Browsing by Author "Castro, Uberdan Guilherme Mendes de"

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    Age-dependent effect of high-fructose and high-fat diets on lipid metabolism and lipid accumulation in liver and kidney of rats.
    (2013) Castro, Uberdan Guilherme Mendes de; Santos, Robson Augusto Souza dos; Silva, Marcelo Eustáquio; Lima, Wanderson Geraldo de; Santos, Maria José Campagnole dos; Alzamora, Andréia Carvalho
    Background: The metabolic syndrome (MS) is characterized by variable coexistence of metabolic and pathophysiological alterations which are important risk factors for developing of type II diabetes and/or cardiovascular diseases. Increased of MS patients in worldwide has stimulated the development of experimental models. However, it is still challenging to find an dietetic model that most closely approximates human MS and, in addition, is not yet fully established the effect of different diets of MS in lipid metabolism in rats of different ages. The aim of this study was to evaluate the effect of different diets of MS in lipid metabolism and ectopic fat deposition and define the most appropriate diet for inducing the characteristic disturbances of the human MS in rats of different ages. Methods: Young (4 weeks old) and adult rats (12 weeks old) were given a high-fat (FAT) or high-fructose diet (FRU) for 13 weeks and biochemical, physiological, histological and biometric parameters were evaluated. Results: In young rats, the FAT diet induced increased mean blood pressure (MAP) and heart rate (HR), body weight after 6 to 10 weeks, and in the 13th week, increased the liver, mesenteric, retroperitoneal and epididymal fat weights,fasting glucose, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and reduced HDL cholesterol; and also induced non-alcoholic fatty liver disease (NAFLD) and renal inflammatory infiltrates. In adult rats, the FRU diet induced transient elevations of MAP and HR in the 6th week, and, at 13 weeks, increased fasting glucose, triglycerides, total cholesterol, AST and ALT; increased liver, kidneys and retroperitoneal fat weights; and induced macrovesicular and microvesicular NAFLD, the presence of fat cells in the kidney, glomerular sclerosis, and liver and kidney inflammation. Additionally, the FAT and FRU diets induced, respectively, increases in liver glycogen in adults and young rats. Conclusions: Our data show that FRU diet in adult rats causes biggest change on metabolism of serum lipids and lipid accumulation in liver and kidney, while the FAT diet in young rats induces elevation of MAP and HR and higher increased visceral lipid stores, constituting the best nutritional interventions to induce MS in rats.
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    Angiotensin-(1-7) antagonist, A-779, microinjection into the caudal ventrolateral medulla of renovascular hypertensive rats restores baroreflex bradycardia.
    (2009) Cangussu, Luiza Michelle; Castro, Uberdan Guilherme Mendes de; Machado, Raquel do Pilar; Silva, Marcelo Eustáquio; Ferreira, Patrícia Maria; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia Carvalho
    In the present study we evaluated the effect of caudal ventrolateral medulla (CVLM) microinjection of the main angiotensin (Ang) peptides, Ang II and Ang-(1-7), and their selective antagonists on baseline arterial pressure (AP) and on baroreceptor-mediated bradycardia in renovascular hypertensive rats (2K1C). Microinjection of Ang II and Ang-(1-7) into the CVLM of 2K1C rats produced similar decrease in AP as observed in Sham rats. In both Sham and 2K1C, the hypotensive effect of Ang II and Ang-(1-7) at the CVLM was blocked, for up to 30 min, by previous CVLM microinjection of the Ang II AT 1 receptor antagonist, Losartan, and Ang-(1-7) Mas antagonist, A-779, respectively. As expected, the baroreflex bradycardia was lower in 2K1C in comparison to Sham rats. CVLM microinjection of A-779 improved the sensitivity of baroreflex bradycardia in 2K1C hypertensive rats. In contrast, Losartan had no effect on the baroreflex bradycardia in either 2K1C or Sham rats. These results suggest that Ang-(1-7) at the CVLM may contribute to the low sensitivity of the baroreflex control of heart rate in renovascular hypertensive rats
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    Antioxidant effects of oral Ang-(1-7) restore insulin pathway and RAS components ameliorating cardiometabolic disturbances in rats.
