Abstract
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.
Highlights
Cytokines are small proteins with multiple biological properties [1,2,3,4,5,6] including growth factors [7], interferons [8], interleukins [9], chemokines [10] and the tumor necrosis factor family [11].Early studies on cytokines focused on inflammation, but today it is recognized that cytokines mediate a multiplicity of biological processes
IL: interleukin; interleukin-1 receptor antagonist (IL-1RA): IL-1 receptor antagonist; IL-2RI: L-2 receptor; IFN-a and IFN-g: interferon a and g; MIG: monokine induced by IFN-g; TNFa: tumor necrosis factor a; EGF: epidermal growth factor; HGFh: epatocyte growth factor; VEGF: vascular endothelial growth factor; MIP-1a and MIP-1b: macrophage inflammatory protein-1a and 1b; G-CSF: granulocyte-colony stimulating factor; granulocytemacrophage CSF (GM-CSF): granulocyte-macrophage stimulating factor; FGF-basic: basic fibroblast growth factor; MCP-1: eotaxin, monocyte chemotactic protein 1; IP-10: inducible protein 10
(IL-17), epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), eotaxin, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon a (IFN-a), interferon g (IFN-g), monokine induced by IFN-g (MIG), inducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein-1a (MIP-1-a), macrophage inflammatory protein-1b (MIP-1-), and tumor necrosis factor a (TNF-a)
Summary
Cytokines are small proteins with multiple biological properties [1,2,3,4,5,6] including growth factors [7], interferons [8], interleukins [9], chemokines [10] and the tumor necrosis factor family [11].Early studies on cytokines focused on inflammation, but today it is recognized that cytokines mediate a multiplicity of biological processes. In spite of the fact that acute hyperglycemia [13] and hypoglycemia [14,15] are associated with increased blood levels of pro-inflammatory cytokines in non-diabetic subjects, to our knowledge, there are no data that correlates anti-inflammatory cytokines with those conditions. In this context, we aimed to evaluate the effect of the acute increase and decrease of glycemia on circulating proinflammatory and anti-inflammatory cytokines levels by assessing patients with clinical symptoms suggesting reactive hypoglycemia. The reason for selecting these specific individuals was the possibility to obtain a glycemic curve with a hyperglycemic followed by a hypoglycemic phase
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