Latent autoimmune diabetes in adults (LADA) is a heterogeneous disease characterized by a less intensive autoimmune process and a broad clinical phenotype compared to classical type 1 diabetes mellitus (T1DM), sharing features with both type 2 diabetes mellitus (T2DM) and T1DM. Since patients affected by LADA are initially insulin independent and recognizable only by testing for islet-cell autoantibodies, it could be difficult to identify LADA in clinical setting and a high misdiagnosis rate still remains among patients with T2DM. Ideally, islet-cell autoantibodies screening should be performed in subjects with newly diagnosed T2DM, ensuring a closer monitoring of those resulted positive and avoiding treatment of hyperglycaemia which might increase the rate of β-cells loss. Thus, since the autoimmune process in LADA seems to be slower than in classical T1DM, there is a wider window for new therapeutic interventions that may slow down β-cell failure. This review summarizes the current understanding of LADA, by evaluating data from most recent studies, the actual gaps in diagnosis and management. Finally, we critically highlight and discuss novel findings and future perspectives on the therapeutic approach in LADA.

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My professional journey to understand the glucose homeostasis began in the 1990s, starting from cloning of the promoter region of glucose transporter type 2 (GLUT2) gene that led us to establish research foundation of my group. When I was a graduate student, I simply thought that hyperglycemia, a typical clinical manifestation of type 2 diabetes mellitus (T2DM), could be caused by a defect in the glucose transport system in the body. Thus, if a molecular mechanism controlling glucose transport system could be understood, treatment of T2DM could be possible. In the early 70s, hyperglycemia was thought to develop primarily due to a defect in the muscle and adipose tissue; thus, muscle/adipose tissue type glucose transporter (GLUT4) became a major research interest in the diabetology. However, glucose utilization occurs not only in muscle/adipose tissue but also in liver and brain. Thus, I was interested in the hepatic glucose transport system, where glucose storage and release are the most actively occurring.

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Globally, diabetic retinopathy (DR) is one of the leading causes of blindness, that diminishes quality of life. This study aimed to describe the prevalence of DR, and its associated risk factors. This cross-sectional study was carried out among 478 diabetic patients in a referral center in Fars province, Iran. The mean±standard deviation age of the participants was 56.64±12.45 years old and DR prevalence was 32.8%. In multivariable analysis, lower education levels (adjusted odds ratio [aOR], 0.43; 95% confidence interval [CI], 0.24 to 0.76), being overweight (aOR, 1.70; 95% CI, 1.02 to 2.83) or obese (aOR, 1.88; 95% CI, 1.09 to 3.26), diabetes duration of 10 to 20 years (aOR, 2.35; 95% CI, 1.48 to 3.73) and over 20 years (aOR, 5.63; 95% CI, 2.97 to 10.68), receiving insulin (aOR, 1.99; 95% CI, 1.27 to 3.10), and having chronic diseases (aOR, 1.71; 95% CI, 1.02 to 2.85) were significantly associated with DR. In conclusion, longer diabetes duration and obesity or having chronic diseases are strongly associated with DR suggesting that control of these risk factors may reduce both the prevalence and impact of retinopathy in Iran.

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