Abstract
Diabetes mellitus (DM) – is a systemic endocrinologic disorder linked to impaired processing of glucose either due to insufficient insulin levels, insluin resistance or excessive dietary carbs. DM puts a significant strain on a healthcare whereas patients with DM have much lower quality of life and imposing list of comorbidities and complications. Sustained long-term inflammation is a key driving factor that should be adressed while treating DM. Dietary factors, obesity, gut dysbiosis all contribute to higher levels of inflammation in DM patients. Endotoxemia (a condition known to reflect the impaired proper gut barrier function) plays an important role in the development of inflammatory state seen in DM patients.
Aim. To evaluate the role of endotoxinemia in DM in the development of systemic inflammation.
Materials and methods. Our prospective cross-sectional study involved 177 patients with verified diagnoses of type 1 diabetes mellitus (insulin-dependent) (DM1) (n=90), type 2 diabetes mellitus (non-insulin-dependent) (DM2) (n=45) and a control group (practically healthy) (n=42). Correlation analysis was used to establish the relationship between HBA1c and sCD14 as a marker of endotoxemia.
Results. Correlation analysis of the DM2 group showed associations of sCD14 with HbA1c (correlation strength 0.404), zonulin (0.398). Zonulin also correlated with endothelin-1 levels and body mass index, two traditional pro-inflammatory associations (0.312 and 0.343, respectively). LSB correlated with VEGF (0.620) and CRP (0.430). The same CRP correlated with such classical “proxies” of chronic systemic inflammation as LDL (0.333) and HbA1c (0.430).
Conclusions. Endotoxinemia in DM2 is metabolic in nature, while in DM1 it is more likely to be “autoimmune”, that is, more mediated through zonulin than through chronic inflammation observed in patients with DM2. For example, this is additionally confirmed by a higher incidence of celiac disease among DM1 patients. The role of endotoxinemia in patients with type 2 and type 1 diabetes remains a poorly understood issue.
Keywords: diabetes mellitus, metabolic endotoxemia, lipopolysaccharide, LPS binding protein.
Aim. To evaluate the role of endotoxinemia in DM in the development of systemic inflammation.
Materials and methods. Our prospective cross-sectional study involved 177 patients with verified diagnoses of type 1 diabetes mellitus (insulin-dependent) (DM1) (n=90), type 2 diabetes mellitus (non-insulin-dependent) (DM2) (n=45) and a control group (practically healthy) (n=42). Correlation analysis was used to establish the relationship between HBA1c and sCD14 as a marker of endotoxemia.
Results. Correlation analysis of the DM2 group showed associations of sCD14 with HbA1c (correlation strength 0.404), zonulin (0.398). Zonulin also correlated with endothelin-1 levels and body mass index, two traditional pro-inflammatory associations (0.312 and 0.343, respectively). LSB correlated with VEGF (0.620) and CRP (0.430). The same CRP correlated with such classical “proxies” of chronic systemic inflammation as LDL (0.333) and HbA1c (0.430).
Conclusions. Endotoxinemia in DM2 is metabolic in nature, while in DM1 it is more likely to be “autoimmune”, that is, more mediated through zonulin than through chronic inflammation observed in patients with DM2. For example, this is additionally confirmed by a higher incidence of celiac disease among DM1 patients. The role of endotoxinemia in patients with type 2 and type 1 diabetes remains a poorly understood issue.
Keywords: diabetes mellitus, metabolic endotoxemia, lipopolysaccharide, LPS binding protein.
For citation:Beloglazov V.A., Gorlov A.A., Yatskov I.A., Ageeva E.S., Repinskaya I.N., Zagidullina E.R. Metabolic endotoxemia in diabetes mellitus type 1 & 2 patients. Clinical review for general practice. 2025; 6 (10): 32–38 (In Russ.). DOI: 10.47407/kr2025.6.10.00690
All accepted articles publish licensed under a Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.
