Postprandial Dysmetabolism and Its Medical Implications

Figures

• 

  Figure 1. Correlation between Western diet and the increased risk of pathologies, of which the lowest common denominator is systemic low-grade inflammation.

• 

  Figure 2. The delicate equilibrium between pro- and anti-inflammatory statuses (IL-interleukin, TNF-tumor necrosis factor, IFN-interferon and TGF-transforming growth factor).

• 

  Figure 3. Causal connection between the immune system and postprandial dysmetabolism. (A) Systemic low-grade chronic inflammation starts with macrophages and dendritic cells, which recognize and bind DAMP molecules through toll-like receptors (TLRs). Consequently, the production of pro-inflammatory cytokines and the recruitment of immune cells to the site of the damage occur. The further spreading of the leukocytes towards insulin-dependent tissues leads to chronic inflammation. (B) Schematic representation of hyperglycemia and innate immune cells. High blood glucose level decreases rolling ability and increases the adhesion capacity of neutrophils to endothelium, impairs NET formation and decreases phagocytosis of both neutrophils and macrophages.

• 

  Figure 4. Correlation between Western diet, inflammation and obesity.

• 

  Figure 5. Insulin resistance and inflammation in diabetes mellitus type 2.