Analysis of pathological histochemical characteristics of yak pancreas induced by Fasciola hepatica.

Fasciola hepatica infection damages yak pancreatic tissue and induces metabolic insulin resistance.

This study investigated pancreatic pathological changes in yaks infected with Fasciola hepatica using advanced microscopic and molecular techniques. Parasites were identified via phalloidin staining and scanning electron microscopy. Histopathological analysis revealed significant pancreatic inflammation, islet atrophy, interstitial hyperplasia, and reduced glycogen storage in infected animals compared to controls. Blood glucose concentrations were significantly elevated in the infection group. Immunohistochemical and Western blot analysis demonstrated markedly increased protein expression of insulin, glucagon, estrogen receptors alpha (ERα), and beta (ERβ) in infected yaks (P<0.01). The findings suggest Fasciola hepatica infection induces pancreatic damage with subsequent dysfunction of glucose metabolism. The antagonistic relationship between elevated insulin and glucagon secretion, coupled with enhanced ERα/ERβ expression, promotes insulin release and indicates development of metabolic insulin resistance. These results provide pathological basis for understanding fascioliasis-related pancreatic complications in yaks and may have implications for clinical diagnosis of parasitic-induced endocrine dysfunction in large animals.

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