pp.86-95
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• 2020

Background: Ginsenoside Rb1 (Rb1), one of the most abundant protopanaxadiol-type ginsenosides, exerts excellent neuroprotective effects even though it has low intracephalic exposure. Purpose: The present study aimed to elucidate the apparent contradiction between the pharmacokinetics and pharmacodynamics of Rb1 by studying the mechanisms underlying neuroprotective effects of Rb1 based on regulation of microflora. Methods: A pseudo germ-free (PGF) rat model was established, and neuroprotective effects of Rb1 were compared between conventional and PGF rats. The relative abundances of common probiotics were quantified to reveal the authentic probiotics that dominate in the neuroprotection of Rb1. The expressions of the gamma-aminobutyric acid (GABA) receptors, including GABAA receptors (α2, β2, and γ2) and GABAB receptors (1b and 2), in the normal, ischemia/reperfusion (I/R), and I/R+Rb1 rat hippocampus and striatum were assessed to reveal the neuroprotective mechanism of Rb1. Results: The results showed that microbiota plays a key role in neuroprotection of Rb1. The relative abundance of Lactobacillus helveticus (Lac.H) increased 15.26 fold after pretreatment with Rb1. I/R surgery induced effects on infarct size, neurological deficit score, and proinflammatory cytokines (IL-1β, IL-6, and TNF-α) were prevented by colonizing the rat gastrointestinal tract with Lac.H (1 × 10⁹ CFU) by gavage 15 d before I/R surgery. Both Rb1 and Lac.H upregulated expression of GABA receptors in I/R rats. Coadministration of a GABA_A receptor antagonist significantly attenuated neuroprotective effects of Rb1 and Lac.H. Conclusion: In sum, Rb1 exerts neuroprotective effects by regulating Lac.H and GABA receptors rather than through direct distribution to the target sites.

• Toxicological Research
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• v.32 no.3
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• pp.177-193
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• 2016

After more than half of century since the Warburg effect was described, this atypical metabolism has been standing true for almost every type of cancer, exhibiting higher glycolysis and lactate metabolism and defective mitochondrial ATP production. This phenomenon had attracted many scientists to the problem of elucidating the mechanism of, and reason for, this effect. Several models based on oncogenic studies have been proposed, such as the accumulation of mitochondrial gene mutations, the switch from oxidative phosphorylation respiration to glycolysis, the enhancement of lactate metabolism, and the alteration of glycolytic genes. Whether the Warburg phenomenon is the consequence of genetic dysregulation in cancer or the cause of cancer remains unknown. Moreover, the exact reasons and physiological values of this peculiar metabolism in cancer remain unclear. Although there are some pharmacological compounds, such as 2-deoxy-D-glucose, dichloroacetic acid, and 3-bromopyruvate, therapeutic strategies, including diet, have been developed based on targeting the Warburg effect. In this review, we will revisit the Warburg effect to determine how much scientists currently understand about this phenomenon and how we can treat the cancer based on targeting metabolism.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.2
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• pp.99-103
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• 2010

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat, a model of spontaneous type 2 diabetes (T2D), develops hyperglycemic obesity with hyperinsulinemia and insulin resistance after the age of 25 weeks, similar to patients with noninsulin-dependent diabetes mellitus (DM). In the present study, we determined whether there are differences in the pattern of gene expression related to glucose and lipid metabolism between OLETF rats and their control counterparts, Long-Evans Tokushima (LETO) rats. The experiment was done using 35-week-old OLETF and LETO rats. At week 35 male OLETF rats showed overt T2D and increases in blood glucose, plasma insulin, plasma triglycerides (TG) and plasma total cholesterol (TC). Livers of diabetic OLETF and LETO rats also showed differences in expression of mRNA for glucose and lipid metabolism related genes. Among glucose metabolism related genes, GAPDH mRNA was significantly higher and FBPase and G6Pase mRNA were significantly lower in OLETF rats. For lipid metabolism related genes, HMGCR, SCD1 and HL mRNA were substantially higher in OLETF rats. These results indicate that gluconeogenesis in OLETF rats is lower and glycolysis is higher, which means that glucose metabolism might be compensated for by a lowering of the blood glucose level. However, lipid synthesis is increased in OLETF rats so diabetes may be aggravated. These differences between OLETF and LETO rats suggest mechanisms that could be targeted during the development of therapeutic agents for diabetes.