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ChREBP deficiency leads to diarrhea-predominant irritable bowel syndrome
Oh, Ah-Reum,Sohn, Seonyong,Lee, Junghoon,Park, Jong-Min,Nam, Ki Taek,Hahm, Ki-Baik,Kim, Young-Bum,Lee, Ho-Jae,Cha, Ji-Young Elsevier 2018 clinical and experimental Vol.85 No.-
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>Fructose malabsorption is a common digestive disorder in which absorption of fructose in the small intestine is impaired. An abnormality of the main intestinal fructose transporter proteins has been proposed as a cause for fructose malabsorption. However the underlying molecular mechanism for this remains unclear. In this study, we investigated whether carbohydrate response element-binding protein (ChREBP) plays a role in intestinal fructose absorption through the regulation of genes involved in fructose transport and metabolism and ion transport.</P> <P><B>Methods</B></P> <P>Wild type (WT) and <I>Chrebp</I> knockout (KO) mice (6 or 8 weeks old) were fed a control diet (55% starch, 15% maltodextrin 10) or high-fructose diet (HFrD, 60% fructose, 10% starch) for 3–12 days. Body weight and food intake were measured, signs of fructose malabsorption were monitored, and the expression of genes involved in fructose transport/metabolism and ion transport was evaluated. Furthermore, transient transfection and chromatin immunoprecipitation were performed to show the direct interaction between ChREBP and carbohydrate response elements in the promoter of <I>Slc2A5</I>, which encodes the fructose transporter GLUT5.</P> <P><B>Results</B></P> <P> <I>Chrebp</I> KO mice fed the control diet maintained a constant body weight, whereas those fed a HFrD showed significant weight loss within 3–5 days. In addition, <I>Chrebp</I> KO mice fed the HFrD exhibited a markedly distended cecum and proximal colon containing both fluid and gas, suggesting incomplete fructose absorption. Fructose-induced increases of genes involved in fructose transport (GLUT5), fructose metabolism (<I>fructokinase</I>, <I>aldolase B</I>, <I>triokinase</I>, and <I>lactate dehydrogenase</I>), and gluconeogenesis (<I>glucose</I>-<I>6</I>-<I>phosphatase</I> and <I>fructose</I>-<I>1</I>,<I>6</I>-<I>bisphosphatase</I>) were observed in the intestine of WT but not of <I>Chrebp</I> KO mice. Moreover the Na<SUP>+</SUP>/H<SUP>+</SUP> exchanger NHE3, which is involved in Na<SUP>+</SUP> and water absorption in the intestine, was significantly decreased in HFrD-fed <I>Chrebp</I> KO mice. Consistent with this finding, the high-fructose diet-fed <I>Chrebp</I> KO mice developed severe diarrhea. Results of chromatin immunoprecipitation assays showed a direct interaction of ChREBP with the <I>Glut5</I> promoter, but not the <I>Nhe3</I> promoter, in the small intestine. Ectopic co-expression of ChREBP and its heterodimer partner Max-like protein X activated the <I>Glut5</I> promoter in Caco-2BBE cells.</P> <P><B>Conclusions</B></P> <P>ChREBP plays a key role in the dietary fructose transport as well as conversion into lactate and glucose through direct transcriptional control of genes involved in fructose transport, fructolysis, and gluconeogenesis. Moreover, ablation of <I>Chrebp</I> results in a severe diarrhea in mice fed a high-fructose diet, which is associated with the insufficient induction of GLUT5 in the intestine.</P> <P><B>Highlights</B></P> <P> <UL> <LI> <I>Chrebp</I> knockout mice show intestinal fructose malabsorption upon high-fructose feeding. </LI> <LI> ChREBP deficiency leads to a severe diarrhea and weight loss upon high-fructose feeding. </LI> <LI> GLUT5 and intestinal fructolytic genes are not induced by fructose in <I>Chrebp</I> knockout mice. </LI> <LI> ChREBP directly regulates <I>Glut5</I> gene expression through binding to functional ChoREs. </LI> </UL> </P>
Oh, Ah-Reum,Lee, Seung-Ku,Kim, Min-Ho,Cheong, Jae-Youn,Cho, Sung-Won,Yang, Kap-Seok,Kwack, Kyu-Bum Korea Genome Organization 2008 Genomics & informatics Vol.6 No.4
RAS guanyl-releasing protein 3 (RasGRP3), a member of the Ras subfamily of GTPases, functions as a guanosine triphosphate (GTP)/guanosine diphosphate (GDP)-regulated switch that cycles between inactive GDP- and active GTP-bound states during signal transduction. Various growth factors enhance hepatocellular carcinoma (HCC) proliferation via activation of the Ras/Raf-1/extracellular signal-regulated kinase (ERK) pathway, which depends on RasGRP3 activation. We investigated the relationship between polymorphisms in RasGRP3 and progression of hepatitis B virus (HBV)-infected HCC in a Korean population. Nineteen RasGRP3 SNPs were genotyped in 206 patients with chronic liver disease (CLD) and 86 patients with HCC. Our results revealed that the T allele of the rs7597095 SNP and the C allele of the rs7592762 SNP increased susceptibility to HCC (OR=1.55, p=0.04 and OR=1.81${\sim}$2.61, p=0.01${\sim}$0.03, respectively). Moreover, patients who possessed the haplotype (ht) 1 (A-T-C-G) or diplotype (dt) 1 (ht1/ht1) variations had increased susceptibility to HCC (OR=1.79${\sim}$2.78, p=0.01${\sim}$0.03). In addition, we identified an association between haplotype1 (ht1) and the age of HCC onset; the age of HCC onset are earlier in ht1 +/+ than ht1 +/- or ht1 -/- (HR=0.42${\sim}$0.66, p=0.006${\sim}$0.015). Thus, our data suggest that RasGRP3 SNPs are significantly associated with an increased risk of developing HCC.
