Diabetes promotes invasive pancreatic cancer by increasing systemic and tumour carbonyl stress in Kras^G12D/+ mice.

ABSTRACT:

Background

Type 1 and 2 diabetes confer an increased risk of pancreatic cancer (PaC) of similar magnitude, suggesting a common mechanism. The recent finding that PaC incidence increases linearly with increasing fasting glucose levels supports a central role for hyperglycaemia, which is known to cause carbonyl stress and advanced glycation end-product (AGE) accumulation through increased glycolytic activity and non-enzymatic reactions. This study investigated the impact of hyperglycaemia on invasive tumour development and the underlying mechanisms involved.

Methods

Pdx1-Cre;LSL-Kras^G12D/+ mice were interbred with mitosis luciferase reporter mice, rendered diabetic with streptozotocin and treated or not with carnosinol (FL-926-16), a selective scavenger of reactive

SUBMITTER: Menini S 

PROVIDER: S-EPMC7418209 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature