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Sexual dimorphism in intestinal absorption and lymphatic transport of dietary lipids.

The Journal of physiology

Liu M, Shen L, Yang Q, Nauli AM, Bingamon M, Wang DQ, Ulrich-Lai YM, Tso P.
PMID: 34648185
J Physiol. 2021 Nov;599(22):5015-5030. doi: 10.1113/JP281621. Epub 2021 Oct 31.

Although the basic process of intestinal lipid absorption and transport is understood, many critical aspects remain unclear. One question in particular is whether intestinal lipid absorption and transport differ between the sexes. Using a well-established lymph fistula model, we...

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Liu M, Shen L, Yang Q, et al. Sexual dimorphism in intestinal absorption and lymphatic transport of dietary lipids. J Physiol. 2021;599(22):5015-5030doi: 10.1113/JP281621.
Liu, M., Shen, L., Yang, Q., Nauli, A. M., Bingamon, M., Wang, D. Q., Ulrich-Lai, Y. M., & Tso, P. (2021). Sexual dimorphism in intestinal absorption and lymphatic transport of dietary lipids. The Journal of physiology, 599(22), 5015-5030. https://doi.org/10.1113/JP281621
Liu, Min, et al. "Sexual dimorphism in intestinal absorption and lymphatic transport of dietary lipids." The Journal of physiology vol. 599,22 (2021): 5015-5030. doi: https://doi.org/10.1113/JP281621
Liu M, Shen L, Yang Q, Nauli AM, Bingamon M, Wang DQ, Ulrich-Lai YM, Tso P. Sexual dimorphism in intestinal absorption and lymphatic transport of dietary lipids. J Physiol. 2021 Nov;599(22):5015-5030. doi: 10.1113/JP281621. Epub 2021 Oct 31. PMID: 34648185; PMCID: PMC8595769.
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Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk.

Journal of clinical medicine

Di Ciaula A, Baj J, Garruti G, Celano G, De Angelis M, Wang HH, Di Palo DM, Bonfrate L, Wang DQ, Portincasa P.
PMID: 32823983
J Clin Med. 2020 Aug 14;9(8). doi: 10.3390/jcm9082648.

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide and parallels comorbidities such as obesity, metabolic syndrome, dyslipidemia, and diabetes. Recent studies describe the presence of NAFLD in non-obese individuals, with mechanisms partially independent from excessive caloric...

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Di Ciaula A, Baj J, Garruti G, et al. Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk. J Clin Med. 2020;9(8)doi: 10.3390/jcm9082648.
Di Ciaula, A., Baj, J., Garruti, G., Celano, G., De Angelis, M., Wang, H. H., Di Palo, D. M., Bonfrate, L., Wang, D. Q., & Portincasa, P. (2020). Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk. Journal of clinical medicine, 9(8), . https://doi.org/10.3390/jcm9082648
Di Ciaula, Agostino, et al. "Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk." Journal of clinical medicine vol. 9,8 (2020). doi: https://doi.org/10.3390/jcm9082648
Di Ciaula A, Baj J, Garruti G, Celano G, De Angelis M, Wang HH, Di Palo DM, Bonfrate L, Wang DQ, Portincasa P. Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk. J Clin Med. 2020 Aug 14;9(8). doi: 10.3390/jcm9082648. PMID: 32823983; PMCID: PMC7465294.
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Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis.

Digestive diseases and sciences

Wang DQ, Portincasa P, Liu M, Tso P.
PMID: 33742290
Dig Dis Sci. 2022 Jan;67(1):11-13. doi: 10.1007/s10620-021-06905-7. Epub 2021 Mar 20.

No abstract available.

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Wang DQ, Portincasa P, Liu M, et al. Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis. Dig Dis Sci. 2021;67(1):11-13doi: 10.1007/s10620-021-06905-7.
Wang, D. Q., Portincasa, P., Liu, M., & Tso, P. (2022). Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis. Digestive diseases and sciences, 67(1), 11-13. https://doi.org/10.1007/s10620-021-06905-7
Wang, David Q-H, et al. "Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis." Digestive diseases and sciences vol. 67,1 (2022): 11-13. doi: https://doi.org/10.1007/s10620-021-06905-7
Wang DQ, Portincasa P, Liu M, Tso P. Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis. Dig Dis Sci. 2022 Jan;67(1):11-13. doi: 10.1007/s10620-021-06905-7. Epub 2021 Mar 20. PMID: 33742290; PMCID: PMC8450299.
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Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4.

