소아에서의 UCP-1 다형성과 비만도 및 혈액 지질수치와의 관련성에 관한 연구

오현희(Oh Hyunhee),신은정(Shin Eunjung),이명숙(Lee Myoungsook) 韓國營養學會 2008 Journal of Nutrition and Health Vol.41 No.8

1) 연구대상자 중 비만아동 빈도수 분석 결과, BIA법에서는 70.0%, BMI에 의한 비만도에서는 32.7%, 신장별체중에 의한 비만도에서는 23.6%로 BAI법에 의해 비만아동의 빈도수가 가장 많았다. 혈청 생화화적 분석 결과는 NCEP의 이상지혈증 기준 이하로 나타났다. 2) UCP-1 유전자 다형성에 의한 신체계측의 결과의 분포는 정상형과 변이형에서 차이를 나타내지 않았고 혈중 생화학 결과에서는 LDL (p = 0.039)과 TC (p = 0.063)이 정상형에 비해 변이형에서 유의적으로 증가하였다. 3) LDL을 130 ㎎/dL 기준으로 고LDL 콜레스테롤혈증과 정상으로 나누었을 때 각각에서 UCP-1 유전자 다형성의 분포는 고LDL 콜레스테롤혈증에서 A allele는 5.4%, G allele는 13.0%로 G allele의 빈도가 높게 분포하였고, 정상에서는 각각 94.6%, 87%의 분포를 나타내었다 (p = 0.062, ORs 2.640). LDL의 농도를 백분위수에 따라 4집단으로 나누고 UCP-1 유전자의 A allele와 G allele에서 LDL 농도의 빈도수를 나타내었을 때 G allele에서는 빈도수가 25th, 50th, 75th, 100th에 따라 유의적으로 증가하였다 (r² = 0.7995, p-trend = 0.032). 따라서 UCP-1 유전자 변이형은 정상형에 비해 고LDL-콜레스테롤혈증의 발병을 증가시키는 것으로 나타났다. UCP-1 유전자의 다형성은 이상지혈증의 위험인자인 LDL 농도를 증가시키는 위험요인으로써 나타났고, 체중을 감안할 때는 이상지혈증의 위험도가 더욱 증가할 것으로 생각되어진다. 따라서 UCP-1 유전자 변이형을 가지는 비만아동은 고LDL-콜레스테롤혈증의 발병과 관련된 식이 및 환경적 인자를 적절히 통제하는 예방 대책을 마련하여야겠다. Uncoupling protein-1 (UCP-1) plays a major role in thermogenesis at brown adipose tissues and has been implicated in the pathogenesis of obesity and metabolic disorders. The purpose of this study was to estimate the effects of A-3826G polymorphism in 117 Korean prepubertal children aged 8-11 years olds. Anthropometry by bioelectrical impedance analysis method, plasma lipid profiles by auto-biochemical analyzer and UCP-1 genotyping by PCR-RFLP were done. The frequencies of UCP-1 genotypes were AA; 17.7%, AG; 57.8%, GG; 26.6%. The frequencies of each G allele (55.5%) was similar to Japanese’s (49%) and higher than Caucacian’s (25%). No correlation UCP-1 polymorphism and BMI (㎏/㎡) or the degree of obesity described by the relative percentiles of the standard weight according to height in prepubertal children. However, plasma total- and LDL-cholesterol were significantly increased in G allele when sex, age and weight were adjusted. Our results suggested that G allele of UCP-1 gene was stronger risk factors in hyperLDLcholesterolemia than A allele. This impact might be progressed as the precaution against the revalence of obesity based-metabolic disease.

Egr-1 and serum response factor are involved in growth factors- and serum-mediated induction of E2-EPF UCP expression that regulates the VHL-HIF pathway

Lim, Jung Hwa,Jung, Cho-Rok,Lee, Chan-Hee,Im, Dong-Soo Wiley Subscription Services, Inc., A Wiley Company 2008 Journal of cellular biochemistry Vol.105 No.4

