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        Ambient temperature regulates uncoupling protein 1 expression but fails to induce adipocyte browning in zebrafish

        Mao Yousheng,Hong KwangHeum,Bhandari Sushil,Li Li,Liao Weifang,Kim SeongJin,Xiong Yinyi,Nam In-Koo,Choe Seong-Kyu,Kwak SeongAe 경희대학교 융합한의과학연구소 2021 Oriental Pharmacy and Experimental Medicine Vol.21 No.2

        Adipocyte browning is a potential strategy to treat obesity. Although uncoupling protein 1 (UCP1) plays an important role in browning and thermogenesis in mammals, it is not known for zebrafish. We found that cold stress, as an efficient way of inducing browning in mammals, failed to induce adipocyte browning in zebrafish, evidenced by the cell morphology and expression of browning genes. Other potential approaches including heat stress and treatment with a chemical known to induce adipocyte browning in mammals also failed to induce browning, suggesting that zebrafish may not be a suitable model to study the browning process. Interestingly however, we found that the liver expresses ucp1 much higher than the adipose tissue in zebrafish. Moreover, the expression of ucp1 in the zebrafish liver is positively regulated by the ambient temperature. These findings suggest that the role of ucp1 in zebrafish may be different from its established role in adipocyte browning in mammals but instead be evolved to adapt to environmental temperature.

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        Coordinated Hospital-Home Fecal Microbiota Transplantation via Percutaneous Endoscopic Cecostomy for Recurrent Steroid-Dependent Ulcerative Colitis

        ( Xiaodong Ni ),( Shengxian Fan ),( Yongliang Zhang ),( Zhiming Wang ),( Lan Ding ),( Yousheng Li ),( Jieshou Li ) 대한소화기학회 2016 Gut and Liver Vol.10 No.6

        Since its introduction as an alternative intestinal microbiota alteration approach, fecal microbiota transplantation (FMT) has been increasingly used as a treatment of choice for patients with ulcerative colitis (UC), but no reports exist regarding FMT via percutaneous endoscopic cecostomy (PEC). This report describes the case of a 24-year-old man with a 7-year history of recurrent, steroid-dependent UC. He received FMT via PEC once per day for 1 month in the hospital. After the remission of gastrointestinal symptoms, he was discharged from the hospital and continued FMT via PEC twice per week for 3 months at home. The frequency of stools decreased, and the characteristics of stools improved soon thereafter. Enteral nutrition was regained after 1 week, and an oral diet was begun 1 month later. Two months after the FMT end point, the patient resumed a normal diet, with formed soft stools once per day. The follow-up colonoscopy showed normal mucus membranes; then, the PEC set was removed. On the subsequent 12 months follow-up, the patient resumed orthobiosis without any gastrointestinal discomfort and returned to work. This case emphasizes that FMT via PEC can not only induce remission but also shorten the duration of hospitalization and reduce the medical costs; therefore, this approach should be considered an alternative option for patients with UC. (Gut Liver 2016;10:975-980)

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        Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression

        Peng-fei Wang,Dan-hua Yao,Yue-yu Hu,Yousheng Li 한국응용약물학회 2019 Biomolecules & Therapeutics(구 응용약물학회지) Vol.27 No.2

        Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protective effect of Vitamin D on intestinal barrier function. However, severe cholestasis leads to vitamin D depletion. This study was designed to test whether vitamin D therapy improves intestinal dysfunction in cirrhosis. Rats were subcutaneously injected with 50% sterile CCl4 (a mixture of pure CCl4 and olive oil, 0.3 mL/100 g) twice a week for 6 weeks. Next, 1,25(OH)2D3 (0.5 μg/100 g) and the vehicle were administered simultaneously with CCl4 to compare the extent of intestinal histologic damage, tight junction protein expression, intestinal barrier function, BT, intestinal proliferation, apoptosis, and enterocyte turnover. Intestinal heme oxygenase-1 (HO-1) expression and oxidative stress were also assessed. We found that vitamin D could maintain intestinal epithelial proliferation and turnover, inhibit intestinal epithelial apoptosis, alleviate structural damage, and prevent BT and intestinal barrier dysfunction. These were achieved partly through restoration of HO-1 and inhibition of oxidative stress. Taken together, our results suggest that vitamin D ameliorated intestinal epithelial turnover and improved the integrity and function of intestinal barrier in CCl4-induced liver cirrhotic rats. HO-1 signaling activation was involved in these above beneficial effects.

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