The Effect of Caffeine on Wnt/β-Catenine and P38 Mitogen-Activated Protein Kinases (MAPK) Signal Pathways and Some...

Obesity is a major noncommunicable public health problem that is rapidly spreading worldwide, arising from an imbalance between energy intake and expenditure, and various interventions have been attempted for its treatment. This study evaluated the impact of caffeine on metabolic and hepatic parameters in rats with obesity induced by a cafeteria diet. Rats were assigned to control, caffeine, obesity, and obesity + caffeine groups. The cafeteria diet effectively promoted obesity, as evidenced by increased body weight, BMI, and Lee Index, accompanied by elevated serum glucose, triglycerides, total cholesterol, low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), and reduced high-density lipoprotein (HDL) levels. Obesity also led to higher plasma asprosin and visfatin levels, decreased hepatic β-catenin and P38 mitogen-activated protein kinases (p38 MAPK) expression, and histopathological alterations in liver tissue. Caffeine administration mitigated body weight gain, improved lipid profiles, and modulated plasma levels of asprosin, preptin, and visfatin, while reducing liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. Although caffeine did not restore β-catenin or p38 MAPK protein levels in obese rats, it alleviated liver histopathological damage. These findings indicate that caffeine may exert protective effects against cafeteria diet-induced obesity by regulating multiple metabolic parameters and improving liver morphology. The study highlights the potential of caffeine as a modulator of obesity-related metabolic dysregulation, while suggesting that further research is necessary to clarify its influence on β-catenin and p38 MAPK signaling pathways.