Background/Aim: High-sensitivity C-reactive protein (hs-CRP) is used in the differential diagnosis of maturity-onset diabetes of the young (MODY)-3, but other inflammatory markers have not been investigated in MODY patients. We aimed to compare the serum levels of antiinflammatory and proinflammatory cytokines between MODY patients and healthy subjects and show the inflammatory features in MODY subtypes. Patients and Methods: Thirty patients with clinically suspected MODY and 34 healthy controls were included in this study. Nextgeneration sequencing (NGS) was used for the molecular diagnosis of MODY subtypes. Serum levels of cytokines were measured using a multiplexed cytokine assay and hs-CRP concentration was determined by the immunoturbidimetric assay. Results: The hs-CRP levels were higher in both NGSconfirmed (MODY, n=17) (p=0.009) and n=13) patients (p<0.001) than those in controls. However, , , , , and sCD40L (p=0.007) levels of MODY patients and IL-1β (p=0.002), IL-31 (p<0.001), , and sCD40L (p=0.039) levels of non-MODY patients were lower than those of controls. While hs-CRP levels were lower in MODY3 patients than non-MODY3 patients (p=0.009), IL-17A (p=0.006) and IL-23 (p=0.016) levels for the first time in this study were found to be higher in patients with MODY3 than in patients with other MODY subtypes (p<0.
05). Conclusion: MODY patients had lower serum levels of the proinflammatory cytokines IL-1β, IL-6, TNF-α, IL-31, and sCD40L compared to healthy controls. High IL-17A and IL-23 levels along with low hs-CRP levels may be potential markers to distinguish MODY3 from other MODY subtypes.Maturity-onset diabetes of the young (MODY) is the most common form of monogenic diabetes and comprises about 1-5% of total diabetes (1). The prevalence of MODY has been increasing like other forms of diabetes in Turkey (2). The diagnostic criteria specified in the Practice Guideline for MODY in 2018 are evidence of endogenous insulin secretion, diabetes-onset before the age of 25 in at least one family member, presence of diabetes in two consecutive generations, and absence of autoantibodies to pancreatic islet antigens (1, 3). Mutations in genes responsible for beta cells' development and function cause MODY. To date, different mutations in fourteen genes (HNF4A/MODY1, GCK/MODY2, HNF1A/MODY3, PDX1/MODY4, HNF1B/MODY5, NEUROD1/MODY6, KLF11/ MODY7, CEL/MODY8, PAX4/MODY9, INS/MODY10, BLK/ MODY11, ABCC8/MODY12, KCNJ11/MODY13, and APPL1/ MODY14) have been described as responsible for the pathogenesis of MODY subtypes (3, 4). Recent studies have suggested that some possible biomarkers such as urine and serum amino acids, complement 5 and 8, transthyretin, urine glucose, apolipoprotein M (ApoM), lipid profile, D-glycan index, and cystatin C are useful for the differential diagnosis of 2490