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Your search keyword '"Mizuko Osaka"' showing total 2 results
Start Over Author "Mizuko Osaka" Journal cell reports
2 results on '"Mizuko Osaka"'

1. Roles for Cell-Cell Adhesion and Contact in Obesity-Induced Hepatic Myeloid Cell Accumulation and Glucose Intolerance

Author

Yasutaka Miyachi, Kyoichiro Tsuchiya, Chikara Komiya, Kumiko Shiba, Noriko Shimazu, Shinobu Yamaguchi, Michiyo Deushi, Mizuko Osaka, Kouji Inoue, Yuta Sato, Sayaka Matsumoto, Junichi Kikuta, Kenjiro Wake, Masayuki Yoshida, Masaru Ishii, and Yoshihiro Ogawa

Subjects
insulin resistance, inflammation, obesity, diabetes, macrophages, neutrophils, monocytes, Notch signaling, liver sinusoidal endothelial cells, Biology (General), QH301-705.5
Abstract

Obesity promotes infiltration of inflammatory cells into various tissues, leading to parenchymal and stromal cell interaction and development of cellular and organ dysfunction. Liver sinusoidal endothelial cells (LSECs) are the first cells that contact portal blood cells and substances in the liver, but their functions in the development of obesity-associated glucose metabolism remain unclear. Here, we find that LSECs are involved in obesity-associated accumulation of myeloid cells via VLA-4-dependent cell-cell adhesion. VLA-4 blockade in mice fed a high-fat diet attenuated myeloid cell accumulation in the liver to improve hepatic inflammation and systemic glucose intolerance. Ex vivo studies further show that cell-cell contact between intrahepatic leukocytes and parenchymal hepatocytes induces gluconeogenesis via a Notch-dependent pathway. These findings suggest that cell-cell interaction between parenchymal and stromal cells regulates hepatic glucose metabolism and offers potential strategies for treatment or prevention of obesity-associated glucose intolerance.

Published
2017
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2. Roles for Cell-Cell Adhesion and Contact in Obesity-Induced Hepatic Myeloid Cell Accumulation and Glucose Intolerance

Author

Masayuki Yoshida, Kenjiro Wake, Masaru Ishii, Junichi Kikuta, Sayaka Matsumoto, Mizuko Osaka, Kouji Inoue, Yoshihiro Ogawa, Kumiko Shiba, Kyoichiro Tsuchiya, Chikara Komiya, Yasutaka Miyachi, Michiyo Deushi, Noriko Shimazu, Shinobu Yamaguchi, and Yuta Sato

Subjects
0301 basic medicine, Male, obesity, Myeloid, Cell, Mice, Obese, Integrin alpha4beta1, neutrophils, Cell Movement, insulin resistance, Leukocytes, Myeloid Cells, lcsh:QH301-705.5, Notch signaling, Receptors, Notch, diabetes, Up-Regulation, macrophages, medicine.anatomical_structure, Liver, monocytes, Infiltration (medical), Signal Transduction, medicine.medical_specialty, Stromal cell, liver sinusoidal endothelial cells, Carbohydrate metabolism, Biology, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Internal medicine, Glucose Intolerance, medicine, Cell Adhesion, Animals, Cell adhesion, Antibodies, Blocking, Gluconeogenesis, Endothelial Cells, Metabolism, medicine.disease, Mice, Inbred C57BL, 030104 developmental biology, Endocrinology, Glucose, Gene Expression Regulation, lcsh:Biology (General), inflammation, Hepatocytes, Cell Adhesion Molecules
Abstract

Obesity promotes infiltration of inflammatory cells into various tissues, leading to parenchymal and stromal cell interaction and development of cellular and organ dysfunction. Liver sinusoidal endothelial cells (LSECs) are the first cells that contact portal blood cells and substances in the liver, but their functions in the development of obesity-associated glucose metabolism remain unclear. Here, we find that LSECs are involved in obesity-associated accumulation of myeloid cells via VLA-4-dependent cell-cell adhesion. VLA-4 blockade in mice fed a high-fat diet attenuated myeloid cell accumulation in the liver to improve hepatic inflammation and systemic glucose intolerance. Ex vivo studies further show that cell-cell contact between intrahepatic leukocytes and parenchymal hepatocytes induces gluconeogenesis via a Notch-dependent pathway. These findings suggest that cell-cell interaction between parenchymal and stromal cells regulates hepatic glucose metabolism and offers potential strategies for treatment or prevention of obesity-associated glucose intolerance.

Published
2017

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