Increased insulin secretion suppresses cortisol levels, exacerbates inflammation and beta-cell dysfunction Increased insulin resistance with cortisol levels and HOMA- beta

Abstract

Aim: The role of inflammatory mechanisms in the formation of insulin resistance (IR), diabetes and metabolic syndrome has been widely discussed in recent years. The aim of this study was to investigate the relationship between IR and pancreatic β-cell function with hematological inflammatory markers and cortisol levels. Material and Methods: Four hundred fifteen adult patients whose samples were accepted to the laboratory between the hours of 08:00-12:00; leukocyte, neu-trophil and lymphocyte count, mean platelet volume (MPV), insulin, glucose, and cortisol levels were examined retrospectively. The neutrophil-lymphocyte ratio (NLR), the homeostasis model assessment (HOMA)-IR and HOMA-β values were calculated according to the collected data. The patients were divided into two groups: with (HOMA-IR≥2.5) and without IR (HOMA-IR<2.5). All data were statistically evaluated using the SPSS package program. Results: A statistically significant difference was found in cortisol levels (p=0.003), leukocyte (p<0.001), neutrophil (p<0.001), lymphocyte counts (p=0.003) and NLR (p=0.011) between the groups. However, there was no significant difference between the MPV levels. Both HOMA-IR and HOMA-β showed a weak positive correlation with leukocyte, neutrophil and lymphocyte counts and showed a negative correlation with cortisol levels. There was a weak positive correlation between NLR levels and HOMA-IR. Although there was a negative correlation between cortisol with insulin and NLR levels, no significant correlation was found between cortisol and glucose, neutrophil-lymphocyte count. Discussion: The significant increase in hematological inflammatory cells in patients with IR suggests that inflammatory mechanisms may have produced insulin resistance. The increase in insulin levels and suppression of cortisol levels may play a role in the progression of inflammation.