Blood levels of pro-inflammatory and anti-inflammatory cytokines during an oral glucose tolerance test in patients with symptoms suggesting reactive hypoglycemia

We evaluated the impact of postprandial glycemia on blood levels of pro-inflammatory and anti-inflammatory cytokines during an oral glucose tolerance test in non-diabetic patients with symptoms suggesting reactive hypoglycemia. Eleven patients with clinical symptoms suggesting reactive hypoglycemia received an oral glucose solution (75 g) Blood was collected at 0 (baseline), 30, 60, 120 and 180 min after glucose ingestion and the plasma concentrations of interferon-α (IFN-α), interferon-γ (IFN-γ), interleukin-1 receptor antagonist (IL-1RA), interleukin 2 (IL-2), interleukin-2 receptor (IL-2R), interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 10 (IL-10), interleukin-12 (IL-12), interleukin 13 (IL-13), interleukin 15 (IL-15), interleukin 17 (IL-17), IFN-γ inducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP1), monokine induced by IFN-γ (MIG), macrophage inflammatory protein-1α (MIP-1α), interleukin-1β (IL-1β), colony stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), basic fibroblast growth factor (FGF-basic), eotaxin, tumor necrosis factor α (TNFα), epidermal growth factor (EGF), hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), macrophage inflammatory protein-1α (MIP-1α), and 1β (MIP-1β) were evaluated. Overall, glycemic levels increased, reached its maximum at 30 min (phase 1), returned to baseline levels at 120 min (phase 2), followed by a mild hypoglycemia at 180 min (phase 3). During phase 1, cytokine blood levels were maintained. However, we observed a synchronous fall (P<0.05) in the concentrations of pro-inflammatory (IL-15, IL-17, MCP-1) and anti-inflammatory cytokines (FGF-basic, IL-13, IL-1RA) during phase 2. Furthermore, a simultaneous rise (P<0.05) of pro-inflammatory (IL-2, IL-5, IL-17) and anti-inflammatory cytokines (IL-4, IL-1RA, IL-2R, IL-13, FGF-basic) occurred during phase 3. Thus, mild acute hypoglycemia but not a physiological increase of glycemia was associated with increased blood levels of anti-inflammatory and pro-inflammatory cytokines.

Cytokines and growth factors in Duchene muscular dystrophy patients

Dystrophin deficiency associated with Duchene muscular dystrophy [DMD] results in chronic inflammation and severe skeletal muscle degeneration, where the extent of muscle fibrosis contributes to disease severity. The microenvironment of dystrophic muscles is associated with variation in levels of cytokine and growth factors. Most of the current researches test for such cytokines and growth factors in tissue biopsies, which is an invasive technique. Of the present study is to investigate whether cytokines and growth factors, as indicators of inflammatory response, can be detected in blood of DMD patients as non-invasive technique. Accordingly the cytokine tumor necrosis factor alpha [TNF TNF-alpha], as well as the growth factors basic fibroblast growth factor [bFGF] and vascular endothelial growth factor [VEGF] were measured in blood of 24 boys with DMD diagnosed clinically and at the molecular level versus 20 age matching healthy boys. Showed a significant increases in TNF-alpha [30.2 +/- 9.5 vs. 3.6 +/- 0.9 pg/ml] and bFGF [21.7 +/- 10.3 vs. 4.75 +/- 2.2 pg/ml.], while VEGF was significantly decreased [190 +/- 115 vs. 210 +/- 142 pg/ml] in blood of DMD patients compared to controls. Results provide further proof that inflammatory response is associated with DMD pathogenesis and favours the use of biomarkers in blood of such patients as a non invasive technique