Induction of Giardia spp. infection and biochemical profiles in rats

The present study investigated the metabolic and hepatic effects of experimental Giardia infection in male rats over a four-week post-infection period. Results demonstrated that Giardia infection significantly disrupted glucose homeostasis, as evidenced by a progressive and time-dependent elevation in serum glucose levels. Infected rats exhibited markedly higher glucose concentrations compared with controls, reaching a peak of 472.40 ± 200.86 mg/dL at four weeks post-infection, indicating impaired intestinal absorption and dysregulated glucose metabolism. Concurrently, serum insulin levels were significantly reduced in infected rats, with the highest post-infection value (2.543 ± 0.5431) remaining lower than the control group. Assessment of insulin resistance using the HOMA-IR index revealed a notable increase in infected groups (59.49 ± 61.73), accompanied by a significant decline in insulin sensitivity (0.345 ± 0.132). These findings suggest that Giardia infection promotes insulin resistance and disrupts systemic glucose regulation, likely through inflammatory mechanisms and alterations in gut epithelial function. levels increased progressively over the four-week period, reaching 180.00 ± 75.54 U/L and 492.45 ± 389.57 U/L, respectively, reflecting hepatocellular stress or damage induced by systemic inflammatory responses associated with intestinal infection. In contrast, serum albumin concentrations were consistently higher in infected rats compared with controls (up to 4.48 ± 0.303 g/dL), though these changes did not reach statistical significance, potentially indicating adaptive hepatic protein synthesis in response to infection. Overall, these results demonstrate that Giardia infection exerts profound systemic metabolic and hepatic effects, including hyperglycemia, hypoinsulinemia, increased insulin resistance, and elevated liver enzymes. The findings highlight the broader physiological impact of intestinal parasitic infections and underscore the need to consider their metabolic consequences in both experimental models and clinical settings.