Affiliation:
1. Laboratório de Análises Clínicas - Centro Universitário Saúde ABC/FMABC – Santo André, Brazil
2. Departamento de
Ciências Farmacêuticas, Universidade Federal de São Paulo, Campus Diadema, Diadema, Brazil
Abstract
Introduction::
Diabetes Mellitus (DM) is a metabolic disorder characterized by persistent
hyperglycemia and/or insulin resistance. If left uncontrolled, it can lead to a combination of
cardiac and renal alterations known as cardiorenal syndrome. Additionally, oxidative stress and
inflammation contribute to tissue damage, thereby reducing the life expectancy of individuals
with diabetes.
Aim::
The aim of this study was to identify early molecular markers associated with cardiorenal
syndrome, oxidative stress, and inflammation, and to investigate their correlation with the duration
of exposure to DM.
Methods::
An experimental DM model was employed using Wistar rats. The rats were divided
into four groups: diabetic rats at 7 days (DM7), diabetic rats at 30 days (DM30), control sham at
7 days (CS7), and control sham at 30 days (CS30). Blood and brain tissue from the brainstem region
were collected at 7 and 30 days after confirming DM induction. Gene expression analysis of
Bnp, Anp, Cat, Gpx, Sod, Tnf-α, and Il-6 was performed.
Results::
The analysis revealed lower expression values of Cat in the brainstem tissue of the
DM7 group compared to the NDS7 group. Moreover, diabetic animals exhibited statistically
lower levels of Tnf-α in their peripheral blood compared to the control animals.
Conclusion::
This study concluded that DM alters the oxidative balance in the brainstem after 7
days of DM induction, resulting in lower Cat expression levels. Although some genes did not
show statistical differences after 30 days of DM induction, other genes exhibited no expression
values, indicating possible gene silencing. The study identified an imbalance in the studied
pathways and concluded that the organism undergoes a compensatory state in response to the initial
metabolic alterations caused by DM.
Publisher
Bentham Science Publishers Ltd.