Hepatocytes Are the Principal Source of Circulating RBP4 in Mice
| Autor: | Jason J. Yuen, Jinjin Cai, Seung-Ah Lee, Manuel Mark, Ashot Sargsyan, Norbert B. Ghyselinck, Rana Smalling, Spencer J Thompson, Timothy E. Graham, William S. Blaner |
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| Přispěvatelé: | University of Utah School of Medicine [Salt Lake City], George Wahlen Veterans Affairs Medical Center [Salt Lake City, UT, USA], Columbia University College of Physicians and Surgeons, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Les Hôpitaux Universitaires de Strasbourg (HUS), univOAK, Archive ouverte |
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male Endocrinology Diabetes and Metabolism Adipose tissue Type 2 diabetes Inbred C57BL chemistry.chemical_compound Mice 0302 clinical medicine Adipocyte Adipocytes Mice Knockout Blotting Reverse Transcriptase Polymerase Chain Reaction Blot Female Western medicine.medical_specialty Genotype Knockout Blotting Western 030209 endocrinology & metabolism Biology 03 medical and health sciences Paracrine signalling Insulin resistance Internal medicine Internal Medicine medicine [SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology Animals Secretion Plasma/genetics/*metabolism [SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology RNA Messenger Autocrine signalling medicine.disease Mice Inbred C57BL Retinol-Binding Proteins Hepatocytes/*metabolism Metabolism 030104 developmental biology Endocrinology chemistry Adipocytes/metabolism Hepatocytes RNA Messenger/genetics Insulin Resistance Retinol-Binding Proteins Plasma |
| Zdroj: | Diabetes Diabetes, 2017, 66 (1), pp.58-63. ⟨10.2337/db16-0286⟩ |
| ISSN: | 0012-1797 1939-327X |
| DOI: | 10.2337/db16-0286⟩ |
| Popis: | RBP4 is produced mainly by hepatocytes. In type 2 diabetes and obesity, circulating RBP4 is increased and may act systemically to cause insulin resistance and glucose intolerance. Observations that adipocyte RBP4 mRNA increases in parallel with circulating RBP4 in these conditions, whereas liver RBP4 mRNA does not, led to a widely held hypothesis that elevated circulating RBP4 is a direct result of increased production by adipocytes. To test this, we generated mice with hepatocyte-specific deletion of RBP4 (liver RBP4 knockout or LRKO mice). Adipose tissue RBP4 expression and secretion remained intact in LRKO mice and increased as expected in the setting of diet-induced insulin resistance. However, circulating RBP4 was undetectable in LRKO mice. We conclude that adipocyte RBP4 is not a significant source of circulating RBP4, even in the setting of insulin resistance. Adipocyte RBP4, therefore, may have a more important autocrine or paracrine function that is confined within the adipose tissue compartment. |
| Databáze: | OpenAIRE |
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