Rat liver carbohydrate alterations in streptozotocin-induced diabetic rats

TLDR: A set of lectins with different carbohydrate affinities is used to investigate impairment in rat liver glycoconjugates influenced by streptozotocin-induced diabetes mellitus and demonstrate the applicability of the original fucose-specific lectin preparation to experimental histopathology.

Abstract: Diabetes mellitus (DM) currently belongs to the most widespread human pathologies, affecting about 4% of the world adult population. Despite the pivotal role of the liver in the development of metabolic disorders, the influence of DM on hepatic glycoconjugates remains obscure. The aim of the present investigation was to use a set of lectins with different carbohydrate affinities to investigate impairment in rat liver glycoconjugates influenced by streptozotocin-induced diabetes mellitus. The lectin panel included 7 conventional lectins – Con A, SNA, RCA, WGA, PNA, SBA, and HPA, supplemented with the original fucose-specific lectin preparation from Laburnum anagyroides bark (LABA). Tissue samples were fixed in 4% neutral formalin, embedded in paraffin, and subjected to lectin-peroxidase-diaminobenzidine staining. In control rats a strong reactivity against Con A, LABA, SBA and SNA with cytoplasmic granularities of hepatocytes was detected, while RCA, WGA and HPA showed a strong reactivity with vascular endothelium, and WGA and HPA with bile capillaries. Experimental diabetes was associated with a redistribution of Con A and LABA receptor sites from centrolobular hepatocytes to hepatocytes with peripheral localization. Among the most remarkable observations was DMinduced exposure of lectin reactivity with hepatocyte and endothelial cell nuclei. The endothelial lining of sinusoidal hemocapillaries, of central veins, and portal tract vessels also displayed a significant and differential rearrangement of carbohydrate determinants when influenced by DM. Diabetes-induced activation of Kupffer cells was accompanied by the expression of SNA, PNA and SBA receptor sites within the cytoplasm of these cells, which was lectin-negative in control specimens. The results reported provide a new insight into the pathogenesis of DM-induced impairment of hepatic carbohydrates, and demonstrate the applicability of the original fucose-specific lectin preparation to experimental histopathology.