Immunocytochemical detection of anti-ACTH reactivity in pancreatic islet cells of normal and steroid diabetic rats.
Morphologically different pancreatic islet cells of the rat reveal immunoreactivity under incubation with anti-ACTH 1-39. In normal rats, anti-ACTH reactivity is detectable predominantly in peripheral, polygonal cells. Paraffin serial section treated alternately with anti-ACTH and anti-glucagon show that the major portion of the anti-ACTH reactivity is localized in A cells. A few A cells, however, lack anti-ACTH reactivity. Anti-ACTH reactivity was also detected in individuals, round-to-oval, occasionally quite large and more centrally situated cells of pancreatic islets. In contrast, islets of steroid diabetic rats reveal a different distribution islets. In contrast, islets of steroid diabetic rats reveal a different distribution of anti-ACTH reactive cells. The number of peripheral reacting cells is greatly reduced; whereas there is an increase in the number of immunoreactive, large, round or polygonal cells, which are distributed throughout the islet. Preliminary investigations indicate that adsorption of ACTH 18-39 and glucagon onto anti-ACTH 1-39 reduces immunoreactivity in normal and steroid diabetic rats, whereas adsorption of ACTH 1-24 does not.
D000324:Adrenocorticotropic Hormone / Q000032:analysis*; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D006651:Histocytochemistry; D007124:Immunoenzyme Techniques; D007515:Islets of Langerhans / Q000032:analysis*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014222:Triamcinolone Acetonide
D000324:Adrenocorticotropic Hormone; D014222:Triamcinolone Acetonide