Short-term High-fat Overfeeding Does Not Induce NF-κB Inflammatory Signaling in Subcutaneous White Adipose Tissue

Abstract

Context It is unclear how white adipose tissue (WAT) inflammatory signaling proteins respond during the early stages of overnutrition. Objective To investigate the effect of short-term, high-fat overfeeding on fasting abdominal subcutaneous WAT total content and phosphorylation of proteins involved in nuclear factor-κB (NF-κB) inflammatory signaling, systemic metabolic and inflammatory biomarkers. Design Individuals consumed a high-fat (65% total energy from total fat), high-energy (50% above estimated energy requirements) diet for 7 days. Results Fifteen participants (aged 27 ± 1 years; body mass index 24.4 ± 0.6 kg/m2) completed the study. Body mass increased following high-fat overfeeding (+1.2 ± 0.2 kg; P < 0.0001). However, total content and phosphorylation of proteins involved in NF-κB inflammatory signaling were unchanged following the intervention. Fasting serum glucose (+0.2 ± 0.0 mmol/L), total cholesterol (+0.4 ± 0.1 mmol/L), low-density lipoprotein cholesterol (+0.3 ± 0.1 mmol/L), high-density lipoprotein cholesterol (+0.2 ± 0.0 mmol/L), and lipopolysaccharide-binding protein (LBP; +4.7 ± 2.1 µg/mL) increased, whereas triacylglycerol concentrations (−0.2 ± 0.1 mmol/L) decreased following overfeeding (all P < 0.05). Systemic biomarkers (insulin, soluble cluster of differentiation 14 [CD14], C-reactive protein, interleukin-6, tumor necrosis factor-α and monocyte chemoattractant protein-1) and the proportion and concentration of circulating CD14+ monocytes were unaffected by overfeeding. Conclusion Acute lipid oversupply did not impact on total content or phosphorylation of proteins involved in WAT NF-κB inflammatory signaling, despite modest weight gain and metabolic alterations. Systemic LBP, which is implicated in the progression of low-grade inflammation during the development of obesity, increased in response to a 7-day high-fat overfeeding period.

Short-term high-fat diet favors the appearances of apoptosis and gliosis by activation of ERK1/2/p38MAPK pathways in brain

“…In addition, many new findings in mice and humans suggest that JNK activation might induce insulin resistance and lead to obesity [ 47 , 48 ]. Meanwhile, NF-κB inflammatory regulation signaling pathway is up-regulated in the brain tissue of 14weeks or 16weeks HFD-feeding mice [ 20 , 49 ] as well NF-κB inflammatory signaling is unchanged in subcutaneous white adipose tissue after short-term high-fat overfeeding [ 16 ]. On the other hand, our results showed that after 7 days or 21 days consumption of HFD led to a significant decrease in phospho-NF-κB p65 and phospho-JNK simultaneously.…”

“…Interestingly, even as little as 3–10 days exposure, short-term HFD consumption has demonstrated that production of proinflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor α (TNFα), apoptosis and memory impairments in humans and rodents in long before obesity symptoms appearance [ 11 – 15 ]. Nevertheless, a literature suggests that short-term HFD overnutrition does not induce NF-κB inflammatory signaling of subcutaneous white adipose tissue in humans [ 16 ].…”