The Pathogenesis of Pancreatic Islet Cell Hyperplasia and Insulin Insensitivity in Obesity

Author(s):  
Richard J. Mahler
1979 ◽  
Vol 66 (5) ◽  
pp. 883-888 ◽  
Author(s):  
Gerald S. Kidd ◽  
Mark Donowitz ◽  
Thomas O'Dorisio ◽  
Samuel Cataland ◽  
Forest Newman

Gut ◽  
1977 ◽  
Vol 18 (12) ◽  
pp. 1032-1035 ◽  
Author(s):  
M Lesna ◽  
A N Hamlyn ◽  
C W Venables ◽  
C O Record

Blood ◽  
1967 ◽  
Vol 30 (3) ◽  
pp. 359-363 ◽  
Author(s):  
J. STEINKE ◽  
F. A. GRIES ◽  
S. G. DRISCOLL ◽  
Maija Grinbush

Abstract It was demonstrated that hemolysed blood and/or crystalline hemoglobin inactivated insulin either by irreversible destruction due to the presence of SH compounds or by reversible binding to hemoglobin. The increased pancreatic insulin content and pancreatic islet cell hyperplasia observed in infants with erythroblastosis fetalis may represent a compensatory response to inactivation of circulating insulin.


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