Diabetes is a complex and rapidly growing disease with heterogeneous clinical presentations. Recent advances in molecular and genetic technologies have led to the identification of various subtypes of diabetes. These advancements offer the potential for a more precise, individualized approach to treatment, known as precision medicine. Recognizing high-risk phenotypes and intervening early and intensively is crucial. A staging system for type 1 diabetes has been proposed and accepted globally. In this article, we will explore the different methods for categorizing and classifying type 2 diabetes (T2D) based on clinical characteristics, progression patterns, risk of complications, and the use of molecular techniques for patient grouping. We, as a team of experts, will also present an easy-to-follow treatment plan and guidance for non-specialists, particularly primary care physicians, that integrates the classification and staging of diabetes. This will help ensure that the most suitable therapy is applied to the different types of T2D at each stage of the disease’s progression.

Type 1 diabetes (T1D) is an autoimmune disorder characterized by the destruction of insulin-producing pancreatic beta-cells, leading to lifelong insulin dependence. This review explores the current understanding of T1D pathogenesis, clinical progression, and emerging therapeutic approaches. We examined the complex interplay between genetic predisposition and environmental factors that could trigger the autoimmune response as well as the immunological mechanisms involved in beta-cell destruction. The clinical phases of T1D are discussed from the preclinical stage through diagnosis and long-term management, highlighting the importance of early detection and intervention. Recent advancements in treatment strategies are presented, including immunomodulatory therapies and potential cell-based treatments aimed at preserving or restoring beta-cell function. Additionally, this review critically evaluates the feasibility and potential benefits of implementing a population-wide screening program for T1D in Spain. The epidemiological, economic, and ethical implications of such an initiative were considered by the national expert panel, focusing on the potential of early diagnosis to improve clinical outcomes in the face of the challenges of large-scale implementation. This comprehensive analysis aims to provide healthcare professionals, researchers, and policymakers with valuable insights into the current landscape of T1D management and prospects for enhanced prevention and treatment strategies in the Spanish context.

There is a high prevalence of nutritional disorders in patients with liver cirrhosis (LC). This study was designed to assess the relationships between liver function, IFG-I/IGFBP-3, nutritional status, leptin, ghrelin and glucagon in 21 patients waiting for liver transplantation (LT). We studied 21 men aged 56±2.1 years who were on the LT list. They were classified according to Child-Pugh(CP) score from low to high liver dysfunction in CPA (n=4),CPB (n=11) and CPC (n=6). Body mass index (BMI) was calculated and body fat (%) was measured by air-displacement plethysmography. Resting energy expenditure (REE) and its variation over Harris-Benedict values (GER%) were assessed by indirect calorimetry. Fasting serum samples were taken to measure albumin, glucose, insulin, HbA1c, leptin, total ghrelin,glucagon, IGF-I and IGFBP3. There were no differences in fat % and leptin values in the three groups according to CP classification. The CPC group showed higher ghrelin values than CPA and CPB(p<0.05). All groups displayed high glucagon levels and GER%values superior to 100%. Positive correlations were found between glucagon and GER% (r=0.56; p<0.01) and between glucagon and ghrelin values (r=0.66; p<0.01). IGF-I and IGFBP3 were low in all groups and showed a positive correlation with plasma albumin (r=0.52; p<0.05 and r=0.45; p<0.05 respectively). These results show an increase in ghrelin plasma values in patients with severe liver dysfunction. Hyperglucagonemia was correlated with GER%, supporting a role of glucagon in the hypermetabolic state associated to LC,raising the possibility of becoming a therapeutic target. The measurement of IGF-I/IGFBP3 represents a good marker of liver function in patients with LC.