Obesity is a chronic disease with high prevalence and associated comorbidities, making it a growing global concern. These comorbidities include type 2 diabetes, hypertension, ventilatory dysfunction, arthrosis, venous and lymphatic circulation diseases, depression, and others, which have a negative impact on health and increase morbidity and mortality. GLP-1 agonists, used to treat type 2 diabetes, have been shown to be effective in promoting weight loss in preclinical and clinical studies. This review summarizes numerous studies conducted on the main drugs in the GLP-1 agonists class, outlining the maximum achievable weight loss. Our aim is to emphasize the active role and main outcomes of GLP-1 agonists in promoting weight loss, as well as in improving hyperglycemia, insulin sensitivity, blood pressure, cardio–metabolic, and renal protection. We highlight the pleiotropic effects of these medications, along with their indications, contraindications, and precautions for both diabetic and non-diabetic patients, based on long-term follow-up studies.

Secondary diabetes mellitus is frequently ignored in specialized literature. In this narrative review, the main endocrinopathies accompanied by increased glycemic values are identified, as well as the mechanisms by which the excess or deficiency of certain hormones impact beta cell function or insulin resistance. The main endocrinopathies (acromegaly, Cushing’s syndrome, Basedow–Graves’ disease, pheochromocytoma, somatostatinoma and glucagonoma) and their characteristics are described along with the impact of hormone changes on blood sugar, body mass index and other parameters associated with diabetes. The overall information regarding the complex molecular mechanisms that cause the risk of secondary diabetes and metabolic syndrome is of crucial importance in order to prevent the development of the disease and its complications and particularly to reduce the cardiovascular risk of these patients. The purpose of this study is to highlight the particular features of endocrine pathologies accompanied by an increased risk of developing diabetes, in the context of personalized therapeutic decision making. The epidemiological, physiopathological, clinical and therapeutic approaches are presented along with the importance of screening for diabetes in endocrine diseases.

This review presents the pathophysiological changes underlying dyslipidemia and hyperuricemia. The way in which these health conditions influence each other is through insulin resistance, persistent inflammatory state, oxidative stress and endothelial damage. Insulin resistance influences lipid metabolism and uric acid elimination, leading to triglyceride accumulation and increased uric acid levels. Inflammatory mediators in adipose tissue and cytokine cascades maintain an inflammatory status, favor lipid peroxidation and decrease renal uric acid clearance. Reactive oxygen species amplified by oxidized lipoproteins and urate compromise nitric oxide signaling pathways and vascular homeostasis. Genetic and epigenetic alterations in genes involved in metabolic transport, cytokine regulation and microRNA expression also occur. This dual pathology favors vascular vulnerability and systemic metabolic dysregulation. Effective management requires more than simple monitoring of serum markers. This should target the molecular mechanisms that fuel cardiovascular and metabolic damage.

Background and Objectives: Hyperuricemia is frequent in patients with uncontrolled type 2 diabetes (T2D) and may reflect intertwined renal and metabolic dysfunction. Simple tools to identify those at highest risk are lacking. Materials and Methods: We retrospectively analyzed 253 adults with uncontrolled T2D (HbA1c ≥ 7%) hospitalized at a tertiary center (2022–2023). Patients were stratified by hyperuricemia status (serum uric acid >7.0 mg/dL in men and >6.0 mg/dL in women). Demographic, clinical, biochemical, and pharmacological data were compared. Independent predictors were explored with multivariable modeling. A two-parameter Renal–Metabolic Risk Score (serum urea and triglyceride-to-LDL cholesterol ratio [TG/LDL]) was derived and evaluated by ROC analysis. Results: Compared with non-hyperuricemic patients (n = 20), those with hyperuricemia (n = 233) had higher serum urea (32.15 ± 21.21 vs. 19.76 ± 10.02 mg/dL; p < 0.001) and numerically higher TG/LDL (2.94 ± 6.73 vs. 1.95 ± 1.28; p = 0.062). Serum uric acid was lower in the hyperuricemia group due to categorical definition thresholds and treatment effects (5.69 ± 1.87 vs. 6.77 ± 2.12 mg/dL; p = 0.038). The derived Renal–Metabolic Risk Score showed an AUC = 0.67 and differed significantly between groups (p ≈ 1.2 × 10⁻⁵). Conclusions: The derived RMRS, based on simple and inexpensive laboratory parameters, offers a preliminary tool for assessing hyperuricemia risk in uncontrolled T2D. From a clinical and assistive practice perspective, this score may help nephrology nurses and multidisciplinary teams identify high-risk patients who require closer monitoring of renal and metabolic complications. It could further guide early dietary counseling, pharmacological optimization, and frailty assessment in chronic kidney disease care. Future studies are needed to validate the score in larger and more diverse populations before its integration into routine practice.

Background and Objectives: Dyslipidemia and hyperuricemia frequently co-exist in uncontrolled type 2 diabetes mellitus (T2DM), amplifying renal and cardiovascular risk. This study aimed to develop and evaluate an optimized Renal–Metabolic Risk Score (RMRS) integrating renal and lipid parameters to identify patients with both conditions. Materials and Methods: We conducted a retrospective observational study including 304 patients with uncontrolled T2DM hospitalized at the Emergency County Hospital Oradea, Romania (2022–2023). Hyperuricemia was defined as uric acid > 6 mg/dL in females and >7 mg/dL in males; dyslipidemia was diagnosed according to standard lipid thresholds. RMRS was calculated from standardized values of urea, TG/HDL ratio, and eGFR, with variable weights derived from logistic regression coefficients. The score was normalized to a 0–100 scale. Receiver operating characteristic (ROC) analysis assessed discriminative performance; quartile analysis explored stratification ability. Results: The prevalence of dyslipidemia and hyperuricemia co-occurrence was 81.6%. RMRS was significantly higher in the co-occurrence group compared to others (median 16.9 vs. 10.0; p < 0.001). ROC analysis showed an AUC of 0.78, indicating good discrimination. Quartile analysis demonstrated a monotonic gradient in co-occurrence prevalence from 64.5% in Q1 to 96.1% in Q4. Conclusions: The Renal–metabolic Risk Score (RMRS) demonstrated moderate discriminative performance in identifying patients with uncontrolled T2DM at risk for combined hyperuricemia and dyslipidemia. Because it relies on inexpensive, routine laboratory parameters, RMRS may be particularly useful in resource-limited settings to support early risk stratification, dietary counseling, and timely referral. Further validation in larger and more diverse cohorts is required before its clinical adoption.

Worldwide, metabolic dysfunction-associated fatty liver disease (MAFLD) is a significant public health concern, especially since more than fifty percent of people with type 2 diabetes are affected by it. This pathological condition includes all states of fatty liver disease, from non-alcoholic fatty liver disease (NAFLD) to steatohepatitis (NASH). Prolonged evolutions can lead to cirrhosis and cancer, so treatment must be started early. Hepatic steatosis may be improved by sodium glucose co-transporter 2 inhibitors (SGLT2 inhibitors), which prevent glucose reabsorption in the proximal renal tubule and increase urinary excretion, thus lowering plasma glucose levels. Experimental studies in animal models have suggested that SGLT2 inhibitors may have beneficial modulatory effects on NAFLD and NASH, while numerous clinical trials have demonstrated their favorable effects on the liver enzymes, body mass index, blood lipids, blood glucose, and insulin resistance in NAFLD patients. This review highlights the state of knowledge regarding the epidemiology, diagnosis and pathogenetic pathways of MAFLD, focusing primarily on the effectiveness of SGLT2 inhibitors as a promising drug class in the treatment of NAFLD.