Role of Adiponectin and Tumor Necrosis Factor-Alpha in the Pathogenesis and Evolution of Type 1 Diabetes Mellitus in Children and Adolescents.
Csilla Enikő SzaboOana Iulia ManAlexandru IstrateEva KissAndreea CatanaVictoria CrețRadu Sorin ȘerbanIoan Victor PopPublished in: Diagnostics (Basel, Switzerland) (2020)
Type 1 diabetes mellitus (T1DM) is a complex condition caused by the destruction of pancreatic beta cells by autoimmune mechanisms. As a result, insulin deficiency and subsequent hyperglycemia occur. The aim of the present study is to investigate the role of adiponectin and tumor necrosis factor alpha (TNF-α) in the development of T1DM. The study is designed as an observational case-control study, involving 52 diabetic patients and 66 controls. Z scores for Body Mass Index (BMI), weight, height, and adiponectin and TNF-α serum levels were assessed in both groups. The T1DM group had significantly higher TNF-α levels and a significantly higher proportion of high-risk patients for inflammation based on TNF-α values as compared to the control group, while both groups had statistically similar adiponectin levels and a similar proportion of high/medium-risk patients based on adiponectin values. TNF-α plays a significant role in the pathogenesis and evolution of T1DM and it may represent an additional marker of disease progression, as well as a potential target of immunotherapeutic strategies. In the present study, no statistically significant differences were recorded in adiponectin levels neither in diabetic patients and controls, nor in high/medium severity risk diabetic patients.
Keyphrases
- body mass index
- rheumatoid arthritis
- metabolic syndrome
- end stage renal disease
- insulin resistance
- newly diagnosed
- ejection fraction
- glycemic control
- chronic kidney disease
- type diabetes
- physical activity
- oxidative stress
- cardiovascular disease
- induced apoptosis
- prognostic factors
- cell proliferation
- weight loss
- climate change
- signaling pathway
- cell cycle arrest
- endoplasmic reticulum stress
- replacement therapy