Diabetes mellitus is a severe chronic disease caused by the inability of the pancreas to synthesize insulin or the inability of the body to functionally use synthesized insulin (WHO, 1999). Diabetes mellitus, according to the mechanism of disease development, can be divided into several subtypes, and the most commonly misdiagnosed type of diabetes is MODY (Maturity-onset Diabetes of the Young). MODY diabetes is a heterogeneous group of disorders caused by mutations in different genes, and the most common type is MODY3 caused by a mutation in the HNF1A gene for the transcription factor of the same name. Mutated transcription factor HNF1A leads to abnormal regulation of insulin synthesis in the β-cells of the pancreatic islets of Langerhans leading to the development of diabetes. Previous research has shown that treatment with sulfonylureas leads to the best therapeutic outcome in MODY patients, but due to the often misdiagnosed initial diagnosis, patients are given metformin which does not lead to improvement and withdrawal of symptoms. Mutations in the HNF1A gene are heterogeneous; some of them are benign, more different leads to the development of the disease, and some have not yet been assigned meaning. Therefore, molecular diagnostic methods in the diagnosis of MODY diabetes are deficient and often provide results that, due to lack of literature data, cannot be assigned clinical significance. It has been recognized that mutations in the transcription factor HNF1A lead to changes in the glycosylation of α-1 acid glycoprotein, and it can be assumed that a comprehensive analysis of the structure and composition of glycans on α-1 acid glycoprotein would provide adequate information on the functionality of transcription factor in HNF1A. patient. In this research work, glycopeptides were analyzed by mass spectrometry coupled to liquid chromatography by which it is possible to compare a large number of samples since the method can simultaneously analyse large cohorts. Glycopeptides were tested in 90 plasma samples, of which 72 belonged to individuals without a mutation in the HNF1A gene, and 18 to individuals with a confirmed damaging HNF1A mutation. Statistical processing of the data using the Mann Whitney test revealed that there was a statistically significant difference in AGP fucosylation between the examined groups.