ArticleDiabetologia2015
Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- Obesity, Bariatric Surgery, and Cancer Risk: Nutritional Perspectives and Long-Term Clinical Implications.Nutrients · 2026Review
- Adipocyte death promotes hepatic infiltration of S100A8+ macrophages and steatotic liver disease progression in mice.The Journal of clinical investigation · 2025Article
- Multiple Roles of Palmitic Acid in Cardiovascular Diseases.Journal of inflammation research · 2025Review
- Novel perspectives on the link between obesity and cancer risk: from mechanisms to clinical implications.Frontiers of medicine · 2024Review
- Autologous Human Immunocompetent White Adipose Tissue-on-Chip.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Influence of overweight and obesity on the mortality of hospitalized patients with community-acquired pneumonia.World journal of clinical cases · 2022Article
- Lipid and glucose metabolism in white adipocytes: pathways, dysfunction and therapeutics.Nature reviews. Endocrinology · 2021Review
- Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes.BMC complementary medicine and therapies · 2021Article
- Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin EBiomedicines · 2021Article
- Norepinephrine promotes triglyceride storage in macrophages via beta2-adrenergic receptor activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Remodeling of Macrophages in White Adipose Tissue under the Conditions of Obesity as well as Lipolysis.Oxidative medicine and cellular longevity · 2021Review
- Review
- Article
- Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans.Scientific reports · 2018Article
- Cadmium Alters the Concentration of Fatty Acids in THP-1 Macrophages.Biological trace element research · 2018Article
- The role of inflammation in adipocytolytic nonsurgical esthetic procedures for body contouring.Clinical, cosmetic and investigational dermatology · 2017Review
- Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD.Gut · 2016Article
- Adipose tissue macrophages: going off track during obesity.Diabetologia · 2016Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisActivation of macrophages by fatty acids (FAs) is a potential mechanism linking obesity to adipose tissue (AT) inflammation and insulin resistance. Here, we investigated the effects of FAs released during adipocyte lipolysis on AT macrophages (ATMs).
methodsHuman THP-1 macrophages were treated with media from human multipotent adipose-derived stem (hMADS) adipocytes stimulated with lipolytic drugs. Macrophages were also treated with mixtures of FAs and an inhibitor of Toll-like receptor 4, since this receptor is activated by saturated FAs. Levels of mRNA and the secretion of inflammation-related molecules were measured in macrophages. FA composition was determined in adipocytes, conditioned media and macrophages. The effect of chronic inhibition or acute activation of fat cell lipolysis on ATM response was investigated in vivo in mice.
resultsWhereas palmitic acid alone activates THP-1, conditioned media from hMADS adipocyte lipolysis had no effect on IL, chemokine and cytokine gene expression, and secretion by macrophages. Mixtures of FAs representing de novo lipogenesis or habitual dietary conditions also had no effect. FAs derived from adipocyte lipolysis were taken up by macrophages and stored as triacylglycerol droplets. In vivo, chronic treatment with an antilipolytic drug did not modify gene expression and number of ATMs in mice with intact or defective Tlr4. Stimulation of adipocyte lipolysis increased storage of neutral lipids by macrophages without change in number and phenotype. CONCLUSIONS/
interpretationOur data suggest that adipocyte lipolysis does not activate inflammatory pathways in ATMs, which instead may act as scavengers of FAs.
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