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Hypothalamic AMPK as a Regulator of Energy Homeostasis
Huynh, My Khanh Q.,Kinyua, Ann W.,Yang, Dong Joo,Kim, Ki Woo Hindawi Publishing Corporation 2016 Neural plasticity Vol.2016 No.-
<P>Activated in energy depletion conditions, AMP-activated protein kinase (AMPK) acts as a cellular energy sensor and regulator in both central nervous system and peripheral organs. Hypothalamic AMPK restores energy balance by promoting feeding behavior to increase energy intake, increasing glucose production, and reducing thermogenesis to decrease energy output. Besides energy state, many hormones have been shown to act in concert with AMPK to mediate their anorexigenic and orexigenic central effects as well as thermogenic influences. Here we explore the factors that affect hypothalamic AMPK activity and give the underlying mechanisms for the role of central AMPK in energy homeostasis together with the physiological effects of hypothalamic AMPK on energy balance restoration.</P>
Hwang, Joo-Yeon,Lee, Seung-Hun,Go, Min-Jin,Kim, Beom-Jun,Kim, Young-Jin,Kim, Dong-Joon,Oh, Ji-Hee,Koo, Hee-Jo,Cha, My-Jung,Lee, Min-Hye,Yun, Ji-Young,Yoo, Hye-Sook,Kang, Young-Ah,Oh, Ki-Won,Kang, Moo- Korea Genome Organization 2011 Genomics & informatics Vol.9 No.2
Osteoporotic fracture (OF), along with bone mineral density (BMD), is an important diagnostic parameter and a clinical predictive risk factor in the assessment of osteoporosis in the elderly population. However, a genome-wide association study (GWAS) on OF has not yet been clarified sufficiently. To identify OF-associated genetic variants and candidate genes, we conducted a GWAS in a population-based cohort (Korean Association Resource [KARE], n=1,427 [case: 288 and control: 1139]) and performed a de novo replication study in hospital-based individuals (Asan and Catholic Medical Center [ACMC], n=1,082 [case: 272 and control: 810]). In a combined meta-analysis, a newly identified genetic locus in an intergenic region at 10p11.2 (near genes FZD8 and ANKRD30A ) showed the most significant association (odd ratio [OR] = 2.00, 95% confidence interval [CI] = 1.47~2.74, p=$1.27{\times}10^{-6}$) in the same direction. We provide the first evidence for a common genetic variant influencing OF and genetic information for further investigation in bone metabolism.
( Hue Thi My Van ),( Hyun Jung Woo ),( Hyung Min Jeong ),( Daulat Bikram Khadka ),( Su Hui Yang ),( Caho Zhao ),( Yi Feng Jin ),( Eung Seok Lee ),( Kwang Youl Lee ),( Young Joo Kwon ),( Won Jea Cho ) 전남대학교 약품개발연구소 2014 약품개발연구지 Vol.23 No.-
A series of 3-heteroarylisoquinolinamines were designed. synthesized and evaluated for cytotoxicity, topoisomerases (topos) inhibitory activities and cell cycle inhibition, Several of the 3heteroarylisoquinolines exhibited selective cytotoxicity against human ductal breast epithelial tumor (T47D) cells over non-cancerous human breast epithelial (MCF-10A) and human prostate cancer (DU14S) cells. Most of the derivatives showed greater cytotoxicity in human colorectal adenocarcinoma (HCT-1S) cells than camptothecin (CPT), etoposide and doxorubicin (DOX). Generally, 3-heteroarylisoquinolinamines displayed greater affinity for topo I than topo n. 3-Heteroarylisoquinolinamines with greater topo 1 inhibitory effect exhibited potent cytotoxicity. Piperazine-substituted derivative. Sb, with potent topo 1 and moderate topo n activities intercalated between DNA bases and interacted with topos through H-bonds at the DNA cleavage site of a docking model. Moreover. flowcytometry indicated that cytotoxic 3heteroarylisoquinolinamines led to accumulation of human cervical (HeLa) cancer cells in the different phases of the cell cycle before apoptosis. Taken together. 3-heteroarylisoquinolinamines possessed potent cytotoxicity with topos and cell cycle inhibitory activities. ⓒ 2014 Elsevier Masson SAS. All rights reserved.
Association of Uncoupling Protein-1 Haplotypes with Body Fat Area
Kim, Young-Joo,Cheong, My-Young,Cha, Min-Ho,Choi, Sun-Mi,Kim, Jong-Yeol,Kim, Kil-Soo,Shin, Seung-Uoo,Park, Young-Kyu,Kim, Hyun-Ju,Suh, Soong-Hyuck,Yoon, Yoo-Sik Korean Society for Bioinformatics and Systems Biol 2009 Interdisciplinary Bio Central (IBC) Vol.1 No.4
Obesity is a major cause of morbidity and mortality and is associated with risks for type 2 diabetes mellitus, heart disease, metabolic syndrome, hypertension, stroke, and certain forms of cancer. The glutamate decarboxylase 2 (GAD2), insulin-induced gene 2 (INSIG2), ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), melanocortin 4 receptor (MC4R), fresh touring origination (FTO), and uncoupling protein-1 (UCP-1) genes have been investigated for their association with obesity. Since the A-3826G SNP in the UCP-1 gene was first shown to be the key genetic determinant of obesity and body fat accumulation, many studies have been performed in various populations to measure the association of the G allele of this SNP with obesity phenotypes. The association of the A-3826G SNP with obesity has been controversial, however, suggesting that one SNP does not sufficiently explain the effects of genomic variation on body fat accumulation. In this study, 9 SNPs were newly identified in the 5'-flanking region of the UCP-1 gene by direct sequencing of genomic DNA from 21 Korean subjects, and 6 haplotypes were obtained by SNP genotyping and haplotype reconstruction. According to our haplotype analysis, ht2 of the G allele of A-3826G, was significantly associated with overall fat measures after age and body weight were adjusted. Ht6 of the A allele of A-3826G, was significantly linked to reduced fat accumulation. These results provide an explanation for the controversies that have been reported in many obesity association studies and suggest that haplotype associations between polymorphic loci and neighbor loci that harbor functional sequence variants can be exploited to identify disease-predisposing alleles.