The Relation between Fructose-Induced Metabolic Syndrome and Altered Renal Haemodynamic and Excretory Function in the Rat

Abdulla, Mohammed H.; Sattar, M. A.; Johns, Edward J.

doi:10.4061/2011/934659

Cited by 49 publications

(43 citation statements)

References 204 publications

(230 reference statements)

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“…Contrary to the findings of Takatori et al, Brito et al, Abdulla et al and Catena, when consumed in drinking water in rats and hamster, fructose did not cause a significant impairment in glucose tolerance; this is in the same line with the results of the pres ent study [1,7,9,28]. As listed earlier, different admin istration routes and different species of animals may explain the controversy observed [6,21,29].…”

Section: Discussionsupporting

confidence: 78%

Original article High fructose solution induces neuronal loss in the nucleus of the solitary tract of rats

Rafati¹,

Anvari²,

Noorafshan³

2013

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Section: Discussionsupporting

confidence: 78%

Original article High fructose solution induces neuronal loss in the nucleus of the solitary tract of rats

Rafati¹,

Anvari²,

Noorafshan³

2013

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“…Fructose is considered a lipogenic sugar, leading to increased triglycerides deposition in white adipose tissues, hypertriglyceridemia, proinflammatory state, and increased ectopic fat deposition, especially in the liver and skeletal muscle. [32][33][34] The increased glycemic response curve in FF rats compared with CTL during the glucose tolerance test, along with the increased levels of serum insulinemia and glycemia and increased HOMA-IR index, as well as the reduced hepatic glycogen content, suggest that FF rats present reduced response of insulin-sensitive tissues, a state of insulin resistance. In contrast, FF+A7 rats had all those parameters normalized, suggesting a dramatic beneficial effect of increasing Ang-(1-7) levels in the brain in preventing the development of insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Increasing Angiotensin-(1–7) Levels in the Brain Attenuates Metabolic Syndrome–Related Risks in Fructose-Fed Rats

et al. 2014

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Metabolic syndrome (MetS) is currently recognized as a worldwide health problem, 1,2 and the substantial increase in fructose intake in human diet, especially as high-fructose corn syrup, has been considered a potential factor predisposing humans to MetS. 3,4 MetS is a cluster of different risk factors, such as increase in visceral fat deposition, glucose intolerance, dyslipidemia, and hypertension, which increases the risk of development of cardiovascular and renal diseases and type II diabetes mellitus. 2,5 Recent studies in rodents have shown that the renin-angiotensin system, through the inappropriate overactivity of angiotensin (Ang) II on Ang II type 1 (AT 1 ) receptor especially in the circulation and in the white adipose tissue, plays a pivotal role on the pathogenesis of MetS. [6][7][8] Peripheral blockade of Ang II synthesis or its action on AT 1 receptor attenuates metabolic disorders in obese rodents. [6][7][8] In contrast, the other functional arm of renin-angiotensin system, represented by the actions of Ang-(1-7) on Mas receptor, has been recognized widely as a counter-regulatory axis of Ang II/AT 1 receptor actions.Recent studies have shown that chronic increases in peripheral Ang-(1-7)/Mas receptor activity play a protective role in the regulation of cardiovascular and energy metabolism. Transgenic rats with increased Ang-(1-7) levels in the circulation [TGR(A1-7)3292] are protected against cardiac dysfunction, fibrosis, and hypertension when subjected to deoxycorticosterone (DOCA) acetate-salt model 9 and have enhanced resting glucose and lipid metabolism. 10 Accordingly, Giani et al 11,12 showed that chronic subcutaneous infusion of Ang-(1-7) improved insulin resistance, hypertension, and cardiac remodeling in fructose-fed rats. However, genetic deletion of Mas receptor alters glucose and lipid metabolism and the neural control of blood pressure, inducing a state of MetS. [13][14][15] Taken together, these data provide a clear evidence of a protective role of peripheral Ang-(1-7)/Mas receptor axis in the regulation of cardiovascular system and energy metabolism.Our group showed recently that chronic increase in Ang-(1-7) levels in the brain attenuates DOCA-salt hypertension, and that this effect is related to a dramatic beneficial role Abstract-We evaluated effects of chronic intracerebroventricular infusion of angiotensin (Ang)-(1-7) on cardiovascular and metabolic parameters in fructose-fed (FF) rats. After 6 weeks of fructose intake (10% in drinking water), SpragueDawley rats were subjected to intracerebroventricular infusion of Ang-(1-7) (200 ng/h; FF+A7 group) or 0.9% sterile saline (FF group) for 4 weeks with continued access to fructose. Compared with control rats, FF rats had increased mean arterial pressure and cardiac sympathetic tone with impaired baroreflex sensitivity. FF rats also presented increased circulating triglycerides, leptin, insulin, and glucose with impaired glucose tolerance. Furthermore, relative weights of liver and retroperitoneal adipose tissue were increased...