    (2019) Figueiredo, Vivian Paulino; Barbosa, Maria Andréa; Castro, Uberdan Guilherme Mendes de; Zacarias, Aline Cruz; Bezerra, Frank Silva; Cota, Renata Guerra de Sá; Lima, Wanderson Geraldo de; Santos, Robson Augusto Souza dos; Alzamora, Andréia Carvalho
    In prevention studies of metabolic syndrome (MetS), Ang-(1-7) has shown to improve the insulin signaling. We evaluated the HPβCD/Ang-(1-7) treatment on lipid metabolism, renin-angiotensin system (RAS) components, oxidative stress, and insulin pathway in the liver and gastrocnemius muscle and hepatic steatosis in rats with established MetS. After 7 weeks of high-fat (FAT) or control (CT) diets, rats were treated with cyclodextrin (HPβCD) or HPβCD/Ang-(1-7) in the last 6 weeks. FATHPβCD/ empty rats showed increased adiposity index and body mass, gene expression of ACE/ANG II/AT1R axis, and oxidative stress. These results were accompanied by imbalances in the insulin pathway, worsening of liver function, hyperglycemia, and dyslipidemia. Oral HPβCD/Ang-(1-7) treatment decreased ACE and AT1R, increased ACE2 gene expression. in the liver, and restored thiobarbituric acid reactive substances (TBARS), catalase (CAT), superoxide dismutase (SOD), insulin receptor substrate (Irs-1), glucose transporter type 4 (GLUT4), and serine/threonine kinase 2 (AKT-2) gene expression in the liver and gastrocnemius muscle improving hepatic function, cholesterol levels, and hyperglycemia in MetS rats. Overall, HPβCD/Ang-(1-7) treatment restored the RAS components, oxidative stress, and insulin signaling in the liver and gastrocnemius muscle contributing to the establishment of blood glucose and lipid homeostasis in MetS rats.
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    Cardiac and renal effects induced by different exercise workloads in renovascular hypertensive rats.
    (2011) Soares, Everton Rocha; Lima, Wanderson Geraldo de; Machado, Raquel do Pilar; Carneiro, Cláudia Martins; Silva, Marcelo Eustáquio; Rodrigues, Míriam Carmo; Castro, Uberdan Guilherme Mendes de; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia Carvalho
    We examined the effect of exercise training (Ex) without (Ex 0%) or with a 3% workload (Ex 3%) on different cardiac and renal parameters in renovascular hypertensive (2K1C) male Fisher rats weighing 150-200 g. Ex was performed for 5 weeks, 1 h/day, 5 days/week. Ex 0% or Ex 3% induced similar attenuation of baseline mean arterial pressure (MAP, 119 ± 5 mmHg in 2K1C Ex 0%, N = 6, and 118 ± 5 mmHg in 2K1C Ex 3%, N = 11, vs 99 ± 4 mmHg in sham sedentary (Sham Sed) controls, N = 10) and heart rate (HR, bpm) (383 ± 13 in 2K1C Ex 0%, N = 6, and 390 ± 14 in 2K1C Ex 3%, N = 11 vs 371 ± 11 in Sham Sed, N = 10). Ex 0%, but not Ex 3%, improved baroreflex bradycardia (0.26 ± 0.06 ms/mmHg, N = 6, vs 0.09 ± 0.03 ms/mmHg in 2K1C Sed, N = 11). Morphometric evaluation suggested concentric left ventricle hypertrophy in sedentary 2K1C rats. Ex 0% prevented concentric cardiac hypertrophy, increased cardiomyocyte diameter and decreased cardiac vasculature thickness in 2K1C rats. In contrast, in 2K1C, Ex 3% reduced the concentric remodeling and prevented the increase in cardiac vasculature wall thickness, decreased the cardiomyocyte diameter and increased collagen deposition. Renal morphometric analysis showed that Ex 3% induced an increase in vasculature wall thickness and collagen deposition in the left kidney of 2K1C rats. These data suggest that Ex 0% has more beneficial effects than Ex 3% in renovascular hypertensive rats.
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    Efeito do óxido nítrico na regulação de parâmetros cardiovasculares pela CVLM em ratos com hipertensão renovascular 2R1C”.
