Name: LAYLA MENDONÇA LÍRIO
Publication date: 20/12/2021
Advisor:
Name | Role |
---|---|
SILVANA DOS SANTOS MEYRELLES | Advisor * |
Examining board:
Name | Role |
---|---|
ALESSANDRA SIMAO PADILHA | Internal Examiner * |
AURÉLIA ARAÚJO FERNANDES | External Examiner * |
EDUARDO FRIZZERA MEIRA | External Examiner * |
IVANITA STEFANON | Internal Examiner * |
SILVANA DOS SANTOS MEYRELLES | Advisor * |
Summary: The change in the population`s dietary pattern in recent years, opting for the
consumption of industrialized products and the food industry school for
sweetening products with fructose, seems to be related to the increase in cases
of metabolic alterations in the population. In addition, some of the metabolic
changes are risk factors, as well as inadequate nutrition, for the development of
cardiovascular diseases and the occurrence of acute events, such as
myocardial infarction. Our hypothesis, therefore, is that high fructose
consumption for a long period of time in normotensive animals interferes with
hemodynamic and metabolic parameters and in the production of reactive
oxygen species after myocardial infarction. Methods: Wistar rats aged 6 weeks
were treated with water or fructose (10%) for 7 weeks, in the seventh week,
ligation of the left anterior descending coronary artery was introduced, the
treatment with fructose suspended and followed for seven days. Capillary blood
glucose was assessed weekly and at the end of the protocol, glucose tolerance
and insulin sensitivity tests were performed in the seventh week and not the
seventh day after the infarction. Catheterization of the femoral artery was
performed for invasive assessment of blood pressure and heart rate, and of the
carotid artery for assessment of hemodynamic parameters of the left ventricle,
both performed on the seventh day after the infarction. Lean mass, abdominal
fat and visceral weight were measured. And the animals` blood was collected for
biochemical analysis and evaluation of the production of reactive oxygen
species. Results: glycemia was shown to be increased in animals that consume
the fructose diet, these animals also added greater insulin resistance and lower
glucose tolerance, worsening after 7 days of infarction. An increase in left
ventricular systolic pressure and a reduction in heart rate variability were
obtained in the fructose-treated group. There was an increase in serum
triglyceride levels and in the production of reactive oxygen species in this same
group. Conclusions: We demonstrate that a high fructose diet promotes
changes in triglyceride levels, insulin sensitivity, glucose tolerance, increased
left ventricular pressure after myocardial infarction, reduced heart rate variability
and increased production of reactive species of oxygen. Suggesting that a diet
rich in fructose worsens cardiac muscle adaptation to myocardial infarction