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“…Os autores agradecem à Fundação de Amparo à Pesquisa do Estado de Alagoas (FAPEAL) pelo auxílio financeiro, concedido sob a forma de bolsa de iniciação científica a Breno T. G. Fonseca e Bianca M. V. Vasconcelos, pelo Programa de Bolsas de Iniciação Científica da Universidade Federal de Alagoas (PIBIC/ UFAL 2015-2016.…”

Section: Agradecimentosunclassified

“…A síndrome metabólica (SMet) é um conjunto de fatores de risco, tais como resistência à insulina, hiperinsulinemia, hipertrigliceridemia, arteriosclerose e hipertensão arterial, que contribuem para aumentar as chances de doenças cardiovasculares, diabetes mellitus tipo 2 e doenças renais (ABDULLA, 2011).…”

Section: Introductionunclassified

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Resposta cardiovascular ao estresse emocional agudo de ratos submetidos à suplementação alimentar rica em frutose

Alves¹,

Vasconcelos²,

Guimarães³

2016

Anais do Congrebio 2016

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RESUMOO estresse é um fator de risco para desenvolvimento de doenças cardiovasculares em seres humanos e diversos estudos têm mostrado que a obesidade induz a uma resposta cardíaca exacerbada a exposição ao estresse. Em adição, o consumo elevado de frutose na atual sociedade, tem se mostrado um fator predisponente ao surgimento da síndrome metabólica, que por sua vez, oferece prejuízos a saúde do coração. Neste contexto, o objetivo deste estudo foi avaliar a capacidade de resposta cardiovascular ao estresse agudo de contenção e outras alterações fisiológicas em uma dieta rica em frutose (CEUA-UFAL 19/ 2015). Para isso, ratos wistar machos (7 semanas de idade) foram submetidos a 10 semanas de dieta rica em frutose (FF) ou água potável (grupo controle -CTL). Foram avaliados: a pressão arterial média (PAM), a frequência cardíaca (FC), a sensibilidade do controle barorreflexo da frequência cardíaca (BRS), a resposta cardiovascular ao estresse agudo de contenção, e o tônus simpático vascular por bloqueio farmacológico (prazosina, 0,1 mg/ kg i.v). Os resultados foram analisados quanto à normalidade e variabilidade da amostragem. Diferenças entre os grupos foram analisadas utilizando o teste t Student (p<0.05). Os ratos FF mostraram um aumento significativo na PAM (FF=129,71 ± 2,0 vs CTL=117,14 ± 1,5 mmHg), e uma tendência ao aumento da FC (FF = 309,86 ± 7,1 vs CTL = 287,29 ± 8,7 bpm; p=0.067) comparado ao CTL. Como esperado, o grupo FF mostrou um prejuízo no BRS (FF = 1.11 ± 0.08 vs CTL=1.62 ± 0.08 ms/mmHg). No que se refere à resposta cardiovascular ao estresse, o grupo FF mostrou uma resposta cardiovascular exacerbada, apresentando maiores variações de PAM (FF = 37,5 ± 4,2 vs CTL = 29,0 ± 3,6 mmHg) e de FC (FF = 150,3 ± 19,5 vs CTL = 79,8 ± 20 bpm) durante e logo após o estresse. Não houve diferença quanto ao tônus simpático vascular (p> 0,05). Conclui-se que a suplementação alimentar crônica rica em frutose, além de promover aumento PAM e FC de repouso, e reduzir a sensibilidade do controle barorreflexo da FC, também contribui para uma resposta cardiovascular exacerbada ao estresse emocional moderado, conferindo a este um potencial fator de risco adicional ao desenvolvimento de doenças cardiovasculares. (FAPEAL). Palavras-chave:Estresse; Síndrome Metabólica; Sistema Nervoso Autônomo. INTRODUÇÃOA síndrome metabólica (SMet) é um conjunto de fatores de risco, tais como resistência à insulina, hiperinsulinemia, hipertrigliceridemia, arteriosclerose e hipertensão arterial, que contribuem para aumentar as chances de doenças cardiovasculares, diabetes mellitus tipo 2 e doenças renais (ABDULLA, 2011).Estudos realizados em humanos e em roedores indicam que o aumento da ingestão em longo prazo de frutose pode estar relacionada com o aparecimento de diferentes alterações cardiovasculares e metabólicas relacionadas à SMet. Esse aumento mundial na ingestão de frutose se deve principalmente a sua maior utilização na indústria alimentícia como xarope de

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The Relation between Fructose-Induced Metabolic Syndrome and Altered Renal Haemodynamic and Excretory Function in the Rat

Cited by 49 publications

References 204 publications

Original article High fructose solution induces neuronal loss in the nucleus of the solitary tract of rats

Original article High fructose solution induces neuronal loss in the nucleus of the solitary tract of rats

Increasing Angiotensin-(1–7) Levels in the Brain Attenuates Metabolic Syndrome–Related Risks in Fructose-Fed Rats

Resposta cardiovascular ao estresse emocional agudo de ratos submetidos à suplementação alimentar rica em frutose

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