• Molecules and Cells
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• 제38권12호
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• pp.1023-1028
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• 2015

Whole body energy balance is achieved through the coordinated regulation of energy intake and energy expenditure in various tissues including liver, muscle and adipose tissues. A positive energy imbalance by excessive energy intake or insufficient energy expenditure results in obesity and related metabolic diseases. Although there have been many obesity treatment trials aimed at the reduction of energy intake, these strategies have achieved only limited success because of their associated adverse effects. An ancient neurotransmitter, serotonin is among those traditional pharmacological targets for anti-obesity treatment because it exhibits strong anorectic effect in the brain. However, recent studies suggest the new functions of peripheral serotonin in energy homeostasis ranging from the endocrine regulation by gut-derived serotonin to the autocrine/paracrine regulation by adipocyte-derived serotonin. Here, we discuss the role of serotonin in the regulation of energy homeostasis and introduce peripheral serotonin as a possible target for anti-obesity treatment.

• Molecules and Cells
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• 제23권3호
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• pp.272-279
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• 2007

The maintenance of normal blood glucose levels at rest and during exercise is critical. The maintenance of blood glucose homeostasis depends on the coordination and integration of several physiological systems, including the sympathetic nervous system and the endocrine system. During prolonged exercise increased demand for glucose by contracting muscle causes to increase glucose uptake to working skeletal muscle. Increase in glucose uptake by working skeletal muscle during prolonged exercise is due to an increase in the translocation of insulin and contraction sensitive glucose transporter-4 (GLUT4) proteins to the plasma membrane. However, normal blood glucose level can be maintained by the augmentation of glucose production and release through the stimulation of liver glycogen breakdown, and the stimulation of the synthesis of glucose from other substances, and by the mobilization of other fuels that may serve as alternatives. Both feedback and feedforward mechanisms allow glycemia to be controlled during exercise. This review focuses on factors that control blood glucose homeostasis during prolonged exercise.

• 한국영양학회:학술대회논문집
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• 한국영양학회 1995년도 추계학술대회 초록
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• pp.41-41
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• 1995

• The Korean Journal of Physiology and Pharmacology
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• 제20권4호
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• pp.387-397
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• 2016

Neurofibrillary tangles (NFTs) of microtubule-associated protein tau are a pathological hallmark of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress has been known to be involved in the pathogenesis of AD. However, the exact role of ER stress in tau pathology has not yet been clearly elucidated. In present study, the possible relationship between tau pathology and ER stress was examined in terms of sorcin, which is a calcium binding protein and plays an important role in calcium homeostasis. Our previous yeast two hybrid study showed that sorcin is a novel tau interacting protein. Caspase-3-cleaved tau (T4C3) showed significantly increased tau-sorcin interaction compared to wild type tau (T4). Thapsigargin-induced ER stress and co-expression of constitutively active $GSK3{\beta}$ ($GSK3{\beta}-S9A$) also exhibited significantly increased tau-sorcin interactions. T4C3-expressing cells showed potentiated thapsigargin -induced apoptosis and disruption of intracellular calcium homeostasis compared to T4-expressing cells. Overexpression of sorcin significantly attenuated thapsigargin-induced apoptosis and disruption of calcium homeostasis. In contrary, siRNA-mediated knock-down of sorcin showed significantly increased thapsigargin-induced apoptosis and disruption of calcium homeostasis. These data strongly suggest that sequestration of sorcin by aberrant forms of tau compromises the function of sorcin, such as calcium homeostasis and cellular resistance by ER stress, which may consequently result in the contribution to the progression of AD.

• 대한화장품학회지
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• 제34권1호
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• pp.1-8
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• 2008

피부장벽을 포함한 표피층은 인체의 조직 가운데에서도 가장 역동적인 기관이다. 다시 말해서 끊임없이 새로운 표피세포의 형성, 분화 및 탈각과정이 반복되면서 표피항상성(epidermal homeostasis)을 유지한다. 표피항상성은 피부기능 가운데 가장 주요한 기능인 permeability barrier homeostasis의 확립으로 연결된다. Permeability barrier homeostasis는 각질층에서 이루어지며 이를 형성하고 유지하기 위해 매우 정교하게 조절되어야 한다. 표피항상성을 조절하는 핵심 조절인자로서 nuclear hormone receptor(NHR)가 중심에 있음이 최근 다양한 연구를 통해 입증되었다. 이들은 각질세포 특이적인 단백질, 즉, involucrin, loricrin 및 trans-glutaminase 1(TG 1) 등의 발현을 유전자 수준에서 조절할 뿐 아니라 표피 지질성분의 생합성을 증가시키는 등 피부장벽을 구성하는 brick 및 mortar의 생성과 유지에 핵심적 역할을 하는 것으로 알려졌다. NHR 가운데 peroxisome proliferator activator receptor(PPAR)와 liver X receptor(LXR)의 activator/ligands가 리놀레인산 등 지방산, leukotriene, prostanoid 및 oxygenated sterol 등이 지질대사과정에서 형성된 지질 종류인 까닭에 liposensor로도 알려지고 있다. 따라서 liposensor들을 비롯한 PPAR과 LXR activator/ligands들은 피부장벽기능이 저해된 아토피성 피부를 포함하여 건조피부를 관리하는 epidermotherapy의 수단으로서 잠재적 가능성이 있다고 생각된다.

