UA is a final product of purine metabolism, and its accumulation has been associated with metabolic disorders [12]. It is produced in various tissues [13], including adipose, and obesity promotes this synthesis by increasing xanthine oxidase activity [14]. In adipose tissue, xanthine oxidase appears to have a role in adipocyte differentiation [15]. In cases of obesity, serum UA levels are positively associated with visceral fat deposits [16], and hypertrophic adipocytes were reported to secrete UA [14]. Furthermore, UA clearance is lower in obese individuals [17]. Serum uric acid levels strongly correlate with obesity [18; 19; 20], and their elevation increases the risk of obesity [20]. To date, the evidence of association between UA levels and CRC remains not sufficiently explored. In a Mendelian randomized study of eight cancers, including CRC, the authors do not find any consistently strong evidence supporting causality between serum UA levels and cancer risk [21]. In contrast, a recent meta-analysis from 2024 demonstrates that both gout and serum UA levels are associated with an increased risk of CRC. Further studies would elucidate whether serum UA and/or gout have a causative role in CRC [22]. Lactate is known as a product of anaerobic glycolysis. However, recent studies have identified lactate as a signaling molecule [23]. Data about its biological effects may be controversial; e.g., studies have identified lactate as an anti-inflammatory molecule, particularly in intestinal cells and macrophages [24]. A study demonstrated its role in anti-tumor immunity, which is independent of the pH-dependent effect of lactic acid, and that lactate might advance cancer immune therapy [25]. In contrast, in a tumor microenvironment, lactate is considered to be probably the only metabolic compound involved and necessary in all main sequuela for carcinogenesis: angiogenesis, immune escape, cell migration, metastasis, and self-sufficient metabolism in the tumor microenvironment [26; 27]. Lactate has been reported to be higher in CRC patients than in healthy controls, and patients with high lactate have lower overall and progression-free survival [28]. White adipose tissue is considered an active producer of lactate, contributing to the metabolism of 50-70% of ingested glucose [29]. As a signaling molecule, lactate binds GPR81 receptors in adipose tissue, where it mediates the antilipolytic activity of insulin [30; 31]. It has been established that serum lactate levels are higher in obese individuals [29; 32], probably due to hypoxia in hypertrophic visceral adipose tissue [32; 33]. Within adipocytes, lactate plays a crucial role in linking obesity to insulin resistance [34]. Deviations from the electrolyte balance have often been attributed to dehydration [35]. Obesity is related to health effects that may change water needs, hydration, and metabolic processes [36]. In general, high salt intake has been associated with obesity in the general population [37; 38]. Sodium stimulates thirst and appetite, thus increasing energy intake and extracellular volume [39; 40]. Electrolyte disorders are common in cancer patients [41; 42] and may worsen patient prognosis [43]. The aim of this study was to study plasma UA, lactate, Na\({}^{+}\), Cl\({}^{-}\), and osmolality in CRC patients in comparison with healthy individuals and to assess their applicability as diagnostic biomarkers to distinguish between CRC and a healthy state. We also aimed to analyze how these parameters depend on gender and BMI. Plasma levels of UA are significantly higher in CRC patients, indicating that metabolic impairments are associated with the disease. UA levels are correlated with obesity and are gender-dependent in CRC patients. Na\({}^{+}\), Cl\({}^{-}\), and osmolality are lower in CRC patients,supporting the statement that electrolyte balance is impaired in CRC. Plasma uric acid, lactate, and osmolality parameters have diagnostic potential as determined with ROC.