Alternative macrophage activation and metabolism
Open accessAbstract
Obesity and its attendant metabolic disorders represent the great public health challenge of our time. Recent evidence suggests that onset of inflammation in metabolic tissues pathogenically links obesity to insulin resistance and type 2 diabetes. In this review, we briefly summarize the extant literature, paying special attention to the central role of the tissue-associated macrophage in the initiation of metabolic inflammation. We argue that rather than representing simple inflammatory disease, obesity and metabolic syndrome represent derangements in macrophage activation with concomitant loss of metabolic coordination. As such, the sequelae of obesity are as much products of the loss of positive macrophage influences as they are of the presence of deleterious inflammation. The therapeutic implications of this conclusion are profound because they suggest that pharmacologic targeting of macrophage activation, rather than simply inflammation, might be efficacious in treating this global epidemic.
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PPAR-δ induces monounsaturated fatty acids, which prompts KCs to modulate the immune response via reduction of TNF-α or IFN-α.
“PPAR-δ induce monounsaturated fatty acids, which in turn prompts KCs to modulate the immune response via a reduction of TNF-α or IFN-α.[144]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [144]
PPAR-δ regulates serum and hepatic triglyceride levels.
“PPAR-δ -/-mice showed a reduction in adiposity compared to wild-type animals, which revealed that PPAR-δ is highly involved in the systemic lipid metabolism [143] and regulation of serum/hepatic triglyceride levels [144,145]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [144]
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References 139 · Cited by 640
- Authors
- Odegaard, J. I., & Chawla, A.
- Affiliations
- Stanford Medicine (US)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2011-02-28
- Volume
- 6
- Issue
- 1
- Pages
- 275-297
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- PMC
- PMC3381938
- OpenAlex
- W2130874539
- Cited by
- 640
- References
- 139
- Citations by year
- 2026: 27 · 2025: 31 · 2024: 42 · 2023: 31 · 2022: 34 · 2021: 41 · 2020: 39 · 2019: 39 · 2018: 39 · 2017: 44 · 2016: 53 · 2015: 57 · 2014: 50 · 2013: 58 · 2012: 36
- FWCI
- 6.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (DP1OD006415)
- National Heart, Lung, and Blood Institute (HL076746, R01HL076746)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK081405, R01DK081405, DK076760, R01DK076760)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- macrophage activation, obesity, metabolic inflammation, insulin resistance, type 2 diabetes, metabolic syndrome, macrophage metabolism, metabolic coordination, anti-inflammatory therapy
- MeSH terms
- Diabetes Mellitus, Type 2, Humans, Inflammation, Macrophage Activation, Macrophages, Obesity
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