Effect of induced hypoglycemia on inflammation and oxidative stress in type 2 diabetes and control subjects

Intensive diabetes control has been associated with increased mortality in type 2 diabetes (T2DM); this has been suggested to be due to increased hypoglycemia. We measured hypoglycemia-induced changes in endothelial parameters, oxidative stress markers and inflammation at baseline and after a 24-hou...

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Bibliographic Details
Published in:Scientific reports Vol. 10; no. 1; p. 4750
Main Authors: Kahal, Hassan, Halama, Anna, Aburima, Ahmed, Bhagwat, Aditya M., Butler, Alexandra E., Graumann, Johannes, Suhre, Karsten, Sathyapalan, Thozhukat, Atkin, Stephen L.
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 16.03.2020
Nature Publishing Group
Subjects:
692/163/2743/137/138
692/163/2743/137/773
Adult
Biomarkers - blood
Blood Glucose
C-Reactive Protein
Case-Control Studies
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - diagnosis
Diabetes Mellitus, Type 2 - drug therapy
Disease control
Female
Heat shock proteins
Humanities and Social Sciences
Humans
Hypoglycemia
Hypoglycemia - diagnosis
Hypoglycemia - etiology
Hypoglycemic Agents - adverse effects
Inflammation
Isoprostanes
Male
Middle Aged
multidisciplinary
Oxidation
Oxidative Stress
Science
Science (multidisciplinary)
Time Factors
ISSN:2045-2322, 2045-2322
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Summary:Intensive diabetes control has been associated with increased mortality in type 2 diabetes (T2DM); this has been suggested to be due to increased hypoglycemia. We measured hypoglycemia-induced changes in endothelial parameters, oxidative stress markers and inflammation at baseline and after a 24-hour period in type 2 diabetic (T2DM) subjects versus age-matched controls. Case-control study: 10 T2DM and 8 control subjects. Blood glucose was reduced from 5 (90 mg/dl) to hypoglycemic levels of 2.8 mmol/L (50 mg/dl) for 1 hour by incremental hyperinsulinemic clamps using baseline and 24 hour samples. Measures of endothelial parameters, oxidative stress and inflammation at baseline and at 24-hours post hypoglycemia were performed: proteomic (Somalogic) analysis for inflammatory markers complemented by C-reactive protein (hsCRP) measurement, and proteomic markers and urinary isoprostanes for oxidative measures, together with endothelial function. Between baseline and 24 -hours after hypoglycemia, 15 of 140 inflammatory proteins differed in T2DM whilst only 1 of 140 differed in controls; all returned to baseline at 24-hours. However, elevated hsCRP levels were seen at 24-hours in T2DM (2.4 mg/L (1.2–5.4) vs. 3.9 mg/L (1.8–6.1), Baseline vs 24-hours, P < 0.05). In patients with T2DM, between baseline and 24-hour after hypoglycemia, only one of 15 oxidative stress proteins differed and this was not seen in controls. An increase (P = 0.016) from baseline (73.4 ng/mL) to 24 hours after hypoglycemia (91.7 ng/mL) was seen for urinary isoprostanes. Hypoglycemia resulted in inflammatory and oxidative stress markers being elevated in T2DM subjects but not controls 24-hours after the event.
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-020-61531-z