The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Adipocyte/macrophage fatty acid–binding proteins contribute to metabolic deterioration through actions in both macrophages and adipocytes in mice
Open accessAbstract
Adipose tissue inflammation is a characteristic of obesity. However, the mechanisms that regulate this inflammatory response and link adipose inflammation to systemic metabolic consequences are not fully understood. In this study, we have taken advantage of the highly restricted coexpression of adipocyte/macrophage fatty acid-binding proteins (FABPs) aP2 (FABP4) and mal1 (FABP5) to examine the contribution of these lipid chaperones in macrophages and adipocytes to local and systemic inflammation and metabolic homeostasis in mice. Deletion of FABPs in adipocytes resulted in reduced expression of inflammatory cytokines in macrophages, whereas the same deletion in macrophages led to enhanced insulin signaling and glucose uptake in adipocytes. Using radiation chimerism through bone marrow transplantation, we generated mice with FABP deficiency in bone marrow and stroma-derived elements in vivo and studied the impact of each cellular target on local and systemic insulin action and glucose metabolism in dietary obesity. The results of these experiments indicated that neither macrophages nor adipocytes individually could account for the total impact of FABPs on systemic metabolism and suggest that interactions between these 2 cell types, particularly in adipose tissue, are critical for the inflammatory basis of metabolic deterioration.
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Metadata
- Authors
- Furuhashi, M., Fucho, R., Görgün, C. Z., Tuncman, G., Cao, H., & Hotamisligil, G. S.
- Affiliations
- Harvard University (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2008-06-01
- Volume
- 118
- Issue
- 7
- Pages
- 2640-50
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2423863
- OpenAlex
- W2025059877
- Semantic Scholar
- 006094a9303b57c51c4cf09b8015eafb6569c638
- Cited by
- 332
- References
- 34
- Citations by year
- 2025: 12 · 2024: 18 · 2023: 14 · 2022: 23 · 2021: 15 · 2020: 17 · 2019: 19 · 2018: 15 · 2017: 18 · 2016: 23 · 2015: 17 · 2014: 18 · 2013: 29 · 2012: 19
- FWCI
- 18.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- Iacocca Family Foundation
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL065405, HL 65405)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK52540, R90DK071507, P30DK040561, DK71507-04)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- fatty acid binding protein, FABP4, FABP5, adipose tissue inflammation, obesity, macrophages, adipocytes, insulin signaling, glucose uptake, inflammatory cytokines, bone marrow chimerism, metabolic homeostasis
- MeSH terms
- Adipose Tissue, Animals, Blood Glucose, Cell Communication, Glucose, Inflammation, Insulin, Liver, Macrophages, Male, Mice, Inbred C57BL, Mice, Transgenic, Neoplasm Proteins, Obesity, Receptor, Insulin, Tumor Necrosis Factor-alpha, Bone Marrow Transplantation, Adipocytes, Mice, Knockout, Chemokine CCL2, Fatty Acid-Binding Proteins, Proto-Oncogene Proteins c-akt, Mice
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