    (Programa de Pós-Graduação em Ciências Biológicas. Núcleo de Pesquisas em Ciências Biológicas, Pró-Reitoria de Pesquisa e Pós Graduação, Universidade Federal de Ouro Preto, 2010) Castro, Uberdan Guilherme Mendes de; Alzamora, Andréia Carvalho
    A hipertensão arterial pode ocorrer devido à hiperatividade de neurônios do bulbo ventrolateral rostral (RVLM) (Chan e cols., 1991; Boone e McMillen, 1994; Suzuki e cols., 1994; Minson e cols., 1996) e/ou devido a um tônus reduzido dos neurônios GABAérgicos do bulbo ventrolateral caudal (CVLM) que se projetam para a RVLM. (Smith e Barron, 1990b; a; Colombari e cols., 2001). Além disso, foi observado que durante a hipertensão ocorre uma elevação dos níveis de óxido nítrico (NO) na CVLM. No entanto, não existem estudos conclusivos acerca do papel do NO na CVLM durante o desenvolvimento e/ou manutenção desta patologia. Diante dessas considerações, o objetivo do presente estudo foi avaliar o efeito do NO na CVLM sobre a pressão arterial média (PAM), freqüência cardíaca (FC) e sensibilidade da bradicardia reflexa em animais com hipertensão renovascular 2R1C. Ratos fisher (150 a 200g) foram anestesiados com uma mistura de quetamina (50 mg/Kg, i.p.) e xilasina (5 mg/Kg, i.p.) para realização da cirurgia para indução da hipertensão renovascular (2R1C) ou fictícia (SHAM). Após 30 dias, os animais foram anestesiados com uretana (1,2g/kg, i.p), posicionados em um aparelho estereotáxico para exposição do bulbo e instrumentados para registro da PAM e FC. A sensibilidade da bradicardia reflexa foi avaliada através da injeção de doses crescentes de fenilefrina (i.v.). Ao final dos experimentos os animais foram sacrificados, os rins e coração pesados e o cérebro submetido à análise histológica. Os animais 2R1C apresentam menor peso relativo do rim esquerdo (clipado) (0,28 ± 0,02g, n=11), maior peso relativo do rim contralateral (0,52 ± 0,05g, n=11), maior peso relativo do coração (0,41 ± 0,02g, n=11) e ventrículo esquerdo (0,31± 0,02, n=11) e aumento da PAM (142 ± 3 mmHg, n=36) em comparação aos ratos SHAM (0,34 ± 0,01g; 0,35 ± 0,01g; 0,30 ± 0,01g; 0,20 ± 0,01g, n=11 e 106 ± 2 mmHg, n=42 respectivamente) A microinjeção de nitro-L-arginina-metil-ester, L-NAME (inibidor não seletivo do NO, 10nmol) na CVLM, produziu uma queda na PAM e na FC em animais 2R1C (-17 ± 3 mmHg e -29 ± 8 bpm, n=7, respectivamente) e em animais SHAM (-17 ± 3 mmHg e -39 ± 15 bpm, n=6, respectivamente). Já a microinjeção de L-ARGININA (precursor do NO, 50nmol) na CVLM produziu uma elevação na PAM de ratos 2R1C (11 ± 3 mmHg, n=6) e SHAM (11 ± 1 mmHg, n=11), além de alterações variadas sobre a FC em ambos os grupos (-12 ± 6 bpm, n=6, grupo SHAM; 8 ± 8 bpm, n=11, grupo 2R1C). IX Em animais 2R1C, observamos que o tempo de duração da bradicardia produzida pela microinjeção de L-NAME na CVLM foi inferior (11 ± 1 min, n=11) ao tempo de duração em animais SHAM (23 ± 3 min, n=6). Adicionalmente, a duração do efeito hipertensor da microinjeção de L-ARGININA em animais 2R1C (26 ± 7 min, n=4) e das alterações variadas produzidas pela mesma sobre a FC (32 ± 5 min, n=6) foram superiores, quando comparado aos ratos SHAM (10 ± 2 min e 14 ± 4 min, n=7-10, respectivamente). Os efeitos cardiovasculares produzidos pela microinjeção da LARGININA na CVLM foram abolidos pela microinjeção prévia de L-NAME na CVLM de ratos