TABLE 4.
Impact of obesity and diabetes on neutrophil metabolism and function.
| References | AS comorbidity | Cells | Cells origin | Treatment/condition | Effect on neutrophil metabolism | Associated effect on neutrophil function | PMID |
|---|---|---|---|---|---|---|---|
| Cichon et al. (2021) | Obesity | Mouse primary neutrophils | Obese mice | HFD | ↓ GLUT1 expression ↓ Glycolysis (tendency) |
↓ NET formation after 1 h LPS stimulation ↑ NET formation after 6 h LPS stimulation |
34299338 |
| HFD and sepsis | ↑ Glycolysis (tendency) | ↑ Spontaneous NET formation ↓ NET formation after LPS stimulation |
|||||
| Joshi et al. (2020) | Diabetes | Human primary neutrophils | Healthy donors | High glucose | ↑ Polyol pathway intermediates (NADPH-dependent formation of 1-anhydrosorbitol via aldose reductase) ↓ Glutathione metabolism (with NADPH required for glutathione synthesis) |
↑ Cytosolic ROS ↑ Neutrophil elastase secretion ↑ spontaneous NADPH oxidase-dependent NET formation but ↓ LPS-induced NET formation |
32827651 |
| High glucose + Aldose reductase inhibitor |
No high glucose-induced increase in cytosolic ROS, neutrophil elastase secretion or spontaneous NET formation, but restored responsiveness to LPS-stimulated NET formation | ||||||
| Alba-Loureiro et al. (2006) | Diabetes | Rat primary neutrophils | STZ-treated rats | ↓ Metabolism of glucose and glutamine ↓ Lactate production and PPP activity |
↓ Phagocytosis ↑ Production of H2O2 |
16461555 | |
AS, atherosclerosis; GLUT-1, glucose transporter 1; HFD, high-fat diet; LPS, lipopolysaccharide; PPP, pentose phosphate pathway; STZ, streptozotocin; ROS, reactive oxygen species.