Omega-3 fatty acids reduce adipose tissue macrophages in human subjects with insulin resistance
Spencer M, Finlin BS, Unal R, Zhu B, Morris AJ, Shipp LR, Lee J, Walton RG, Adu A, Erfani R, Campbell M, McGehee RE, Peterson CA, Kern PA
Diabetes · 138 citas
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Institutes of Health
- Gobierno
- National Institute of Diabetes and Digestive and Kidney Diseases
- Gobierno
- National Center for Research Resources
- Gobierno
- National Center for Advancing Translational Sciences
- Gobierno
- NIDDK NIH HHS
- Gobierno
- NCRR NIH HHS
- Gobierno
- NCATS NIH HHS
- Subvenciones
- National Center for Research Resources (P20-RR021954); National Center for Research Resources (UL1RR-033173); National Center for Research Resources (S10 RR024598); National Institute of Diabetes and Digestive and Kidney Diseases (DK-71349); National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK071349); National Institute of Diabetes and Digestive and Kidney Diseases (DK-80327); National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK080327); National Institutes of Health (UL1TR000117)
Según 7 financiadores declarados.
Publicación
- Publicado
- 2013-01-18 · Diabetes · vol. 62 · número 5 · págs. 1709–1717
- Editorial
- American Diabetes Association
- Citado
- 181 citas · más que el 99% de estudios similares · 14.4× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 47 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY-NC-ND
- Áreas de investigación
- Fatty Acid Research and Health · Adipokines, Inflammation, and Metabolic Diseases · Adipose Tissue and Metabolism
- Palabras clave
- omega-3 fatty acids, fish oil, omega-3 acid ethyl esters, insulin resistance, adipose tissue macrophages, macrophage infiltration, MCP-1, adipocyte inflammation, M1 macrophages, adipose tissue inflammation, muscle inflammation, adiponectin, TNF-α
- MeSH
- muscles, capillaries, cells, cultured, macrophages, humans, insulin resistance, obesity, fatty acids, omega-3, docosahexaenoic acids, eicosapentaenoic acid, fish oils, rna, messenger, anti-inflammatory agents, non-steroidal, drug combinations, angiogenesis inducing agents, body mass index, coculture techniques, down-regulation, dietary supplements, middle aged, female, male, abdominal fat, chemokine ccl2, metabolic syndrome
14 autores
- Michael L. Spencer🇺🇸University of Kentucky
- Brian S. Finlin🇺🇸University of Kentucky
- Reşat Ünal🇺🇸University of Kentucky
- Beibei Zhu🇺🇸University of Kentucky
- Andrew J. Morris🇺🇸University of Kentucky
- Lindsey R. Shipp🇺🇸University of Kentucky
- Jonah D. Lee🇺🇸University of Kentucky
- R. Grace Walton🇺🇸University of Kentucky
- Akosua K. Adu🇺🇸University of Kentucky
- Rod A. Erfani🇺🇸University of Kentucky
- Marilyn S. Campbell🇺🇸University of Kentucky
- Robert E. McGehee🇺🇸University of Arkansas for Medical Sciences
- Charlotte A. Peterson🇺🇸University of Kentucky
- Philip A. Kern🇺🇸 · autor de correspondenciaUniversity of Kentucky
Resumen
El texto original del estudio, en el idioma en que se publicó.
Fish oils (FOs) have anti-inflammatory effects and lower serum triglycerides. This study examined adipose and muscle inflammatory markers after treatment of humans with FOs and measured the effects of ω-3 fatty acids on adipocytes and macrophages in vitro. Insulin-resistant, nondiabetic subjects were treated with Omega-3-Acid Ethyl Esters (4 g/day) or placebo for 12 weeks. Plasma macrophage chemoattractant protein 1 (MCP-1) levels were reduced by FO, but the levels of other cytokines were unchanged. The adipose (but not muscle) of FO-treated subjects demonstrated a decrease in macrophages, a decrease in MCP-1, and an increase in capillaries, and subjects with the most macrophages demonstrated the greatest response to treatment. Adipose and muscle ω-3 fatty acid content increased after treatment; however, there was no change in insulin sensitivity or adiponectin. In vitro, M1-polarized macrophages expressed high levels of MCP-1. The addition of ω-3 fatty acids reduced MCP-1 expression with no effect on TNF-α. In addition, ω-3 fatty acids suppressed the upregulation of adipocyte MCP-1 that occurred when adipocytes were cocultured with macrophages. Thus, FO reduced adipose macrophages, increased capillaries, and reduced MCP-1 expression in insulin-resistant humans and in macrophages and adipocytes in vitro; however, there was no measureable effect on insulin sensitivity.
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