SHAM e 2R1C. A bradicardia reflexa dos animais 2R1C foi menor (0,11 ± 0,02 ms/mmHg, n=17) quando comparada aos ratos SHAM (0,42 ± 0,08 ms/mmHg, n=14). A microinjeção do LNAME na CVLM produziu um aumento da sensibilidade da bradicardia reflexa em animais 2R1C (0,18 ± 0,04 ms/mmHg, n=8) em comparação com a sensibilidade da bradicardia reflexa antes da microinjeção do L-NAME (0,07 ± 0,01 ms/mmHg, n=10). Já a microinjeção de L-ARGININA na CVLM produziu uma redução da sensibilidade da bradicardia reflexa nos ratos SHAM (0,29 ± 0,03 ms/mmHg, n=6) em relação à sensibilidade da bradicardia reflexa antes da microinjeção de L- ARGININA (de 0,52 ± 0,08 ms/mmHg, n=6). Os resultados do presente estudo reforçam a idéia de que o NO esteja aumentado na CVLM durante a hipertensão arterial. Esses níveis elevados de NO parecem ter um papel inibitório sobre os neurônios da CVLM, contribuindo para o desenvolvimento e/ou manutenção da hipertensão renovascular e para a baixa sensibilidade do barorreflexo que ocorre nesta patologia.
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    Nitric oxide at the CVLM is involved in the attenuation of the reflex bradycardia in renovascular hypertensive rats.
    (2012) Castro, Uberdan Guilherme Mendes de; Souza, Graziele Galdino de; Machado, Raquel do Pilar; Isoldi, Mauro César; Silva, Marcelo Eustáquio; Nadu, Ana Paula; Souza, Luiz Eduardo de; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia Carvalho
    Hypertension is associated to an increase in central oxidative stress and an attenuation of the baroreflex control of arterial pressure. The present study evaluated the effect of alterations in the levels of nitric oxide (NO) and superoxide anion in the caudal ventrolateral medulla (CVLM), a key area of the brainstem for the baroreflex control of arterial pressure, in renovascular hypertensive rats (2K1C). Baseline mean arterial pressure (MAP), heart rate (HR), and reflex bradycardia were evaluated 30 days after renal artery occlusion in anesthetized (urethane, 1.2 g/kg, i.p.) 2K1C or normotensive (SHAM) rats. The MAP, HR, and baroreflex control of HR were evaluated before and after CVLM microinjections of the non-selective NOS inhibitor L-NAME (10 nmol), the NO precursor L-ARG (50 nmol), or the antioxidant ascorbic acid, Vit C (10 nmol). In both 2K1C and SHAM animals, CVLM microinjection of L-NAME produced a decrease in MAP, whereas L-ARG induced a significant increase in MAP. However, microinjection of Vit C into the CVLM produced a decrease in MAP and HR only in 2K1C and not in SHAM rats. Cardiovascular effects produced by microinjection of L-ARG into the CVLM were abolished by prior microinjection of L-NAME in the CVLM of 2K1C and SHAM rats. Microinjection of L-NAME into the CVLM increased the sensitivity of reflex bradycardia in 2K1C animals. In contrast, the CVLM microinjection of L-ARG reduced reflex bradycardia only in SHAM rats. Vit C in the CVLM did not change reflex bradycardia in either 2K1C or in SHAM rats. These results suggest that increased oxidative stress in the CVLM during hypertension contributes to the reduced baroreflex sensitivity and to maintain hypertension in the 2K1C model.
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    Oral Ang-(1-7) treatment improves white adipose tissue remodeling and hypertension in rats with metabolic syndrome.
