Vitamin C supplementation decreases insulin glycation and improves glucose homeostasis in obese hyperglycemic (ob/ob) mice


Autoria(s): Abdel-Wahab, Y.H.A.; O'Harte, F.P.M.; Mooney, Mark; Barnett, C.R.; Flatt, P.R.
Data(s)

2002

Resumo

The effects of dietary vitamin C supplementation on glucose homeostasis and insulin glycation were examined in adult lean and obese hyperglycemic (ob/ob) mice. In lean mice, supplementation of the drinking water with vitamin C (25 g/L) for 14 days did not affect food intake, fluid intake, glycated hemoglobin, plasma glucose, or plasma insulin concentrations. Total pancreatic insulin content and the percentage of glycated pancreatic insulin were also similar to control lean mice. In ob/ob mice, vitamin C supplementation caused significant reductions by 26% to 48% in food intake and fluid intake, glycated hemoglobin, plasma glucose, and insulin concentrations compared with untreated control ob/ob mice. The total insulin content and the extent of insulin glycation in the pancreas of ob/ob mice were also significantly decreased by 42% to 45% after vitamin C supplementation. This change was accompanied by a significant 80% decrease in the percentage of glycated insulin in the circulation of vitamin C- supplemented ob/ob mice. These data demonstrate that vitamin C supplementation can decrease insulin glycation and ameliorate aspects of the obesity-diabetes syndrome in ob/ob mice. Copyright 2002, Elsevier Science (USA). All rights reserved.

Identificador

http://pure.qub.ac.uk/portal/en/publications/vitamin-c-supplementation-decreases-insulin-glycation-and-improves-glucose-homeostasis-in-obese-hyperglycemic-obob-mice(8a94c768-1c35-464d-aea1-946626553d68).html

http://dx.doi.org/10.1053/meta.2002.30528

Idioma(s)

eng

Direitos

info:eu-repo/semantics/restrictedAccess

Fonte

Abdel-Wahab , Y H A , O'Harte , F P M , Mooney , M , Barnett , C R & Flatt , P R 2002 , ' Vitamin C supplementation decreases insulin glycation and improves glucose homeostasis in obese hyperglycemic (ob/ob) mice ' Metabolism , vol 51 , no. 4 , pp. 514-517 . DOI: 10.1053/meta.2002.30528

Palavras-Chave #/dk/atira/pure/subjectarea/asjc/1300/1310 #Endocrinology #/dk/atira/pure/subjectarea/asjc/2700/2712 #Endocrinology, Diabetes and Metabolism
Tipo

article