Pancreatic D-cell disorder in coxsackievirus B4-induced diabetic mice.
Pancreatic D-cell disorder was analyzed in Coxsackievirus B4-induced diabetic mice employing molecular hybridization with a radiolabelled probe to quantitate somatostatin mRNA, and specific immunoprecipitation to measure somatostatin synthesis and its release. Many infected mice showed blood glucose lower than noninfected control animals at 72 h postinfection and 85% became hyperglycemic at 6-8 weeks postinfection. Pancreatic somatostatin decreased by 24% and 43% at 72 h and 6 weeks postinfection, respectively, while somatostatin release in islets from the infected mice increased by 2-fold or more. Residual islet somatostatin content after release was initially higher than control at 72 h and then declined at 6 weeks. Islet cellular RNA content decreased by 35% at 6 weeks, somatostatin mRNA content decreased by approximately 45% at 72 h and 6 weeks postinfection. D-cell disorder - somatostatin mRNA supply, synthesis, and release - is clearly evident in this model, which could be of significance in type I diabetes.
Chatterjee
N K
NK
Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201-0509.
Gerling
I
I
Nejman
C
C
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003384:Coxsackievirus Infections / Q000150:complications / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000209:etiology / Q000503:physiopathology*; D029822:Enterovirus B, Human; D005786:Gene Expression Regulation; D007515:Islets of Langerhans / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D012333:RNA, Messenger / Q000032:analysis; D013004:Somatostatin / Q000096:biosynthesis / Q000378:metabolism*
D001786:Blood Glucose; D012333:RNA, Messenger; D013004:Somatostatin