    (2019) Barbosa, Maria Andréa; Sousa, Graziele Galdino de; Castro, Uberdan Guilherme Mendes de; Carneiro, Cláudia Martins; Figueiredo, Vivian Paulino; Cota, Renata Guerra de Sá; Santos, Robson Augusto Souza dos; Alzamora, Andréia Carvalho
    Objective: Angiotensin (Ang)-(1-7) has preventive effects on metabolic syndrome (MetS). The aim of this study was to evaluate the therapeutic effect of oral Ang-(1-7) on mean arterial pressure (MAP), insulin resistance (IR), inflammatory process, and remodeling of white adipose tissue (WAT) in rats with establishedMetS. Methods: Rats were subjected to control (CT; AIN-93M) or high-fat (HF) diets for 13 wk to induce MetS and treated with Ang-(1-7) or vehicle (V) for the last 6 wk. At the end of 13 wk, MAP, biochemical and histological parameters, and uncoupling protein (UCP) and inflammatory gene expression were determined by quantitative reverse transcription polymerase chain reaction. Results: HF-V rats showed increased visceral fat deposition, inflammatory cytokine expression, hyperplasia, and hypertrophy in retroperitoneal (WAT) and brown adipose tissue (BAT). Additionally, the gastrocnemius muscle reduced UCP-3 and increased the UCP-1 expression in BAT. HF-V also elevated levels of plasma insulin, glucose, homeostatic model assessment (HOMA) of IR and HOMA-b, and increased body mass, adiposity, and MAP. Ang-(1-7) treatment in rats with MetS [HF-Ang-(1-7)] reduced WAT area, number of adipocytes, and expression of proinflammatory adipokines in WAT and BAT and increased UCP-3 in gastrocnemius muscle and UCP-1 expression in BAT compared with the HF-V group. These events prevented body mass gain, reduced adiposity, and normalized fasting plasma glucose, insulin levels, HOMA-IR, HOMA-b, and MAP. Conclusion: Data from the present study demonstrated that oral Ang-(1-7) treatment is effective in restoring biochemical parameters and hypertension in established MetS by improving hypertrophy and hyperplasia in WAT and inflammation in adipose tissue, and regulating metabolic processes in the gastrocnemius muscle and BAT.
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    Physical training improves thermogenesis and insulin pathway, and induces remodeling in white and brown adipose tissues.
    (2018) Barbosa, Maria Andréa; Cota, Renata Guerra de Sá; Castro, Uberdan Guilherme Mendes de; Lima, Wanderson Geraldo de; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia Carvalho
    Physical training (PT) has been considered as a treatment in metabolic syndrome (MS), since it induces thermogenic activity in brown (BAT) and white (WAT) adipose tissues. We evaluated the therapeutic effect of PT on activity of WAT and BAT in rats with MS induced by high-fat diet (30% lard) for 13 weeks and submitted, for the last 6 weeks, to swimming or kept sedentary (SED) rats. MS-SED rats compared to control diet (CT-SED) rats showed low physical fitness and high levels of glucose, insulin, homeostasis evaluation of insulin resistance (HOMA-IR), homeostasis evaluation of the functional capacity of β-cells (HOMA-β), and blood pressure. The gastrocnemius muscle decreased in peroxisome proliferator-activated receptor gamma coactivator 1-alpha and beta (PGC-1α, PGC-1β), and uncoupled protein 2 and 3 (UCP2 and UCP3) expressions. Both WAT and BAT increased in the adipocyte area and decreased in blood vessels and fibroblast numbers. WAT increased in expression of pro-inflammatory adipokines and decreased in anti-inflammatory adipokine and adiponectin. WAT and gastrocnemius showed impairment in the insulin signaling pathway. In response to PT, MS rats showed increased physical fitness and restoration of certain biometric and biochemical parameters and blood pressure. PT also induced thermogenic modulations in skeletal muscle, WAT and BAT, and also improved the insulin signaling pathway. Collectively, PT was effective in treating MS by inducing improvement in physical fitness and interchangeable effects between skeletal muscle, WAT and BAT, suggesting a development of brown-like adipocyte cells.
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    Swimming training induces liver adaptations to oxidative stress and insulin sensitivity in rats submitted to high-fat diet.
