Obesity has been associated with a chronic low degree inflammatory response, characterized by an increase of inflammatory adipocytokines like tumoral necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) as well as the synthesis of acute phase reactants such as haptoglobin.
Obesity is per se associated with increased adipose expression and plasma levels of leptin, lower expression of adiponectin, and marginally elevated expression of IL-6, but PCOS does not appear to have an independent effect on the adipose expression of leptin, adiponectin, and IL-6 or the circulating adipocytokines.
Obese subjects had increased levels of oxidative damage: 4-HNE (+37%; P0.03) and PC (+63%; P0.02); evidence of increased adaptive response to oxidative stress because of elevated levels of copper/zinc SOD (Cu/ZnSOD) protein content (+84%; P0.01); increased markers of inflammation: CRP (+737%; P0.0001) and IL-6 (+85%; P0.03), and these correlated with increased markers of obesity; and increased leptin (+262%; P0.0001) with lower adiponectin (-27%; P0.01) levels vs lean controls.
Obesity in WT mice fed a HFD associated with elevated serum IL-6 levels, fatty liver, upregulation of carnitine palmitoyltransferase 1 (CPT1) and signal transducer and activator of transcription-3 (STAT3), increased AMP kinase phosphorylation (p-AMPK), and downregulation of the hepatic lipogenic enzymes fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD1).
Obesity and diabetes were associated with increased leptin and decreased adiponectin plasma levels, higher protein expression of leptin and IL-6 in SAT, and higher visfatin protein expression in EAT.
Obesity and diet composition were both positively associated to pro-inflammatory biomarkers, CRP and IL1b; while diet composition shared with physical activity levels the correlation with IL6 (positive with energy, fat, carbohydrate and saturated fatty acid intake, and negative with cholesterol intake and average physical activity in boys), NGF and glucose (in both cases correlations were negative with diet composition and physical activity variables) (P < 0.05, in all cases).
IL-6 and IL-15 protein concentrations were higher in SAT than in VAT for both obese (p = 0.003 and p < 0.0001, respectively) and control individuals (p = 0.004 and p = 0.001, respectively), while for IL-1β this was observed only in obese subjects (p = 0.047).
A polymorphism in the promoter region of the IL6 gene (-174G/C), has been previously reported to be involved in obesity and metabolic syndrome development.
Acute high-intensity interval exercise induces comparable levels of circulating cell-free DNA and Interleukin-6 in obese and normal-weight individuals.
Additionally, mediation effects of high-sensitive C-reactive protein and interleukin-6 (IL6) measured in blood were related to obesity and WMH using linear regression and structural equation models.
Adoptive transfer experiments of cytokine-deficient mast cells show that these cells, by producing interleukin-6 (IL-6) and interferon-gamma (IFN-gamma), contribute to mouse adipose tissue cysteine protease cathepsin expression, apoptosis and angiogenesis, thereby promoting diet-induced obesity and glucose intolerance.
All PPAR SNPs were not associated with obesity and Met-S in the suburban population of Kampar, Malaysia, where only PPARα V162 and PPARγ2 T161 alleles were associated with plasma IL-6 and HOMA-IR, respectively.