Journal of hepatology

Wei G, Cao J, Huang P, An P, Badlani D, Vaid KA, Zhao S, Wang DQ, Zhuo J, Yin L, Frassetto A, Markel A, Presnyak V, Gandham S, Hua S, Lukacs C, Finn PF, Giangrande PH, Martini PGV, Popov YV.
PMID: 33340584
J Hepatol. 2021 Jun;74(6):1416-1428. doi: 10.1016/j.jhep.2020.12.010. Epub 2020 Dec 17.

BACKGROUND & AIMS: Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a rare lethal autosomal recessive liver disorder caused by loss-of-function variations of the ABCB4 gene, encoding a phosphatidylcholine transporter (ABCB4/MDR3). Currently, no effective treatment exists for PFIC3 outside...

Cite
Wei G, Cao J, Huang P, et al. Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4. J Hepatol. 2020;74(6):1416-1428doi: 10.1016/j.jhep.2020.12.010.
Wei, G., Cao, J., Huang, P., An, P., Badlani, D., Vaid, K. A., Zhao, S., Wang, D. Q., Zhuo, J., Yin, L., Frassetto, A., Markel, A., Presnyak, V., Gandham, S., Hua, S., Lukacs, C., Finn, P. F., Giangrande, P. H., Martini, P. G. V., & Popov, Y. V. (2021). Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4. Journal of hepatology, 74(6), 1416-1428. https://doi.org/10.1016/j.jhep.2020.12.010
Wei, Guangyan, et al. "Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4." Journal of hepatology vol. 74,6 (2021): 1416-1428. doi: https://doi.org/10.1016/j.jhep.2020.12.010
Wei G, Cao J, Huang P, An P, Badlani D, Vaid KA, Zhao S, Wang DQ, Zhuo J, Yin L, Frassetto A, Markel A, Presnyak V, Gandham S, Hua S, Lukacs C, Finn PF, Giangrande PH, Martini PGV, Popov YV. Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4. J Hepatol. 2021 Jun;74(6):1416-1428. doi: 10.1016/j.jhep.2020.12.010. Epub 2020 Dec 17. PMID: 33340584; PMCID: PMC8188846.
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Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis.

Digestive diseases and sciences

Wang DQ, Portincasa P, Liu M, Tso P.
PMID: 33742290
Dig Dis Sci. 2022 Jan;67(1):11-13. doi: 10.1007/s10620-021-06905-7. Epub 2021 Mar 20.

No abstract available.

Cite
Wang DQ, Portincasa P, Liu M, et al. Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis. Dig Dis Sci. 2021;67(1):11-13doi: 10.1007/s10620-021-06905-7.
Wang, D. Q., Portincasa, P., Liu, M., & Tso, P. (2022). Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis. Digestive diseases and sciences, 67(1), 11-13. https://doi.org/10.1007/s10620-021-06905-7
Wang, David Q-H, et al. "Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis." Digestive diseases and sciences vol. 67,1 (2022): 11-13. doi: https://doi.org/10.1007/s10620-021-06905-7
Wang DQ, Portincasa P, Liu M, Tso P. Overcoming Ductal Block: Emergency ERCP and Sphincterotomy Plus Common Bile Duct Stenting Improves Therapeutic Outcomes in Severe Gallstone Pancreatitis. Dig Dis Sci. 2022 Jan;67(1):11-13. doi: 10.1007/s10620-021-06905-7. Epub 2021 Mar 20. PMID: 33742290; PMCID: PMC8450299.
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Novel insights in health-promoting properties of sweet cherries.

Journal of functional foods

Faienza MF, Corbo F, Carocci A, Catalano A, Clodoveo ML, Grano M, Wang DQ, D'Amato G, Muraglia M, Franchini C, Brunetti G, Portincasa P.
PMID: 34422115
J Funct Foods. 2020 Jun;69. doi: 10.1016/j.jff.2020.103945. Epub 2020 Apr 07.