    (2017) Zacarias, Aline Cruz; Barbosa, Maria Andréa; Cota, Renata Guerra de Sá; Castro, Uberdan Guilherme Mendes de; Bezerra, Frank Silva; Lima, Wanderson Geraldo de; Cardoso, Leonardo Máximo; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia Carvalho
    Oxidative stress, physical inactivity and high-fat (FAT) diets are associated with hepatic disorders such as metabolic syndrome (MS). The therapeutic effects of physical training (PT) were evaluated in rats with MS induced by FAT diet for 13 weeks, on oxidative stress and insulin signaling in the liver, during the last 6 weeks. FAT-sedentary (SED) rats increased body mass, retroperitoneal fat, mean arterial pressure (MAP) and heart rate (HR), and total cholesterol, serum alanine aminotransferase, glucose and insulin. Livers of FAT-SED rats increased superoxide dismutase activity, thiobarbituric acid-reactive substances, protein carbonyl and oxidized glutathione (GSSG); and decreased catalase activity, reduced glutathione/GSSG ratio, and the mRNA expression of insulin receptor substrate 1 (IRS-1) and serine/threonine kinase 2. FAT-PT rats improved in fitness and reduced their body mass, retroperitoneal fat, and glucose, insulin, total cholesterol, MAP and HR; and their livers increased superoxide dismutase and catalase activities, the reduced glutathione/GSSG ratio and the expression of peroxisome proliferator-activated receptor gamma and insulin receptor compared to FAT-SED rats. These findings indicated adaptive responses to PT by restoring the oxidative balance and insulin signaling in the liver and certain biometric and biochemical parameters as well as MAP in MS rats.
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    Tratamento com hpβcd/ang-(1-7) reverte distúrbios da síndrome metabólica através da redução do processo inflamatório do tecido adiposo, da melhora da via da insulina e do aumento da termogênese adaptativa.
    (2015) Castro, Uberdan Guilherme Mendes de; Alzamora, Andréia Carvalho; Silva, Marcelo Eustáquio; Costa, Daniela Caldeira; Oliveira Júnior, Antônio Ribeiro de; Oliveira, Tânia Toledo de
    O objetivo do presente estudo foi avaliar o potencial terapêutico da formulação oral de Ang-(1-7), a HPβCD/Ang-(1-7), sobre o processo inflamatório do tecido adiposo branco visceral (TAV) e tecido adiposo marrom (TAM), sobre as vias de sinalização intracelular da insulina e sobre a termogênese adaptativa, na reversão de distúrbios metabólicos da síndrome metabólica (SM), induzidos pela dieta hiperlipídica. Ratos recém-desmamados com 4 semanas de idade, foram submetidas à dieta controle AIN-93 (dieta CT) ou à dieta hiperlipídica (dieta SM) por 7 semanas para indução da SM. Após este período, os grupos foram subdivididos em ratos tratados com HPβCD/Ang-(1-7) ou com ciclodextrina vazia (V) por mais 6 semanas. Ao final das 13 semanas de experimento foram realizadas avaliações biométricas, bioquímicas, Elisa e expressões gênicas por qRT-PCR. Os ratos SM-V apresentaram aumento da expressão de citocinas inflamatórias no TAV retroperitoneal e no TAM, redução da expressão do PPARγ2 no fígado, piora da via intracelular da insulina no fígado, no TAV retroperitoneal e no músculo gastrocnêmico, redução na expressão de PGC1-α, PGC1-β, UCP-2 e UCP-3 no gastrocnêmico e aumento da expressão de UCP-1 no TAM. Esses eventos ocorreram simultaneamente com a elevação da glicemia de jejum, da insulina, do HOMA-IR e do HOMA-ß e com o aumento do peso corporal, do índice de adiposidade, do colesterol total, do LDL e da alanina transferase (ALT). O tratamento com HPβCD/Ang-(1-7) reduziu a expressão das adipocinas pró-inflamatórias do TAV e TAM, normalizou a expressão de PPARγ2 no fígado, melhorou a via intracelular da insulina no fígado, no TAB retroperitoneal e no músculo gastrocnêmico e aumentou a expressão de UCP-3 no músculo gastrocnêmico e a expressão de UCP-1 no TAM, quando comparado ao grupo controle CT-V. Esses eventos impediram o aumento do peso corporal, reduziram o índice de adiposidade e os níveis de colesterol total, além de normalizar a glicemia de jejum, os níveis de insulina, o HOMA-IR, o HOMA-ß, e os níveis de ALT. Nossos dados demonstram a eficácia do tratamento com HPβCD-Ang-(1-7) ao mostrar que essa formulação reverte distúrbios metabólicos da SM em ratos, a partir de alterações benéficas teciduais.