Name: GLAUCIENE JANUÁRIO DE SOUSA
Publication date: 17/03/2022
Advisor:
Name |
Role |
|---|---|
| NAZARE SOUZA BISSOLI | Advisor * |
Examining board:
| Name |
Role |
|---|---|
| ALESSANDRA SIMAO PADILHA | Internal Examiner * |
| IZABELA FACCO CALIMAN | External Examiner * |
| MARCELO PERIM BALDO | External Examiner * |
| NAZARE SOUZA BISSOLI | Advisor * |
| SONIA ALVES GOUVEA | Internal Examiner * |
Summary: Introduction: Chronic high fructose intake mimics the early stages of metabolic
syndrome (MS), leading to progressive cardiometabolic changes. Since the renin-
angiotensin-aldosterone system (RAAS) is implicated in cardiovascular diseases in
general, we hypothesized that treatment with enalapril and spironolactone would blunt
the vascular and metabolic alterations of fructose overload.
Methodology: Six-week-old male Wistar rats were assigned to receive drinking water
(controls: CON) or 10% fructose solution (FRU) for 6 weeks. During the last three weeks,
a sample of FRU rats received enalapril (F-ENA) or spironolactone (F-ESP). Systolic
blood pressure was evaluated by tail plethysmography. Fasting glucose, insulin and
glucose tolerance were measured at the end of the follow-up by strip-based glucometer.
Mesenteric vascular bed reactivity was evaluated in a perfusion system. Western Blot
analysis were performed for TNF-α, COX-2, SOD-1, SOD-2 and Catalase.
Results: Fructose increased visceral fat without affecting body weight gain, while only
enalapril prevented excessive fat accumulation and also decreased body weight. Blood
pressure remained unchanged in all groups during the six weeks. FRU group had
increased blood fasting glucose, which was mitigated only by spironolactone. Fructose
also reduced in both glucose tolerance and insulin sensitivity, which was reverted by
enalapril, while spironolactone only prevented glucose tolerance changes. FRU rats had
increased vasoconstriction elicited by norepinephrine, which was fully prevented by
enalapril, but not by spironolactone. Differences among the groups were maintained after
nitric oxide synthase inhibition and disappeared after COX inhibition. Antioxidant
defenses were affected by fructose but poorly by the treatments.
Conclusions: The metabolic changes by fructose overload were accompanied by
increased vasoconstriction related to constrictor prostanoids. These changes were
strongly related to angiotensin-II but poorly to mineralocorticoids.
