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.

A Randomized Double-Masked Study of 50 mg of Acarbose versus 0.2 mg Voglibose in Overweight Type 2 Diabetes Patients Age Between 30 and 50 Years Having Isolated Postprandial Glycemia.

Objective: To compare the efficacy of 50 mg acarbose versus 0.2 mg of voglibose in treating postprandial hyperglycemia. Material and methods: A randomized double-masked study was conducted at the Hassan Obesity and Diabetes Wellness Centre, Hassan, Karnataka, in coordination with Rajiv Gandhi University of Health Sciences, Karnataka. Sixty cases of isolated high postprandial blood sugar (PPBS > 200 mg/dL FBS < 126 mg/dL), including both males and females between age group 30 and 50 years, were included in the study group. Observation and results: Out of 30 patients in the group treated with acarbose 50 mg, the mean reduction of glycosylated hemoglobin (HbA1C) to their baseline values was 0.8% and mean reduction in the postprandial values was 64 mg/dL. Out of 30 patients in the group treated with voglibose 0.2 mg, the mean reduction in the HbA1C was 0.6% and mean reduction in the postprandial values was 57 mg/dL. Conclusions: Reduction of postprandial blood glucose and HbA1C were more in the group treated with acarbose with the difference of 0.2% in HbA1C and 7-8 mg/dL (mean) in postprandial plasma glucose. The side effects were more in the group treated with acarbose when compared with group treated with voglibose.