The global increase in early-onset cancers among adolescents and young adults has happened at the same time as the rise in the consumption of ultra-processed foods (UPFs). Far beyond their poor nutritional quality, UPFs are increasingly seen as Trojan horses, complex biological agents that interfere with many functions of the human organism. In this review, we utilise the Trojan horse model to explain the quiet and building health risks from UPFs as foods that seem harmless, convenient, and affordable while secretly delivering endocrine-disrupting chemicals (EDCs), causing chronic low-grade inflammation, altering the microbiome, and producing epigenetic alterations. We bring together new proof showing that UPFs mess up hormonal signals, harm the body’s ability to fight off harmful germs, lead to an imbalance of microbes, and cause detrimental changes linked to cancer. Important components, such as bisphenols and phthalates, can migrate from containers into food, while additional ingredients and effects from cooking disrupt the normal balance of cells. These exposures are especially harmful during vulnerable developmental periods and may lay the groundwork for disease many years later. The Trojan horse model illustrates the hidden nature of UPF-related damage, not through a sudden toxin but via chronic dysregulation of metabolic, hormonal, and genetic control. This model changes focus from usual diet worries to a bigger-picture view of UPFs as causes of life-disrupting damage. Ultimately, this review aims to identify gaps in current knowledge and epidemiological approaches and highlight the need for multi-omics, long-term studies and personalised nutrition plans to assess and reduce the cancer risk associated with UPFs. Recognising UPFs as a silent disruptor is crucial in shaping public health policies and cancer prevention programs targeting younger people.

Background and Objectives: This study aimed to investigate the novel adiponectin–resistin (AR) index as a predictor of the development of metabolic syndrome (MetS) in individuals with type 2 diabetes mellitus (T2DM). MetS is common in T2DM and increases cardiovascular risk. Adiponectin and resistin, adipokines with opposing effects on insulin sensitivity and inflammation, make the AR index a potential marker for metabolic risk. Materials and Methods: This prospective observational study included 80 T2DM participants (ages 30–60) from Sarajevo, Bosnia and Herzegovina, over 24 months. The participants were divided into two groups: T2DM with MetS (n = 48) and T2DM without MetS (n = 32). Anthropometric data, biochemical analyses, and serum levels of adiponectin and resistin were measured at baseline and every six months. The AR index was calculated using the formula AR = 1 + log10(R) − 1 + log10(A), where R and A represent resistin and adiponectin concentrations. Logistic regression identified predictors of MetS. Results: T2DM patients who developed MetS showed a significant decline in adiponectin levels (40.19 to 32.49 ng/mL, p = 0.02) and a rise in resistin levels (284.50 to 315.21 pg/mL, p = 0.001). The AR index increased from 2.85 to 2.98 (p = 0.001). The AR index and resistin were independent predictors of MetS after 18 months, with the AR index showing a stronger predictive value (p = 0.007; EXP(B) = 1.265). Conclusions: The AR index is a practical marker for predicting MetS development in T2DM participants, improving metabolic risk stratification. Incorporating it into clinical assessments may enhance early detection and treatment strategies.

Background: Metabolic syndrome (MetS) denotes a cluster of co-occurring medical conditions associated with regulating hyperglycemia and acute cardiovascular events and complications. The escalating frequency of MetS among individuals afflicted with type 2 diabetes mellitus (T2DM) underscores its burgeoning significance as a critical public health concern and a complex clinical conundrum. Timely identification is imperative to avert the expedited progression of diabetic complications. Objective: To investigate the role of CRP/HDL-C and Monocyte/HDL ratios in predicting MetS in T2DM individuals. Methods: The study was designed as a two-year prospective study and included 80 T2DM patients divided into MetS and non-MetS groups based on MetS development over two years. The patients’ serums were analyzed for complete blood count parameters, lipid profile, and C-reactive protein (CRP). Based on the laboratory test results, Monocyte/HDL-C and CRP/HDL-C ratios were calculated and analyzed. The receiver operating characteristic (ROC) curve and their corresponding areas under the curve (AUC) were used to determine prognostic accuracy. Results: Monocyte/HDL-C ratio and CRP/HDL-C ratio were significantly higher in MetS-T2DM2 than in nonMetS-T2DM (p=0.003 and p=0.029, respectively). The results of ROC curve analysis have shown that the CRP/HDL-C ratio (AUC of 0.695) and Monocytes/HDL-C ratio (AUC of 0.645) can serve as good predictors of MetS in T2DM patients. Conclusion: This study confirms the reliability of the Monocytes/HDL-C and CRP/HDL-C ratios as novel, simple, low-cost, and valuable predictors of MetS development in T2DM.

Steatosis extends beyond the liver to the pancreas, heart, and skeletal muscle, yet prevailing definitions remain narrowly organ-focused. This narrative review introduces the Metabolic Steatotic Axis (MSA) as a framework that captures the dynamic, bidirectional interactions among these organs, driving systemic metabolic dysfunction. We synthesize evidence linking lipotoxicity, inflammatory signaling, and endocrine cross-talk into a self-amplifying network accelerating insulin resistance, β-cell failure, and cardiometabolic risk. The MSA concept provides a rationale for axis-based staging systems and composite biomarker panels to quantify cumulative disease burden better and refine risk stratification. We highlight phenotypic heterogeneity within MSA stages, the possible hierarchy of organ vulnerability, and the implications for prognosis and therapy. Viewing pharmacological and lifestyle interventions through the MSA lens reframes them as systemic modulators rather than organ-specific treatments, underscoring the need for multi-organ endpoints in clinical trials. Finally, we outline priorities for longitudinal imaging, multi-omics integration, and global harmonization to translate the MSA from a conceptual construct to a clinically actionable paradigm. By unifying fragmented observations into a systemic model, the MSA has the potential to reshape disease classification, therapeutic strategies, and precision medicine in metabolic disorders.

One effective anthracycline human chemotherapy drug thatis frequently used to treat solid and haematological cancers isdoxorubicin (DOX). The dose-dependent cardiotoxicity of somemedications can result in irreversible heart failure, limiting theirclinical utility. Understanding the pathophysiology and earlydetection of DOX-induced cardiac injury is made possible byanimal models, especially rats, using acute models of DOXcardiotoxicity due to less time-consuming operations. The aimof this research is to determine a potential cardiotoxic DOX dosein gender-specific Wistar wild-type rats using light microscopyfor evaluating morphological changes of the heart.Adult Wistar rats (n=10), including males (n=5) and females(n=5), were treated with doxorubicin intraperitoneal injection indifferent doses (25 mg/kg, 30 mg/kg and 40 mg/kg) per male ratand female rat, respectively. Rats were sacrificed after 48 hoursand 72 hours for the models of 25 mg/kg and 30 mg/kg, whilethe rats of the 40 mg/kg model group were sacrificed 24 hoursafter. The myocardium of the left ventricle is analysed using alight microscope under magnifications of ten and twenty times.Male Wistar rats developed more pronounced morphologicalchanges of the left ventricle compared to female Wistar rats,resulting in myocardial interstitial oedema and disorganisationof myocyte architecture.Male Wistar wild-type rats develop a more aggressive form ofacute cardiotoxicity caused by doxorubicin compared to femaleWistar wild-type rats.