Sweet cherry (Prunus avium L.) is one of the most popular and appreciated temperate fruit not only for its sensory and nutritional properties, but also for its content in bioactive compounds. Consumption of sweet cherries brings beneficial effects on...

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Faienza MF, Corbo F, Carocci A, et al. Novel insights in health-promoting properties of sweet cherries. J Funct Foods. 2020;69doi: 10.1016/j.jff.2020.103945.
Faienza, M. F., Corbo, F., Carocci, A., Catalano, A., Clodoveo, M. L., Grano, M., Wang, D. Q., D'Amato, G., Muraglia, M., Franchini, C., Brunetti, G., & Portincasa, P. (2020). Novel insights in health-promoting properties of sweet cherries. Journal of functional foods, 69. https://doi.org/10.1016/j.jff.2020.103945
Faienza, Maria Felicia, et al. "Novel insights in health-promoting properties of sweet cherries." Journal of functional foods vol. 69 (2020). doi: https://doi.org/10.1016/j.jff.2020.103945
Faienza MF, Corbo F, Carocci A, Catalano A, Clodoveo ML, Grano M, Wang DQ, D'Amato G, Muraglia M, Franchini C, Brunetti G, Portincasa P. Novel insights in health-promoting properties of sweet cherries. J Funct Foods. 2020 Jun;69. doi: 10.1016/j.jff.2020.103945. Epub 2020 Apr 07. PMID: 34422115; PMCID: PMC8376227.
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BDNF/TrkB signaling mediates the anorectic action of estradiol in the nucleus tractus solitarius.

Oncotarget

Shen L, Wang DQH, Xu M, Woods SC, Liu M.
PMID: 29137402
Oncotarget. 2017 Sep 19;8(48):84028-84038. doi: 10.18632/oncotarget.21062. eCollection 2017 Oct 13.

Although compelling evidence indicates that estradiol (E2) acts in the nucleus tractus solitarius (NTS) to reduce food intake, the underlying mechanisms are largely unknown. We now report that estrogen's anorectic action occurs through enhancing the strength of brain-derived neurotrophic...

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Shen L, Wang DQH, Xu M, et al. BDNF/TrkB signaling mediates the anorectic action of estradiol in the nucleus tractus solitarius. Oncotarget. 2017;8(48):84028-84038doi: 10.18632/oncotarget.21062.
Shen, L., Wang, D. Q. H., Xu, M., Woods, S. C., & Liu, M. (2017). BDNF/TrkB signaling mediates the anorectic action of estradiol in the nucleus tractus solitarius. Oncotarget, 8(48), 84028-84038. https://doi.org/10.18632/oncotarget.21062
Shen, Ling, et al. "BDNF/TrkB signaling mediates the anorectic action of estradiol in the nucleus tractus solitarius." Oncotarget vol. 8,48 (2017): 84028-84038. doi: https://doi.org/10.18632/oncotarget.21062
Shen L, Wang DQH, Xu M, Woods SC, Liu M. BDNF/TrkB signaling mediates the anorectic action of estradiol in the nucleus tractus solitarius. Oncotarget. 2017 Sep 19;8(48):84028-84038. doi: 10.18632/oncotarget.21062. eCollection 2017 Oct 13. PMID: 29137402; PMCID: PMC5663574.
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The deletion of the estrogen receptor α gene reduces susceptibility to estrogen-induced cholesterol cholelithiasis in female mice.

Biochimica et biophysica acta

de Bari O, Wang HH, Portincasa P, Liu M, Wang DQ.
PMID: 26232687
Biochim Biophys Acta. 2015 Oct;1852(10):2161-9. doi: 10.1016/j.bbadis.2015.07.020. Epub 2015 Jul 30.

Compelling evidence has demonstrated that estrogen is a critical risk factor for gallstone formation and enhances cholesterol cholelithogenesis through the hepatic estrogen receptor α (ERα), but not ERβ. To study the lithogenic mechanisms of estrogen through ERα, we investigated...

