Cafeteria Diet Increases Fat Mass and Chronically Elevates Lumbar Sympathetic Nerve Activity in Rats

Muntzel, Martin S.; Al-Naimi, Omar Ali S.; Barclay, Alicia; Ajasin, David

doi:10.1161/hypertensionaha.112.194886

Cited by 52 publications

(51 citation statements)

References 38 publications

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“…2 Increases in brown and white adipose tissue (but not body weight) were accompanied by increases in plasma leptin (but not glucose) concentration and heart rate; however, mean arterial pressure was not significantly changed compared with control rats. Increases in lumbar sympathetic nerve activity became significant at day 12.…”

Section: Obesity-related Hypertensionmentioning

confidence: 89%

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Sympathetic Nervous System and Hypertension

2013

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With the development and implementation of device-based therapeutic interventions to decrease renal and systemic nerve activity in patients with resistant hypertension, there has been an increase in research dealing with the role of the sympathetic nervous system in hypertension. These interventions have produced substantial decreases in blood pressure in patients wherein pharmacological treatments, including agents which inhibit the effects of the renin-angiotensin-aldosterone system, have failed serves to confirm and reassert the essential role of the sympathetic nervous system in hypertension. This review will encompass recent publications dealing with the sympathetic nervous system and hypertension, focusing on those recently published in Hypertension. Sympathetic Activation in Animal Models Obesity-Related HypertensionAlthough there has been a debate as to whether sympathetic activation is a cause or consequence of obesity, the studies noted below support the view that it is the obesity that leads to sympathetic activation. The importance of this sympathetic activation for the development of the hypertension is supported by the finding that renal denervation prevents the development of obesity hypertension in the dog.Studies have now focused on the developmental phase of obesity hypertension regarding the renal sympathoexcitation. In rabbits fed high-fat diets, body weight, plasma insulin and leptin concentrations, mean arterial pressure, heart rate, and renal sympathetic nerve activity were all increased after 1 week.1 Mean arterial pressure and body weight continued to increase over 3 weeks of high-fat diet, whereas heart rate and renal sympathetic nerve activity did not change further. Arterial baroreflex control of renal sympathetic nerve activity was attenuated from the first week of the high-fat diet. Excitatory responses to air jet stress diminished over 3 weeks of high-fat diet. Resumption of normal diet normalized glucose, insulin, leptin, and heart rate, but body weight, visceral fat content, mean arterial pressure, and renal sympathetic nerve activity remained elevated. Increased renal sympathetic nerve activity and its impaired baroreflex control, which occur with 1 week of high-fat feeding, seem integral to the rapid development of obesity hypertension. Increased plasma leptin and insulin may contribute to the initiation of hypertension but are not required for maintenance of the hypertension, which is related to the sustained increase in renal sympathetic nerve activity. As the air jet stress response is transduced by hypothalamic neurons, the authors speculate that this site is involved in the maintenance phase of the hypertension with a sustained increase in renal sympathetic nerve activity.The early effects of diet-induced fat accumulation on lumbar sympathetic nerve activity were also examined in rats over 15 days.2 Increases in brown and white adipose tissue (but not body weight) were accompanied by increases in plasma leptin (but not glucose) concentration and heart rate; however, mean a...

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Section: Obesity-related Hypertensionmentioning

confidence: 89%

“…The increase in lumbar sympathetic nerve activity occurred together with an increase in brown and white adipose tissue, whereas body weight was not significantly changed. 2 The…”

Section: Obesity-related Hypertensionmentioning

confidence: 99%

Sympathetic Nervous System and Hypertension

2013

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“…Dados semelhantes também são encontrados em estudos clínicos. 4 O efeito deletério sobre o metabolismo pode ser justificado a partir do modelo experimental, afinal, é sabido que o modelo de dieta hipercalórica, também conhecida como dieta de cafeteria, aumenta a massa de gordura visceral e a atividade simpá-tica dos animais; 29 induz hiperinsulinemia e hiperleptinemia e determina aumento dos marcadores de inflamação e de radicais livres. 30 Nos animais MSG, sabe-se que os níveis aumentados de cortisol decorrentes da lesão hipotalâmica, assim como da leptina, decorrentes do acúmulo de gordura visceral e da insulina, consequente à resistência à insulina, podem determinar aumento da atividade simpática, com maior liberação de catecolaminas na terminação nervosa, facilitando o efluxo simpático central.…”