• Molecules and Cells
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• 제44권10호
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• pp.736-745
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• 2021

Although various marine ingredients have been exploited for the development of cosmetic products, no previous study has examined the potential of seaweed extracellular vesicles (EV) in such applications. Our results revealed that EV from Codium fragile and Sargassum fusiforme effectively decreased α-MSH-mediated melanin synthesis in MNT-1 human melanoma cells, associated with downregulation of MITF (microphthalmia-associated transcription factor), tyrosinase and TRP1 (tyrosinase-related proteins 1). The most effective inhibitory concentrations of EV were 250 ㎍/ml for S. fusiforme and 25 ㎍/ml for C. fragile, without affecting the viability of MNT-1 cells. Both EV reduced melanin synthesis in the epidermal basal layer of a three-dimensional model of human epidermis. Moreover, the application of the prototype cream containing C. fragile EV (final 5 ㎍/ml) yielded 1.31% improvement in skin brightness in a clinical trial. Together, these results suggest that EV from C. fragile and S. fusiforme reduce melanin synthesis and may be potential therapeutic and/or supplementary whitening agents.

• Environmental Analysis Health and Toxicology
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• 제19권4호
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• pp.389-399
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• 2004

Metallothionein (MT), a small protein molecule which can bind or release metal ions, is involved in the regulation of cellular metal homeostasis. This study was investigated the accumulation of cadmium in blood, tissue (liver, kidney and brain), and the effect of cadmium on several key genes (MT-I, MT-II, ZnT-1) in zinc metabolism in the mouse. Mouses weighing 20∼25 g were randomly assigned to control and cadmium treated group (Cd group). Cd group was intraperitoneally injected with cadmium 2, 4, 8 mg/kg and control group was administerd with saline. Mouses of each group were sacrificed by decapitation 4 hours after the administration of cadmium. Cadmium contents in blood, liver, kidney and brain were increased by a dose-dependent manner. Accumulation of cadmium was mainly occurred in liver and kidney. Induction of MT-I and MT-II protein was increased, but ZnT-1 expression was decreased in a dose-dependent manner by the treatment of 2∼8 mg/kg cadmium. These results suggested that cadmium can be transported to brain and alter the expression of several key genes in zinc homeostasis.

• BMB Reports
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• 제49권5호
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• pp.263-269
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• 2016

The intestine represents the largest and most elaborate immune system organ, in which dynamic and reciprocal interplay among numerous immune and epithelial cells, commensal microbiota, and external antigens contributes to establishing both homeostatic and pathologic conditions. The mechanisms that sustain gut homeostasis are pivotal in maintaining gut health in the harsh environment of the gut lumen. Intestinal epithelial cells are critical players in creating the mucosal platform for interplay between host immune cells and luminal stress inducers. Thus, knowledge of the epithelial interface between immune cells and the luminal environment is a prerequisite for a better understanding of gut homeostasis and pathophysiologies such as inflammation. In this review, we explore the importance of the epithelium in limiting or promoting gut inflammation (e.g., inflammatory bowel disease). We also introduce recent findings on how small RNAs such as microRNAs orchestrate pathophysiologic gene regulation.

• Molecules and Cells
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• 제37권8호
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• pp.628-635
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• 2014

2-(Trimethylammonium) ethyl (R)-3-methoxy-3-oxo-2-stearamidopropyl phosphate [(R)-TEMOSPho], a derivative of an organic chemical identified from a natural product library, promotes highly efficient megakaryopoiesis. Here, we show that (R)-TEMOSPho blocks osteoclast maturation from progenitor cells of hematopoietic origin, as well as blocking the resorptive function of mature osteoclasts. The inhibitory effect of (R)-TEMOSPho on osteoclasts was due to a disruption of the actin cytoskeleton, resulting from impaired downstream signaling of c-Fms, a receptor for macrophage-colony stimulating factor linked to c-Cbl, phosphoinositol-3-kinase (PI3K), Vav3, and Rac1. In addition, (R)-TEMOSPho blocked inflammation-induced bone destruction by reducing the numbers of osteoclasts produced in mice. Thus, (R)-TEMOSPho may represent a promising new class of antiresorptive drugs for the treatment of bone loss associated with increased osteoclast maturation and activity.

• Journal of Ginseng Research
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• 제45권6호
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• pp.744-753
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• 2021

Background: Gintonin-enriched fraction (GEF) is a new non-saponin component glycolipoprotein isolated from ginseng root. This study examined the effect of GEF on age-related sarcopenia in old C57BL/6J mice. Methods: Young (3-6 months) and old (20-24 months) C57BL/6J mice received oral GEF (50 mg/kg/day or 150 mg/kg/day) daily for 5 weeks. During the oral administration period, body weight and grip strength were measured weekly. After sacrifice, muscles from the hindlimb were excised and used for hematoxylin and eosin staining and western blotting to determine the effects of GEF on sarcopenia. The thymus was photographed to compare size, and flow cytometry was performed to examine the effect of GEF on immune homeostasis in the thymus and spleen. Blood samples were collected, and the concentrations of pro-inflammatory cytokines and IGF-1 were measured. Results: GEF caused a significant increase in muscle strength, mass, and fiber size in old mice. GEF restored age-related disruption of immune homeostasis by maintaining T cell compartments and regulating inflammatory biomarkers. Thus, GEF reduced common low-grade chronic inflammatory parameters, which are the main cause of muscle loss. Conclusion: GEF maintained immune homeostasis and inhibited markers of chronic inflammation, resulting in anti-sarcopenia effects in aged C57BL/6J mice. Thus, GEF is a potential therapeutic agent that slows sarcopenia in the elderly.