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secretion of MCP-1, resistin, and other proinflammatory cytokines is increased by obesity, the adipose secretion of the anti-inflammatory protein adiponectin is decreased

the peroxisome proliferators- activated receptor (PPAR) family are involved in the regulation of inflammation and energy homestasis

natural agonists, including unsaturated fatty acids and eicosanoids

PPARα also regulates inflammatory processes, mainly by inhibiting inflammatory gene expression

upregulation of COX-2 is seen in alcoholic steatohepatitis and nonalcoholic steatohepatitis and has been directly linked to the progression of steatosis to steatohepatitis, the inhibitory effect of PPARα on COX-2 may reduce steatohepatitis

PPARα agonists have a clear anorexic effect resulting in decreased food intake, evidence is accumulating that PPARα may also directly influence adipose tissue function, including its inflammatory status.

PPARα may govern adipose tissue inflammation in three different ways: (1) by decreasing adipocyte hypertrophy, which is known to be connected with a higher inflammatory status of the tissue [3, 11, 59], (2) by direct regulation of inflammatory gene expression via locally expressed PPARα, or (3) by systemic events likely originating from liver

PPARγ is considered the master regulator of adipogenesis

Unsaturated fatty acids and several eicosanoids serve as endogenous agonists of PPARγ

PPARγ2, which is adipose-tissue specific

two different molecular mechanisms have been proposed by which anti-inflammatory actions of PPARγ are effectuated: (1) via interference with proinflammatory transcription factors including STAT, NF-κB, and AP-1

and (2) by preventing removal of corepressor complexes from gene promoter regions resulting in suppression of inflammatory gene transcription

diet-induced obesity is associated with increased inflammatory gene expression in adipose tissue via adipocyte hypertrophy and macrophage infiltration

PPARγ is able to reverse macrophage infiltration, and subsequently reduces inflammatory gene expression

Inflammatory adipokines mainly originate from macrophages which are part of the stromal vascular fraction of adipose tissue [18, 19], and accordingly, the downregulation of inflammatory adipokines in WAT by PPARγ probably occurs via effects on macrophages

By interfering with NF-κB signaling pathways, PPARγ is known to decrease inflammation in activated macrophages

Recent data suggest that activation of PPARγ in fatty liver may protect against inflammation

PPARs may influence the inflammatory response either by direct transcriptional downregulation of proinflammatory genes

anti-inflammatory properties of PPARs in human obesity

Expression of PPARγ is highest in adipose tissue,

PPARγ also plays a key role in the entraining of adipose tissue lipid metabolism to nutritional state

Its expression is highest postprandially

its activation leads to upregulation of genes that mediate FA uptake and trapping

PPARγ may also promote futile cycling in adipocytes between triglyceride (TG) esterification and de-esterification

its high expression in macrophages, which are now known to infiltrate the dysfunctional adipose tissue of obese subjects