Section: Discussionunclassified

Efeito do estresse sobre o metabolismo glicídico de camundongos tornados obesos

Gozoli¹,

Zeca

Calzzetta

et al. 2017

Rev. Fac. Ciênc. Méd. Sorocaba

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RESUMOIntrodução: Distúrbios do sono, isoladamente ou em associação a uma dieta rica em calorias, podem determinar alterações metabólicas no sistema nervoso autônomo e no eixo hipotálamo-hipófise-adrenal, os quais podem aumentar a glicemia e produzir intolerância à glicose. O estado de intolerância à glicose geralmente precede o aparecimento de diabetes tipo 2. Objetivo: Este estudo visou avaliar os efeitos da associação da privação de sono paradoxal e dieta hipercalórica sobre o comportamento alimentar e a tolerância à glicose de camundongos. Métodos: Camundongos Swiss foram distribuídos em seis grupos: (1) controle; (2) dieta hipercalórica; (3) privação de sono paradoxal; (4) privação de sono paradoxal + dieta hipercalórica; (5) monoglutamato de sódio (MSG); e (6) privação de sono paradoxal + monoglutamato de sódio (MSG+PSP). Durante as oito semanas de acompanhamento, o consumo alimentar foi avaliado e os camundongos pesados periodicamente. A privação de sono foi realizada semanalmente. Após oito semanas executou-se o teste de tolerância oral à glicose (TTGO) e de sensibilidade à insulina (TTI). Ao final, houve pesagem do coração e da gordura epididimal. Resultados: Houve aumento significante do peso corporal nos camundongos tornados obesos, que se associou com o avanço do conteúdo de gordura visceral. Todos os animais, obesos e com privação de sono paradoxal, tiveram piora no metabolismo de glicose medido pelo TTGO e TTI. Não houve mudança no peso cardíaco. Conclusão: A administração de uma dieta hipercalórica e a privação de sono paradoxal determinam intolerância à glicose e resistência à insulina, que nesse trabalho não foi sinérgico. Palavras-chave: sono REM; obesidade; transtornos do metabolismo de glucose; camundongos. ABSTRACT Introduction: Sleep disorders, alone or in association with a high-calorie diet, may determine metabolic changes in the autonomic nervous system and in the hypothalamic-pituitary-adrenal axis, which may increase glycemia and produce glucose intolerance. The state of glucose intolerance usually precedes the onset of type 2 diabetes. Objective: This study aims to evaluate the effects of the association of paradoxical sleep deprivation and hypercaloric diet on the eating behavior and glucose tolerance of mice. Methods: Swiss mice were distributed into six groups: (1) control; (2) hypercaloric diet; (3) paradoxical sleep deprivation; (4) paradoxical sleep deprivation + hypercaloric diet; (5) monossodium glutamate (PSP); and (6) paradoxical sleep deprivation + monossodium glutamate. During the eight-week follow-up, food consumption was assessed and mice were weighed periodically. Sleep deprivation was performed weekly. After eight weeks, the oral glucose tolerance (TTGO) and insulin sensitivity test (TTI) were performed. At the end, heart and epididymal fat were weighed. Results: There was a significant increase in body weight in obese mice, which was associated with increased visceral fat content. All animals, obese and PSP, showed worsening in the parameters that measured the glucose...

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“…However, body weight, coronary flow to heart weight ratio and capillary to muscle fiber ratio were affected by CD and this CD-mediated effect regarding these parameters could be inhibited by Ang (1-7). First, the lack of cardiovascular effect of CD needs discussion: Others have described the development of hypertension following CD (e.g., Coatmellec-Taglioni et al, 2000;Muntzel et al, 2012;Steiner et al, 2013) and attributed this to increased sympathetic activity (Muntzel et al, 2012) or to the RAAS system (Miesel et al, 2010;Müller-Fielitz et al, 2014). Regarding the cafeteria diet, the authors used 2-20 weeks protocols, so that our protocol seems comparable.…”

Section: Discussionmentioning

confidence: 99%

Effect of Angiotensin (1-7) on Heart Function in an Experimental Rat Model of Obesity

Blanke¹,

Schlegel²,

Salameh³

et al. 2016

Thorac cardiovasc Surg

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Aim: Obesity is a risk factor for the development of cardiovascular diseases. Recently it was shown that overexpression of the Mas-receptor antagonist angiotensin(1-7) could prevent from diet-induced obesity. However, it remained unclear whether diet-induced obesity and angiotensin(1-7) overexpression might also have effects on the cardiovascular system in these rats.Methods: Twenty three male Sprague Dawley rats were fed with standard chow (SD+chow, n = 5) or a cafeteria diet (SD+CD, n = 6) for 5 months. To investigate the effect of angiotensin(1-7) transgenic rats, expressing an angiotensin(1-7)-producing fusion protein in testis were used. These transgenic rats also received a 5 month's feeding period with either chow (TGR+chow, n = 6) or cafeteria diet (TGR+CD, n = 6), respectively. Hemodynamic measurements (pressure-volume loops) were carried out to assess cardiac function and blood pressure. Subsequently, hearts were explanted and investigated according to the Langendorff technique. Furthermore, cardiac remodeling in these animals was investigated histologically.Results: After 5 months cafeteria diet feeding rats showed a significantly increased body weight, which could be prevented in transgenic rats. However, there was no effect on cardiac performance after cafeteria diet in non-transgenic and transgenic rats. Moreover, overexpression of angiotensin(1-7) deteriorated cardiac contractility as indicated by impaired dp/dt. Furthermore, histological analysis revealed that cafeteria diet led to myocardial fibrosis in both, control and transgenic rats and this was not inhibited by an overproduction of angiotensin(1-7). Conclusion:These results indicate that an overexpression of circulating angiotensin(1-7) prevents a cafeteria diet-induced increase in body weight, but does not affect cardiac performance in this experimental rat model of obesity. Furthermore, overexpression of angiotensin(1-7) alone resulted in an impairment of cardiac function.

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Cafeteria Diet Increases Fat Mass and Chronically Elevates Lumbar Sympathetic Nerve Activity in Rats

Cited by 52 publications

References 38 publications

Sympathetic Nervous System and Hypertension

Sympathetic Nervous System and Hypertension

Efeito do estresse sobre o metabolismo glicídico de camundongos tornados obesos

Effect of Angiotensin (1-7) on Heart Function in an Experimental Rat Model of Obesity

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