Name: LAYLA MENDONÇA LÍRIO

Publication date: 16/05/2016
Advisor:

Namesort descending Role
MARCELO PERIM BALDO Advisor *

Examining board:

Namesort descending Role
ALESSANDRA SIMAO PADILHA Internal Examiner *
CAMILLE DE MOURA BALARINI External Examiner *
MARCELO PERIM BALDO Advisor *

Summary: The growing epidemic of metabolic syndrome has been related to the increased
use of fructose by individuals, increasing its use for the production of processed
foods. Recently, the use of fructose as an ingredient has increased in
sweetened beverages, such as sodas and juices. We thus hypothesized that
fructose intake by hypertensive rats would have a worse prognosis in
developing metabolic disorder and non-alcoholic fatty liver disease. Methods.
Male Wistar and spontaneously hypertensive aged 6 weeks were given water or
fructose (10%) for 6 weeks. Blood glucose was measured every two weeks, and
insulin and glucose sensitivity test were assessed at the end of the treatment.
Systolic blood pressure was measure by plethysmography. Lean mass and
abdominal fat mass was collected. Liver was analyzed to determine interstitial
fat deposition and fibrosis. Results. Fasting glucose increased in animals that
underwent a high fructose intake, independent of blood pressure. Also, insulin
resistance was observed in both groups normotensive and hypertensive rats
after fructose intake. Fructose intake caused a 2.5-fold increase in triglycerides
levels in both groups. The lean mass gain did not change with fructose intake.
However, we found that fructose intake significantly increased abdominal fat
mass deposition in normotensive rats but not in hypertensive rats.
Nevertheless, chronic fructose intake only increased fat deposition and fibrosis
in the liver of hypertensive rats. Conclusions. We demonstrated that,
normotensive and hypertensive rats, fructose intake increased triglycerides,
abdominal fat deposition, and insulin resistance. However, hypertensive rats
underwent fructose intake also develop interstitial fat deposition and fibrosis in liver. Thus, essential hypertension is worsens outcomes in the development of
metabolic syndrome and liver disorders in hypertensive animals when
compared to normotensive animals.
Keywords: Fructose; Metabolic disorder; Visceral fat; Hypertension; Fatliver
disease.

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