<P>E2-EPF ubiquitin carrier protein (UCP) has been shown to be highly expressed in common human cancers and target von Hippel-Lindau (VHL) for proteosomal degradation in cells, thereby stabilizing hypoxia-inducible factor (HIF)-1α. Here, we investigated cellular factors that regulate the expression of UCP gene. Promoter deletion assay identified binding sites for early growth response-1 (Egr-1) and serum response factor (SRF) in the UCP promoter. Hepatocyte or epidermal growth factor (EGF), or phorbol 12-myristate 13-acetate induced UCP expression following early induction of Egr-1 expression in HeLa cells. Serum increased mRNA and protein levels of SRF and UCP in the cell. By electrophoretic mobility shift and chromatin immunoprecipitation assays, sequence-specific DNA-binding of Egr-1 and SRF to the UCP promoter was detected in nuclear extracts from HeLa cells treated with EGF and serum, respectively. Overexpression of Egr-1 or SRF increased UCP expression. RNA interference-mediated depletion of endogenous Egr-1 or SRF impaired EGF- or serum-mediated induction of UCP expression, which was required for cancer cell proliferation. Systemic delivery of EGF into mice also increased UCP expression following early induction of Egr-1 expression in mouse liver. The induced UCP expression by the growth factors or serum increased HIF-1α protein level under non-hypoxic conditions, suggesting that the Egr-1/SRF-UCP-VHL pathway is in part responsible for the increased HIF-1α protein level in vitro and in vivo. Thus, growth factors and serum induce expression of Egr-1 and SRF, respectively, which in turn induces UCP expression that positively regulates cancer cell growth. J. Cell. Biochem. 105: 1117–1127, 2008. © 2008 Wiley-Liss, Inc.</P>

Curcumin Stimulates UCP1-independent Thermogenesis in 3T3-L1 White Adipocytes but Suppresses in C2C12 Muscle Cells

최민지,술라그나 무케르지,윤종원 한국생물공학회 2022 Biotechnology and Bioprocess Engineering Vol.27 No.6

Non-shivering thermogenesis may be an effective way to alter the energy balance in adipocytes and skeletal muscle. Curcumin stimulates adipocyte browning and improves the mitochondrial function in adipocytes via uncoupling protein 1 (UCP1)-dependent thermogenic activity. On the other hand, the UCP1-independent thermogenic effect of curcumin on adipose tissues and muscle remains unexplored. This study examined whether curcumin can also induce UCP1-independent thermogenesis in 3T3-L1 white adipocytes and C2C12 muscle cells. Curcumin stimulated the expression of α1-adrenergic receptor (α1-AR), UCP1-independent thermogenic markers, sarcoendoplasmic reticulum Ca2+-ATPase (SERCA) 2b, and ryanodine receptor 2 in adipocytes, whereas it suppressed SERCA/sarcolipinbased thermogenesis in muscle cells. Curcumin stimulated non-shivering thermogenesis by activating mitochondrial uncoupling and the SERCA/SLN axis in white adipocytes but not muscle cells. In addition, curcumin stimulated thermogenesis by activating the creatine metabolism-related thermogenic pathway in white adipocytes. Taken together, curcumin induces UCP1-independent creatine-mediated and α1-AR/SERCA-based thermogenesis through ATP-consuming futile processes. Together with previous results, the antiobesity effect of curcumin involves mainly two interacting parts, one mediated via β3-AR and cAMP (UCP1-dependent) and the other via α1-AR and increase in cytosolic Ca2+ levels (UCP1-independent) in beige fat but not in muscle cells.

eUCP에서의 전자제시의 심사기준과 관행

김종칠(Jong-Chill Kim) 중앙대학교 한국전자무역연구소 2010 전자무역연구 Vol.8 No.3

ICC는 전자결제서류의 사용에 대비하여 UCP 500의 보칙으로 eUCP version 1.0을2002년에 제정하였다. eUCP는 전자기록의 자체 또는 종이문서와 결합된 제시에 적용할 목적으로 제정되었으며, UCP 600이 2007년 개정되자 eUCP version 1.1 또한 개정되었다.따라서 본 연구는 eUCP 신용장이 사용되는 전자제시의 적용과 심사기준 및 국제표준은행 관행을 UCP 600과 eUCP를 비교하여 검토하였다.본 논문의 목적은 UCP 600과 eUCP version 1.1상의 서류심사 기준에 대한 규정을 비교검토하고 전자제시에서의 한계점을 제시하고자 한다. The eUCP Version 1.0 enforced by ICC is a supplement to the UCP 500, which governed the use of electronic presentation. The eUCP Version 1.0 was in force as of 1 April 2002. The intention of the eUCP as a supplement to the UCP is to accommodate the presentation of electronic records alone or in combination with paper documents. As changed UCP 600 in 2007, eUCP version 1.1 of supplement of UCP 600 was revised in 2007, too. This paper examines the criterion and banking practice of examination of electronic presentation and their problems associated with using eUCP credit. The purpose of this paper is contribute to enhance the understanding of the eUCP Version 1.1 by studying the main substance of eUCP version 1.1 and standard for examining documents under UCP 600 and eUCP Version 1.1.

