Sympathetic overactivity precedes metabolic dysfunction in a fructose model of glucose intolerance in mice
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
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Data(s) |
30/10/2013
30/10/2013
2012
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Resumo |
De Angelis K, Senador DD, Mostarda C, Irigoyen MC, Morris M. Sympathetic overactivity precedes metabolic dysfunction in a fructose model of glucose intolerance in mice. Am J Physiol Regul Integr Comp Physiol 302: R950-R957, 2012. First published February 8, 2012; doi: 10.1152/ajpregu.00450.2011.-Consumption of high levels of fructose in humans and animals leads to metabolic and cardiovascular dysfunction. There are questions as to the role of the autonomic changes in the time course of fructose-induced dysfunction. C57/BL male mice were given tap water or fructose water (100 g/l) to drink for up to 2 mo. Groups were control (C), 15-day fructose (F15), and 60-day fructose (F60). Light-dark patterns of arterial pressure (AP) and heart rate (HR), and their respective variabilities were measured. Plasma glucose, lipids, insulin, leptin, resistin, adiponectin, and glucose tolerance were quantified. Fructose increased systolic AP (SAP) at 15 and 60 days during both light (F15: 123 +/- 2 and F60: 118 +/- 2 mmHg) and dark periods (F15: 136 +/- 4 and F60: 136 +/- 5 mmHg) compared with controls (light: 111 +/- 2 and dark: 117 +/- 2 mmHg). SAP variance (VAR) and the low-frequency component (LF) were increased in F15 (>60% and >80%) and F60 (>170% and >140%) compared with C. Cardiac sympatho-vagal balance was enhanced, while baroreflex function was attenuated in fructose groups. Metabolic parameters were unchanged in F15. However, F60 showed significant increases in plasma glucose (26%), cholesterol (44%), triglycerides (22%), insulin (95%), and leptin (63%), as well as glucose intolerance. LF of SAP was positively correlated with SAP. Plasma leptin was correlated with triglycerides, insulin, and glucose tolerance. Results show that increased sympathetic modulation of vessels and heart preceded metabolic dysfunction in fructose-consuming mice. Data suggest that changes in autonomic modulation may be an initiating mechanism underlying the cluster of symptoms associated with cardiometabolic disease. FAPESP FAPESP [2006/51551-3, 2007/57595-5] CNPq [482520/2009-4, 306011/2010-7, 479766/2011-8] CNPq National Institutes of Health National Institutes of Health [R-01-HL-093567] CNPq-BPQ CNPqBPQ Foundation for the Improvement of Postsecondary Education [Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)] [Process 010405-1] Foundation for the Improvement of Postsecondary Education |
Identificador |
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, BETHESDA, v. 302, n. 8, supl. 1, Part 6, pp. R950-R957, APR, 2012 0363-6119 http://www.producao.usp.br/handle/BDPI/36892 10.1152/ajpregu.00450.2011 |
Idioma(s) |
eng |
Publicador |
AMER PHYSIOLOGICAL SOC BETHESDA |
Relação |
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY |
Direitos |
restrictedAccess Copyright AMER PHYSIOLOGICAL SOC |
Palavras-Chave | #METABOLIC SYNDROME #AUTONOMIC NERVOUS SYSTEM #LEPTIN #INSULIN RESISTANCE #SPECTRAL ANALYSIS #RADIOTELEMETRY #HEART-RATE-VARIABILITY #INSULIN-RESISTANCE #BLOOD-PRESSURE #NERVOUS-SYSTEM #PARASYMPATHETIC DYSFUNCTION #INDUCED HYPERTENSION #RATS #HYPERINSULINEMIA #DISEASE #DIET #PHYSIOLOGY |
Tipo |
article original article publishedVersion |