ABSTRACT Objetivo: Maturity onset diabetes of the young (MODY) patients have clinical heterogeneity as shown by many studies. Thus, often it is misdiagnosed to type 1 or type 2 diabetes(T2DM). The aim of this study is to evaluate MODY mutations in adult T2DM patients suspicious in terms of MODY, and to show clinical and laboratory differences between these two situations. Subjects and methods: In this study, we analyzed 72 type 2 diabetic patients and their relatives (35F/37M) who had been suspected for MODY and referred to genetic department for mutation analysis. The gene mutations for MODY have been assessed in the laboratory of Marmara University genetics. Totally 67 (32F/35M; median age 36.1) diabetic patients were analyzed for 7 MODY mutations. Twelve patients who have uncertain mutation (VUS) were excluded from study for further evaluation. MODY(+) (n:30) patients and T2DM patients (n:25) were compared for clinical and laboratory parameters. Results: In MODY(+) subjects, mutations in GCK (MODY 2) (n:12; 40%) were the most common followed by HNF4A (MODY 1) (n:4; 13.3%). Diabetes diagnosis age was younger in MODY(+) group but not statistically significant. Sixty-six percent of MODY(+) subjects had diabetes history at 3-consecutive generations in their family compared with 28% of T2DM patients statistically significant (p:0.006). Gender, BMI, C-peptide, HbA1c, lipid parameters, creatinine, GFR, microalbuminuria, vitamin D and calcium were not statistically different between the groups. Conclusion: According to present study results, MODY mutation positivity is most probable in young autoantibody (-) diabetic patients diagnosed before 30 years of age, who have first degree family history of diabetes.

ABSTRACT Objective: Obesity and diabetes are the risk factors for cancer development including differentiated thyroid cancer (DTC). Contradictory accumulated data indicates the possible negative effects of obesity and hyperglyceamia as a factor for aggressiveness of DTC. The aim of the present study is to investigate the association of high body mass index (BMI) and presence of type 2 diabetes mellitus (T2DM) on the histological aggressiveness and clinical outcomes in DTC patients followed for over 4 years in a single center. Materials and methods: Consequative 526 DTC patients who had undergone total thyroidectomy and/or radioactive iodine (RAI) ablation were reviewed retrospectively. Patients were divided into groups based on their BMI: normal weight, overweight, obese and also were evalauted in 3 groups presence of diabetes, prediabetes and nomoglyceamia. Histological aggressiveness of DTC at the time of diagnosis and clinical response at the time of last clinical visit were reassessed according to the criteria suggested by ATA 2015 guideline. Results: No differences in histopathologic features, risk of recurrence, cumulative dose of RAI ablation and prevalence of 131I avid metastatic disease were demonstrated among the groups both classified according to BMI and hyperglycemia. Mean of 3.4 year follow-up also showed no differences in the clinial repsonse to therapy and percentage of nonthyroid primary cancer in DTC patients. Conclusion: In this retrospective study we demonstrated that obesity and T2DM have no additive effect on DTC aggressiveness and response to therapy. DTC patients with obesity and diabetes can be treated according to present guidelines without requirement for spesific attention.

Abstract Background: A growing body of evidence suggest that obese individuals are under risk of renal parenchymal disorders when compared to nonobese counterparts. Microalbuminuria is the early marker of renal involvement. Although most of obese patients carries multiple risk factors for microalbuminuria, some obese individuals without risk factor may progress to microalbuminuria. The present study was performed to examine the role of ICAM-1 gene 1462A>G (K469E) polymorphism on microalbuminuria in obese subjects without diabetes mellitus, hypertension, hiperlipidemia and older age. Methods: Ninety eight obese and 96 nonobese individuals without a comorbidity enrolled into the study. Serum ICAM-1 level was measured by enzyme linked immunoabsorbent assay (ELISA) method. ICAM-1 gene 1462A>G (K469E) polymorphism was examined by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR). Nepholometric method was used to examine urinary albumin loss, and microalbuminuria was measured by albumin to creatinine ratio. Results: Obese individuals had significantly higher microalbuminuria and proteinuria level compared to nonobese subjects (p: 0.043 and p: 0.011; respectively). GG genotype of ICAM-1 carriers have significantly higher microalbuminuria compared to individuals with AA or AG genotype carriers (p: 0.042). Serum ICAM-1 level was significantly correlated with creatinine and microalbuminuria (p: 0.002 and p: 0.03; respectively). Logistic regression analysis indicated a 7.39 fold increased risk of microalbuminuria in individuals with GG genotype of ICAM-1 gene 1462A>G (K469E) polymorphism. Conclusions: GG genotype of ICAM-1 gene K469E polymorphism is associated with increased microalbuminuria in obese individuals without another metabolic risk factor.

Resumen Introducción: Un conjunto de datos en aumento indica que los individuos obesos corren más riesgo de sufrir trastornos del parénquima renal si se los compara con sus homólogos no obesos. La oligoalbuminuria es un primer rasgo de afectación renal. Aunque la mayoría de los pacientes obesos presentan múltiples factores de riesgo de oligoalbuminuria, esta puede manifestarse en algunos individuos obesos sin factores de riesgo. El presente estudio se realizó para analizar el papel del polimorfismo 1462A>G (K469E) del gen ICAM-1 en la oligoalbuminuria de individuos obesos sin diabetes mellitus, hipertensión, hiperlipidemia ni vejez. Métodos: Para el estudio fueron reclutados 98 individuos obesos y 96 individuos no obesos sin comorbilidad. Se midió el nivel sérico de ICAM-1 mediante el ensayo de inmunoabsorción enzimática (ELISA). Se analizó el polimorfismo 1462A>G (K469E) del gen ICAM-1 por reacción en cadena de la polimerasay polimorfismo de longitud de los fragmentos de restricción (RFLP-PCR). El método nefolométrico se utilizó para analizar la pérdida urinaria de albúmina, y la oligoalbuminuria se midió con la tasa de albúmina/creatinina. Resultados: Los individuos obesos presentaron unos niveles de oligoalbuminuria y proteinuria considerablemente más elevados que los individuos no obesos (p: 0,043 y p: 0,011, respectivamente). La oligoalbuminuria en los portadores del genotipo GG de ICAM-1 fue bastante mayor que la de los portadores del genotipo AA o AG (p: 0,042). El nivel sérico de ICAM-1 se correlacionó notablemente con la creatinina y la oligoalbuminuria (p: 0,002 y p: 0,03, respectivamente). El análisis de regresión logística mostró un riesgo 7,39 veces mayor de oligoalbuminuria en los individuos con el genotipo GG del polimorfismo 1462A>G (K469E) del gen ICAM-1. Conclusiones: El genotipo GG del polimorfismo 1462A>G (K469E) del gen ICAM-1 se asocia con un aumento de la oligoalbuminuria en personas obesas sin otro factor de riesgo metabólico.