Naringin promotes fat browning mediated by UCP1 activation via the AMPK signaling pathway in 3T3-L1 adipocytes

Ho Seon Lee,Chan Uk Heo,Young‑Ho Song,Kyeong Lee,Chang‑Ik Choi 대한약학회 2023 Archives of Pharmacal Research Vol.46 No.3

Induction of the brown adipocyte-like phenotype in white adipocytes (fat browning) is considered a promising therapeutic strategy to treat obesity. Naringin, a citrus flavonoid, has antioxidant, anti-inflammatory, and anticancer activities. We examined the application of naringin as an anti-obesity compound based on an investigation of its induction of fat browning in 3T3-L1 adipocytes. Naringin did not induce lipid accumulation in differentiated 3T3-L1 adipocytes. Additionally, naringin reduced the expression levels of proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα) involved in adipogenesis during lipid metabolism and increased the levels of PPARα and adiponectin involved in fatty acid oxidation. The expression levels of fat browning markers uncoupling protein 1 (UCP1; involved in thermogenesis) and PR domain containing 16 (PRDM16) increased. In addition, naringin treatment resulted in the activation of PPARγ coactivator 1-alpha (PGC-1α), a factor related to UCP1 transcription and mitochondrial biogenesis. Moreover, the expression of beige adipocyte-specific genes such as Cd137, Cited1, Tbx1, and Tmem26 was also induced. The small multi-lipid droplets characteristic of beige adipocytes indicated that naringin treatment increased the levels of all lipolysis markers (hormone-sensitive lipase [HSL], adipose triglyceride lipase [ATGL], perilipin [PLIN], and protein kinase A [PKA]). Adenosine monophosphate-activated protein kinase (AMPK) and UCP1 levels increased by treatment with naringin alone; this was possibly mediated by the stimulation of the AMPK signaling pathway. According to mechanistic studies, naringin activated the thermogenic protein UCP1 via the AMPK signaling pathway. In conclusion, naringin induces fat browning and is a promising therapeutic agent for metabolic disorders based on the regulation of lipid metabolism.

Analysis of UCP1 Expression in Rainbow Trout Gonadal Cell Line RTG-2 Indicates its Marginal Response to Adipogenic Inducers Compared to Mammalian Cell Lines

Nam Sang-Eun,Yun Young-Joo,Rhee Jae-Sung,Park Hyoung Sook (사)한국해양생명과학회 2023 한국해양생명과학회지 Vol.8 No.2

Uncoupling protein 1 (UCP1) is a unique mitochondrial membranous protein expressed in brown adipose tissue (BAT) in mammals. While its expression in response to cold temperatures and adipogenic inducers is well-characterized in mammals and human infants, the molecular characterization and expression of UCP1 in fish remain unexplored. To address this gap, we analyzed UCP1 expression in response to adipogenic inducers in a fish cell line, rainbow trout gonadal cells (RTG-2), and compared it with UCP1 expression in three mammalian preadipocytes, 3T3-L1, T37i, and WT1 exposed to the Peroxisome proliferator-activated receptor gamma (PPARγ) agonists, rosiglitazone (Rosi). In mammalian preadipocytes, UCP1 protein was highly expressed by Rosi, with an induction of adipogenesis observed in a time-dependent manner. This suggests that UCP1 plays a significant role in adipogenesis in mammals. However, RTG-2 cells showed no response to adipogenic inducers and exhibited only marginal expressions of UCP1. These results imply that RTG-2 cells may lack crucial responsive mechanisms to adipogenic signals or that the adipogenic response is regulated by other mechanisms. Further studies are needed to confirm these phenomena in fish preadipocytes when an appropriate cell line is established in future research.

한국인(韓國人) 비만여성(肥滿女性)과 UCP-1 유전자다형성(遺傳子多形性)의 상관성(相關性) 연구(硏究)

신승우 ( Seung Uoo Shin ),김성수 ( Sung Soo Kim ) 한방재활의학과학회 2007 한방재활의학과학회지 Vol.17 No.3

Objectives:This study was conducted to investigate the effects of UCP-1(Uncoupling protein-1) polymorphism on obesity phenotypes.For this, we analyzed association between SNPs(single nucleotide polymorphisms) of UCP-1-3954A>G,-1766A>G, +940A>G, +6537A>T, and their haplotypes and obesity phenotypes.Methods:A total of 426 Korean female subjects were recruited from an obesity clinic.All subjects were obesity on BMI(Body mass index) (□25 ㎏/㎡).For genotyping of SNPs, genomic DNA(Deoxyribonucleic acid) from each subject was extracted from whole blood and genotyped by TaqMan Method.Haplotypes and their frequencies were inferred using the algorithm, HapAnalyzer program.BMI, body fat mass, percent body fat, abdominal fat mass, waist circumference, lipid profile, and blood pressure were measured and associations between these and SNPs and haplotypes of UCP-1 were analyzed by age-adjusted general linear model.Results & Conclusions:There was significant, but not close association between-3954A>G, +940G>A, and haplotype 1-3 of UCP-1 with increased body fat of Korean female subjects.It was found that body fat mass and other obesity phenotype were significantly increased in G allele carriers of-1766A>G polymorphism, while decreased in T allele carriers of +6537A>T polymorphism and haplotype4[GAAT] carriers.

