Hypoxia-induced inflammatory cytokine secretion in human adipose tissue stromovascular cells

Aims Hypoxia has been implicated as a cause of adipose tissue inflammation in obesity, although the inflammatory response of human adipose tissue to hypoxia is not well understood. The goal of this study was to define in vitro inflammatory responses of human adipose tissue to hypoxia and identify mo...

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Bibliographic Details
Published in:	Diabetologia Vol. 54; no. 6; pp. 1480 - 1490
Main Authors:	O’Rourke, R. W., White, A. E., Metcalf, M. D., Olivas, A. S., Mitra, P., Larison, W. G., Cheang, E. C., Varlamov, O., Corless, C. L., Roberts, C. T., Marks, D. L.
Format:	Journal Article
Language:	English
Published:	Berlin/Heidelberg Springer-Verlag 01.06.2011 Springer Springer Nature B.V
Subjects:	Adipocytes Adult Biological and medical sciences Body fat Cells, Cultured Cytokines Cytokines - metabolism Diabetes Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endoplasmic reticulum Enzymes Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gastrointestinal surgery Human Physiology Humans Hypoxia Hypoxia - physiopathology Inflammation Internal Medicine Intra-Abdominal Fat - metabolism Intra-Abdominal Fat - pathology Killer Cells, Natural - pathology Kinases Lymphocytes Macrophages - pathology Male MAP Kinase Kinase 4 - metabolism Medical sciences Medicine Medicine & Public Health Metabolic Diseases Metabolic disorders Middle Aged Obesity Obesity - metabolism Obesity - pathology p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Science Subcutaneous Fat - metabolism Subcutaneous Fat - pathology T-Lymphocytes - pathology Thinness - metabolism Thinness - pathology Oregon United States > US Obesity Adipose tissue p38 JNK T cell Hypoxia Inflammation Macrophage Endocrinopathy Human Oxygen Secretion Diabetes mellitus Nutrition disorder Cytokine Environmental factor T-Lymphocyte Nutritional status
ISSN:	0012-186X, 1432-0428, 1432-0428
Online Access:	Get full text
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