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de Bari O, Wang HH, Portincasa P, et al. The deletion of the estrogen receptor α gene reduces susceptibility to estrogen-induced cholesterol cholelithiasis in female mice. Biochim Biophys Acta. 2015;1852(10):2161-9doi: 10.1016/j.bbadis.2015.07.020.
de Bari, O., Wang, H. H., Portincasa, P., Liu, M., & Wang, D. Q. (2015). The deletion of the estrogen receptor α gene reduces susceptibility to estrogen-induced cholesterol cholelithiasis in female mice. Biochimica et biophysica acta, 1852(10), 2161-9. https://doi.org/10.1016/j.bbadis.2015.07.020
de Bari, Ornella, et al. "The deletion of the estrogen receptor α gene reduces susceptibility to estrogen-induced cholesterol cholelithiasis in female mice." Biochimica et biophysica acta vol. 1852,10 (2015): 2161-9. doi: https://doi.org/10.1016/j.bbadis.2015.07.020
de Bari O, Wang HH, Portincasa P, Liu M, Wang DQ. The deletion of the estrogen receptor α gene reduces susceptibility to estrogen-induced cholesterol cholelithiasis in female mice. Biochim Biophys Acta. 2015 Oct;1852(10):2161-9. doi: 10.1016/j.bbadis.2015.07.020. Epub 2015 Jul 30. PMID: 26232687; PMCID: PMC4701041.
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Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4.

Journal of hepatology

Wei G, Cao J, Huang P, An P, Badlani D, Vaid KA, Zhao S, Wang DQ, Zhuo J, Yin L, Frassetto A, Markel A, Presnyak V, Gandham S, Hua S, Lukacs C, Finn PF, Giangrande PH, Martini PGV, Popov YV.
PMID: 33340584
J Hepatol. 2021 Jun;74(6):1416-1428. doi: 10.1016/j.jhep.2020.12.010. Epub 2020 Dec 17.

BACKGROUND & AIMS: Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a rare lethal autosomal recessive liver disorder caused by loss-of-function variations of the ABCB4 gene, encoding a phosphatidylcholine transporter (ABCB4/MDR3). Currently, no effective treatment exists for PFIC3 outside...

Cite
Wei G, Cao J, Huang P, et al. Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4. J Hepatol. 2020;74(6):1416-1428doi: 10.1016/j.jhep.2020.12.010.
Wei, G., Cao, J., Huang, P., An, P., Badlani, D., Vaid, K. A., Zhao, S., Wang, D. Q., Zhuo, J., Yin, L., Frassetto, A., Markel, A., Presnyak, V., Gandham, S., Hua, S., Lukacs, C., Finn, P. F., Giangrande, P. H., Martini, P. G. V., & Popov, Y. V. (2021). Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4. Journal of hepatology, 74(6), 1416-1428. https://doi.org/10.1016/j.jhep.2020.12.010
Wei, Guangyan, et al. "Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4." Journal of hepatology vol. 74,6 (2021): 1416-1428. doi: https://doi.org/10.1016/j.jhep.2020.12.010
Wei G, Cao J, Huang P, An P, Badlani D, Vaid KA, Zhao S, Wang DQ, Zhuo J, Yin L, Frassetto A, Markel A, Presnyak V, Gandham S, Hua S, Lukacs C, Finn PF, Giangrande PH, Martini PGV, Popov YV. Synthetic human ABCB4 mRNA therapy rescues severe liver disease phenotype in a BALB/c.Abcb4. J Hepatol. 2021 Jun;74(6):1416-1428. doi: 10.1016/j.jhep.2020.12.010. Epub 2020 Dec 17. PMID: 33340584; PMCID: PMC8188846.
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Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease.

Molecular metabolism

Xu Y, Zhu Y, Hu S, Pan X, Bawa FC, Wang HH, Wang DQ, Yin L, Zhang Y.
PMID: 33930596
Mol Metab. 2021 Sep;51:101244. doi: 10.1016/j.molmet.2021.101244. Epub 2021 Apr 28.

OBJECTIVE: Hepatic miR-34a expression is elevated in diet-induced or genetically obese mice and patients with non-alcoholic steatohepatitis (NASH), yet hepatocyte miR-34a's role in the progression of non-alcoholic fatty liver disease (NAFLD) from non-alcoholic fatty liver (NAFL) to NASH remains...

