Influência da leptina na reatividade vascular em anéis de aorta de ratos obesos
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Data
2015-06-25
Autores
Rocha, Vanessa da Silva
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Editor
Universidade Federal do Espírito Santo
Resumo
Obesity is a metabolic chronic disease characterized by excessive accumulation of
body fat and an independent risk factor for development of cardiovascular disorders.
Experimental studies show that the unsaturated high-fat diet-induced obesity
promotes vascular alterations characterized by improved endothelial L-arginine/Nitric
Oxide (NO) pathway. Research suggest that leptin is involved in this process, being
able to promote vasodilation by increase of NO synthesis and/or release. The
objective of this study was to evaluate the involvement of leptin on vascular reactivity
in aortic rings of rats submitted to obesity by unsaturated high-diet fat. Thirty-day-old
male Wistar rats were randomized into two groups: control (C, n=9) and obese (Ob,
n=7). The C group was fed a standard diet and the Ob group was alternately
submitted to four palatable high-fat diets for 27 weeks. Final body weight, total body
fat and adiposity index were assessed. The glycemic profile was evaluated by
glucose tolerance test (GTT) and systolic blood pressure (SBP) by tailcuff plethysmography method. The analysis of vascular reactivity was carried out in
aortic segments and assessed by the concentration-response curves to
phenylephrine (10-11 to 3x10-4 M), acetylcholine (10-12 to 10-4 M) and leptin (10-14 to
3x10-6 M) in the presence and absence of L-NAME (nonspecific inhibitor of NO
synthase, 100 µM). Data were expressed using descriptive measures of variability
position and submitted to Students T-test and two-way ANOVA followed by a
Bonferroni post-hoc test. The level of significance was considered to be 5%. The
results show that unsaturated high-fat diet used in this study promoted greater calorie
intake, elevation of body weight and body fat, adiposity index, featuring a
reproducible model of obesity. However, comorbidities frequently associated to
experimental obesity were not visualized, such as glucose intolerance, dyslipidemia
and hypertension. Obesity reduced the maximum response to phenylephrine (Rmax -
C: 88.5 ± 4.8% vs Ob: 61.1 ± 5.4%*; p<0.05) and sensibility (pD2 - C: -6.78 ± 0.10 vs
Ob: -7.31 ± 0.12 *; p<0.05). After incubation of aortic rings with L-NAME, in Ob group
persisted significant decrease in pD2 (L-NAME/C: -7.41 ± 0.13 vs L-NAME/Ob: -7.80
± 0.10#
; p<0.05) than C. Obesity lead did not change the vasodilation induced by
acetylcholine between groups. However, after administration of L-NAME, the Rmax
(L-NAME/Ob: 4.10 ± 1.89%#
vs L-NAME/C: 26.54 ± 5.30%; p<0.05) was lower in the
Ob group compared to C. Furthermore, the vasodilation induced by leptin in the
presence and absence of L-NAME were not altered by obesity. In conclusion, obesity
induced unsaturated fat diet leads to decreased contractile response without
changing the vasodilator response. Furthermore, the findings show that leptininduced relaxation response is not altered due to the obesity, but are dependent on
the release of NO.
Descrição
Palavras-chave
Obesity , High-fat diet , Endothelium , Leptin , Dieta hiperlipídica , Aorta , Obesidade , Dieta hiperlipídica , Endotélio , Leptina