Reports : Ursodeoxycholic acid decreases age-related adiposity and inflammation in mice
( Ah-reum Oh ),( Jin-sik Bae ),( Junghoon Lee ),( Eunji Shin ),( Byung-chul Oh ),( Sang-chul Park ),( Ji-young Cha ) 생화학분자생물학회(구 한국생화학분자생물학회) 2016 BMB Reports Vol.49 No.2
Ursodeoxycholic acid (UDCA), a natural, hydrophilic nontoxic bile acid, is clinically effective for treating cholestatic and chronic liver diseases. We investigated the chronic effects of UDCA on age-related lipid homeostasis and underlying molecular mechanisms. Twenty-week-old C57BL/6 male and female mice were fed a diet with or without 0.3% UDCA supplementation for 25 weeks. UDCA significantly reduced weight gain, adiposity, hepatic triglyceride, and hepatic cholesterol without incidental hepatic injury. UDCA-mediated hepatic triglyceride reduction was associated with downregulated hepatic expression of peroxisome proliferator-activated receptor-y, and of other genes involved in lipogenesis (Chrebp, Acaca, Fasn, Scd1, and Me1) and fatty acid uptake (Ldlr, Cd36). The inflammatory cytokines Tnfa, Ccl2, and Il6 were significantly decreased in liver and/or white adipose tissues of UDCA-fed mice. These data suggest that UDCA exerts beneficial effects on age-related metabolic disorders by lowering the hepatic lipid accumulation, while concurrently reducing hepatocyte and adipocyte susceptibility to inflammatory stimuli. [BMB Reports 2016; 49(2): 105-110]
오아름(Ah-Reum Oh) 한국유아교육·보육복지학회 2023 유아교육·보육복지연구 Vol.27 No.1
본 연구는 한국 유아를 대상으로 놀이성을 알아보기 위하여 사용되고 있는 Barnett(1990, 1991)이 제작한 놀이성 검사 도구(CPS)를 타당화하는 것을 목적으로 하였다. 자료수집을 위해 214명의 한국 유아를 대상으로 각 담임교사가 놀이성 검사 도구(CPS)로 유아의 놀이성 측정을 실시하였다. 수집된 자료는SPSS 25.0 프로그램과 AMOS 26.0 프로그램으로 통계처리를 실시하였다. 그 결과 한국어로 번안된Barnett(1990, 1991)의 놀이성 검사 도구(CPS)는 교사가 유아들을 대상으로 요인별로 놀이성을 살펴보기보다는 놀이성 전체를 한 가지 요인으로 보고 측정할 때 사용할 수 있는 것으로 볼 수 있다. 각 요인이갖는 놀이성 특성을 고려하여 측정하기 위해서는 내용타당도에 관한 연구를 거쳐 문항 내용을 수정‧보완한 후 수렴 및 판별타당도를 확인하여 사용해야 할 것이다. The purpose of this study was to validate the Children's Playfulness Scale (CPS) produced by Barnett (1990 and 1991), which is used to find out playfulness for Korean children. To this end, each class teacher measured the playfulness of children with a Children's Playfulness Scale (CPS) for 214 Korean children. The collected data were statistically processed with the SPSS 25.0 program and the AMOS 26.0 program. As a result of the analysis, Barnett's (1990 and 1991) Children's Playfulness Scale (CPS), which was translated into Korean, can be used by teachers to see and measure playfulness as one factor rather than looking at playfulness for children by factor. In order to measure the playfulness characteristics of each factor, it is necessary to modify and supplement the contents of the questions through research on content validity, and then check the convergence and discriminant validity.
작은 무릎 굽힘 동안 시각적 바이오피드백을 이용한 엉덩이 조임이 엉덩관절 폄 근육의 근 활성도에 미치는 영향
오아름(Ah-Reum Oh),오재섭(Jae-Seop Oh),유원규(Won-Gyu Yoo),안덕현(Duk-Hyun An),조원녕(Won-Nyeong Cho) 한국임상움직임치료학회 2021 한국임상움직임치료학회지 Vol.1 No.1
Background : In recent studies on back pain control, various exercises for strengthening the gluteus maximus have been suggested, however most of them imply load bearing exercise or giving resistance. Small knee bending is a movement evaluation that is frequently used in clinical practice and provides basic data for therapeutic intervention. It is also introduced as a safe way to exercise without applying a large load. Objectives : This study was conducted to investigate how the hip squeeze exercise using a tension sensor affects the muscle activity of the hip joint extension muscle during small knee bending. Methods : In this study, 30 subjects without back pain conducted to two conditions, with and without real-time visual biofeedback for small knee flexion. The hip squeeze force was measured using a tension sensor, and this was confirmed by real-time visual biofeedback. The muscle activities of hip extensors acting on the extension of the hip joint were measured by superficial EMG. To compare the difference in muscle activity under the two conditions, it was analyzed using a paired t-test. Results : As a result, the hip extensor muscle (gluteus maximus, both erector spinae) activity (maximum voluntary isometric contraction, %MVIC) significantly increased (p < 0.05) when real-time visual biofeedback using a tension sensor was applied compared to when it was not applied. Conclusions : Our study confirms that even a low-intensity exercise, such as a small knee flexion, can increase selective muscle activity if appropriate visual biofeedback is applied. In addition, the proposed hip squeezing method using a tension sensor induces selective muscle activity in a low-intensity exercise, which renders this method appropriate for subjects who do not exercise with great force, such as the elderly or women.