UCP 600을 위한 주요개정내용에 관한 연구 - 2005. 11월 1차개정완결초안을 중심으로

한재필(Jae-phil Hahn) 한국국제상학회 2006 國際商學 Vol.21 No.2

  This paper is aiming at analyzing critical issues for UCP 600 as shown in the First Complete Draft of the proposed Articles, November 2005, so as to make available by banks, traders, transporters and insurance companies to cope with a challenge and an opportunity launched on these new rules. In the course of identifying the issues, two papers by Roger Kreitman, "UCP 600: The end in sight?", October 2005 and by ICC-US Council for International Business, "UCP Drafting Group Makes Progress", from the July-September 2004 issue of DCInsight, have been mainly referred to.<BR>  In this paper, special issues and definitions of the first complete draft are analysed, such as 1) "On its face", 2) Time restriction for examination of documents, 3) discounting of deferred payment undertaking, 4) liabilities of a notifying bank, 5) acceptance or rejection of the amendment by the beneficiary, 6) data inconsistency between documents, 7) "Honour" and "Negotiation" and so on. The Complete Draft is a draft not a revision itself. Since the draft is, however, the product made as a result of 3 (three) year study by the Working Group, it is expected that UCP 600 would not be greatly deviated from this draft. It should be further studied on the article by article of UCP 600 in comparison with UCP 500 with a view to its implementation.

HDAC6 regulates thermogenesis through activating PKA to induce UCP1 expression

( Joo-yong Lee ) 한국장기요양학회 2018 한국장기요양학회 추계학술대회자료집 Vol.2018 No.-

HDAC6 is a unique cytosolic deacetylase that regulates multiple cellular processes against various stresses. At first, HDAC6 deacetylates tubulin, a cellular highway to transport numerous molecules and vesicles. Interestingly, HDAC6 binds ubiquitinated misfolded protein and transports to aggresome, “a cellular junkyard”, to minimize misfolded protein stress. At the same line, HDAC6 also binds damaged mitochondria and makes “mitoaggresome”. Moreover, HDAC6 regulates mitochondrial fusion to reduce mitochondrial reactive oxygen against metabolic stresses. Recently, we found that the body temperature of HDAC6 knockout mice is slightly decreased in normal hosing condition. Interestingly, UCP1 was downregulated in BAT of HDAC6 knockout mice, which extensively linked mitochondrial thermogenesis. Mechanistically, we showed that cAMP-PKA signaling plays a key role in HDAC6-dependent UCP1 expression. Notably, the size of brown adipocytes and lipid droplets in HDAC6 knockout BAT is increased. Taken together, our findings suggested that HDAC6 contributes to mitochondrial thermogenesis in BAT by increasing UCP1 expression through cAMP-PKA signaling pathway. [NRF-2015R1D1A1A01058257, -2016M3A9E1918329, -2014R1A6A9064166]

Conjugated Linoleic Acids Influence Ucp2 and Ucp3 Expression in an Isofomr and Stage-Specific Manner during 3T3-L1 Preadipocyte Differentiation

Kwon, So Young;Kang, Keum Jee 덕성여자대학교 자연과학연구소 2011 자연과학 논문집 Vol.17 No.-

To examine the effects of conjugated linoleic acid (CLA) isomers on cellular activities and the expressions of Ucp2 and Ucp3 genes during the time course of preadipocyte differentiation. Cis~9, trans-11 (c9t11) or trans-10 and cis12 (t10c12) CLA isomers (50 uM) were added to the medium of differentiating 3T3-L1 preadipocytes for six or nine days. Cytochemical and RT-PCR analyses were used to evaluate cellular activities including cell proliferation, differentiation, and pycnotic chromatin formation, and Ucp2 and Ucp3 gene expression, respectively. CLA isomers significantly inhibited both cell proliferation and differentiation at day 6, but not at day 9. Cell death significantly increased in (t10c12) CLA-treated cells at day 6 and 9. Ucp2 expression increased markedly at day 6 after treatment with both CLA isomers and to a lesser extent at day 9. However, Ucp3 expression increased clearly only in the CLA isomer groups. These Ucps expression changes occurred concurrently with increased cell proliferation, decreased lipid accumulation, and increased pycnotic chromatin at different stages of 3T3-L1 preadipocyte differentiation. In conclusion, specific increases or decreases in levels of Ucp isoforms in the presence of CLA isomers suggest that these supplements influence the different isoforms of Ucp during the course of preadipocyte differentiation in vitro. These changes occurred in the same cells undergoing different cellular activities (proliferation, differentiation, and death) during 3T3-L1 preadipocyte differentiation.