Abstract
Background In type 2 diabetes, insulin resistance is observed, and
β-cells are incapable of responding to glycemia demands, leading to
hyperglycemia. Although the nature of β-cells dysfunction in this
disease is not fully understood, a link between the induction of pancreatic
β-cell premature senescence and its metabolic implications has been
proposed. This study aimed to understand the relationship between diabetes and
pancreatic senescence, particularly at the beginning of the disease.
Methods C57Bl/6 J mice were fed two different diets, a
normal diet and a high-fat diet, for 16 weeks. Pancreatic histomorphology
analysis, insulin quantification, inflammation parameters, and senescence
biomarkers for the experimental animals were assessed at weeks 12 and 16.
Results The results proved that diabetes onset occurred at week 16 in the
High Fat Diet group, supported by glycaemia, weight and blood lipid levels.
Increased β-cells size and number accompanied by increased insulin
expression were observed. Also, an inflammatory status of the diabetic group was
noted by increased levels of systemic IL-1β and increased pancreatic
fibrosis. Finally, the expression of galactosidase-beta 1 (GLB1) was
significantly increased in pancreatic β-cells.
Conclusion The study findings indicate that senescence, as revealed by an
increase in GLB1 expression, is a key factor in the initial stage of
diabetes.
Key words
Diabetes- pancreatic cells, cellular senescence, histomorphology, markers
