Fatima Itzel Soto Rios

Cardiovascular disease remains the leading cause of mortality worldwide, and traditional risk stratification models based on static variables are often insufficient to explain the complexity of cardiometabolic disorders. In this context, metabolic flexibility—defined as the ability of the organism to adapt substrate utilization according to physiological demands—has emerged as a relevant integrative concept linking endocrinology and cardiovascular disease. This review analyzes metabolic flexibility as a central mechanism in cardiovascular risk, exploring its physiological basis, its relationship with insulin resistance and metabolic disorders, and its implications in cardiovascular pathology. Evidence shows that impaired metabolic flexibility is associated with altered substrate utilization, mitochondrial dysfunction, systemic inflammation, and increased cardiovascular risk. These alterations contribute to inefficient myocardial energy metabolism, vascular dysfunction, and disease progression. Additionally, current therapeutic strategies that improve metabolic regulation have demonstrated significant cardiovascular benefits, supporting the relevance of metabolic pathways in disease prevention and management. The analysis also highlights the importance of considering metabolic flexibility in populations with a high burden of cardiometabolic disease, particularly in Latin American countries such as Mexico, Colombia, and Ecuador.

Chronic diseases in internal medicine have traditionally been approached as isolated entities; however, emerging evidence supports their interpretation as interconnected processes sustained by metabolic–inflammatory networks. This review aimed to analyze and integrate current high-impact evidence on immunometabolism, chronic inflammation, and systemic dysregulation in order to propose a systems-based framework applicable to clinical practice and medical education. A structured narrative review was conducted using 20 peer-reviewed references indexed in major biomedical databases. The analysis focused on key mechanisms including metaflammation, insulin resistance, adipose tissue inflammation, vascular dysfunction, gut microbiota interactions, skeletal muscle signaling, and ageing-related inflammatory changes. The results demonstrated a consistent convergence across mechanistic, biological, and clinical domains, highlighting chronic inflammation as a central driver linking obesity, type 2 diabetes mellitus, atherosclerosis, and multimorbidity. Furthermore, the evidence revealed that these processes are dynamically influenced by lifestyle factors, environmental exposures, and ageing. The integration of these findings supports a network-based model of disease that transcends traditional organ-specific approaches. This framework offers potential benefits in clinical reasoning, risk stratification, preventive strategies, and medical education, particularly in regions with a high burden of chronic disease such as Mexico, Colombia, and Ecuador. In conclusion, metabolic–inflammatory networks represent a fundamental organizing principle in chronic disease, providing a coherent and clinically relevant perspective for modern internal medicine.

Clinical complexity in internal medicine has increasingly shifted from isolated organ-based disease models toward integrative, systems-based approaches. This review analyzes the interaction between gastrointestinal and urological systems as a representative model of multisystem disease. A narrative synthesis of high-impact literature was conducted, focusing on shared pathophysiological mechanisms, including systemic inflammation, metabolic dysregulation, microbiota alterations, neuroautonomic dysfunction, and organ crosstalk. The findings demonstrate that gastrointestinal and urological disorders frequently coexist and are interconnected through dynamic biological networks rather than independent processes. Multimorbidity emerges as a central framework in which conditions influence each other’s progression and clinical expression. The gut–kidney–bladder axis, along with the role of the microbiome and metabolic syndrome, provides key insights into these interactions. Furthermore, integrated care approaches show a clear advantage over fragmented management, improving clinical outcomes through coordinated and mechanism-based strategies. These results support the need for a paradigm shift in internal medicine toward systems-based thinking, particularly in clinical and educational settings. The integration of gastrointestinal and urological perspectives offers a more comprehensive understanding of disease and contributes to more effective, patient-centered care.

The growing prevalence of diabetic kidney disease (DKD) underscores the urgent need for therapies that go beyond glycemic control to achieve meaningful renal protection. This multicenter international study evaluated the impact of GLP-1 receptor agonists—semaglutide (Ozempic) and tirzepatide (Mounjaro)—on kidney outcomes in adults with type 2 diabetes mellitus and chronic kidney disease across Mexico, Colombia, and Ecuador. A total of 1,200 participants were followed for 12 months and compared with matched controls under standard care. Both semaglutide and tirzepatide significantly reduced the incidence of the composite renal endpoint (≥40% decline in eGFR, renal replacement therapy, or cardiovascular death) by 22% and 26%, respectively, versus control. The annual decline in estimated glomerular filtration rate was markedly slower in treated groups (−1.2 to −1.3 mL/min/1.73m²/year) compared with standard care (−3.4 mL/min/1.73m²/year), and urinary albumin-to-creatinine ratio decreased by 35–40%. These benefits were consistent across subgroups, including sex, age, CKD stage, and country, and remained significant after adjustment for confounders. The nephroprotective effects observed likely reflect multifactorial mechanisms—hemodynamic stabilization, anti-inflammatory modulation, endothelial protection, and synergy with SGLT2 inhibitors and RAAS blockade. Results parallel those from major global trials such as FLOW, SURPASS-4, and REWIND, confirming reproducible benefits in Latin American populations. Integrating GLP-1 receptor agonists into diabetic kidney disease management may represent a transformative, evidence-based strategy to delay renal failure and reduce cardiovascular mortality worldwide.