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Xu Y, Zhu Y, Hu S, et al. Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease. Mol Metab. 2021;51:101244doi: 10.1016/j.molmet.2021.101244.
Xu, Y., Zhu, Y., Hu, S., Pan, X., Bawa, F. C., Wang, H. H., Wang, D. Q., Yin, L., & Zhang, Y. (2021). Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease. Molecular metabolism, 51101244. https://doi.org/10.1016/j.molmet.2021.101244
Xu, Yanyong, et al. "Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease." Molecular metabolism vol. 51 (2021): 101244. doi: https://doi.org/10.1016/j.molmet.2021.101244
Xu Y, Zhu Y, Hu S, Pan X, Bawa FC, Wang HH, Wang DQ, Yin L, Zhang Y. Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease. Mol Metab. 2021 Sep;51:101244. doi: 10.1016/j.molmet.2021.101244. Epub 2021 Apr 28. PMID: 33930596; PMCID: PMC8141777.
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Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease.

Molecular metabolism

Xu Y, Zhu Y, Hu S, Pan X, Bawa FC, Wang HH, Wang DQ, Yin L, Zhang Y.
PMID: 33930596
Mol Metab. 2021 Sep;51:101244. doi: 10.1016/j.molmet.2021.101244. Epub 2021 Apr 28.

OBJECTIVE: Hepatic miR-34a expression is elevated in diet-induced or genetically obese mice and patients with non-alcoholic steatohepatitis (NASH), yet hepatocyte miR-34a's role in the progression of non-alcoholic fatty liver disease (NAFLD) from non-alcoholic fatty liver (NAFL) to NASH remains...

Cite
Xu Y, Zhu Y, Hu S, et al. Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease. Mol Metab. 2021;51:101244doi: 10.1016/j.molmet.2021.101244.
Xu, Y., Zhu, Y., Hu, S., Pan, X., Bawa, F. C., Wang, H. H., Wang, D. Q., Yin, L., & Zhang, Y. (2021). Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease. Molecular metabolism, 51101244. https://doi.org/10.1016/j.molmet.2021.101244
Xu, Yanyong, et al. "Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease." Molecular metabolism vol. 51 (2021): 101244. doi: https://doi.org/10.1016/j.molmet.2021.101244
Xu Y, Zhu Y, Hu S, Pan X, Bawa FC, Wang HH, Wang DQ, Yin L, Zhang Y. Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease. Mol Metab. 2021 Sep;51:101244. doi: 10.1016/j.molmet.2021.101244. Epub 2021 Apr 28. PMID: 33930596; PMCID: PMC8141777.
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New insights into the role of .

Liver research

Wang HH, Li T, Portincasa P, Ford DA, Neuschwander-Tetri BA, Tso P, Wang DQ.
PMID: 34367715
Liver Res. 2017 Jun;1(1):42-53. doi: 10.1016/j.livres.2017.05.005. Epub 2017 Jun 03.

Cholesterol gallstone formation represents a failure of biliary cholesterol homeostasis in which the physical-chemical balance of cholesterol solubility in bile is disturbed. Lithogenic bile is mainly caused by persistent hepatic hypersecretion of biliary cholesterol and sustained cholesterol-supersaturated bile is...

Cite
Wang HH, Li T, Portincasa P, et al. New insights into the role of . Liver Res. 2017;1(1):42-53doi: 10.1016/j.livres.2017.05.005.
Wang, H. H., Li, T., Portincasa, P., Ford, D. A., Neuschwander-Tetri, B. A., Tso, P., & Wang, D. Q. (2017). New insights into the role of . Liver research, 1(1), 42-53. https://doi.org/10.1016/j.livres.2017.05.005
Wang, Helen H, et al. "New insights into the role of ." Liver research vol. 1,1 (2017): 42-53. doi: https://doi.org/10.1016/j.livres.2017.05.005
Wang HH, Li T, Portincasa P, Ford DA, Neuschwander-Tetri BA, Tso P, Wang DQ. New insights into the role of . Liver Res. 2017 Jun;1(1):42-53. doi: 10.1016/j.livres.2017.05.005. Epub 2017 Jun 03. PMID: 34367715; PMCID: PMC8341472.
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Showing 1 to 12 of 18 entries