Catecholamine Metabolism in Primary Anorexia Nervosa

Gross, Howard A.; Lake, C. Raymond; Ebert, M H; Kopin, Irwin J.

doi:10.1210/jcem-49-6-805

Cited by 146 publications

(58 citation statements)

References 24 publications

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“…Diet-induced changes in SNS activity were first described in fasting (1) and sucrose-fed (2) rats in studies utilizing NE turnover techniques to measure sympathetic activity in different organs (9,15 studies have clearly demonstrated that diet affects SNS activity in human subjects as well (7,(16)(17)(18)(19)(20)(21). The effect of carbohydrates, particularly glucose and sucrose, has been studied most intensively; a stimulatory effect on the SNS in rats (2,3,22) and humans (18,19,23,24) is generally recognized.…”

Section: Discussionmentioning

confidence: 99%

Effect of dietary fat on sympathetic nervous system activity in the rat.

Schwartz¹,

Young²,

Landsberg³

1983

J. Clin. Invest.

129

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A B S T R A C T Previous studies from our laboratory have demonstrated that dietary intake affects the sympathetic nervous system (SNS); carbohydrate intake, in particular, has been shown to stimulate sympathetic activity. The present studies were undertaken to characterize the effect of dietary fat on SNS activity in the rat. Sympathetic activity was assessed by measurement of norepinephrine (NE) turnover in heart, interscapular brown adipose tissue (IBAT), and pancreas and by excretion of NE in the urine. When fed a fatenriched diet (50% chow, 50% lard), fractional NE turnover in heart (k) increased from 6.3±0.6% h in ad lib. fed controls to 14.7±1.3% h in the high-fat group (P < 0.001); calculated NE turnover rate increased from 24.5±2.4 ng/heart per h to 36.8±3.5 (P < 0.05). Urinary NE excretion more than doubled after 6 d of the same high fat diet (P < 0.001). Ganglionic blockade produced a greater effect on NE turnover in fat-fed, as compared with chow-fed animals, consistent with increased sympathetic activity in the fat-fed group. When fat absorption was blocked with a bile acid binding resin (cholestyramine), the same high-fat diet did not increase cardiac NE turnover, indicating that fat absorption is required for the stimulatory effect on sympathetic activity. In another series of experiments, in which chow (and hence protein) intake was held constant, the effect of fat and isocaloric sucrose supplements on NE turnover was assessed in heart, IBAT, and pancreas. The caloric value of the supplements was 50, 100, and 335% of the chow in the different experiments. An effect of fat on NE turnover in heart and IBAT was demonstrable at the lowest level of fat supplement. Fat increased pancreatic NE turnover when added in amounts sufficient to double the caloric Presented in part before the American Federation for Clinical Research and published in abstract form (Clin. Res., 1982, 30:247A).Received for publication 29 November 1982 and in re-vised form 14 March 1983. intake. The stimulatory effect of sucrose and fat on NE turnover in heart and IBAT was similar. These experiments demonstrate that fat increases SNS activity in the rat and that the magnitude of the effect is similar to that of sucrose. The results imply that fat may contribute to dietary thermogenesis in this species. INTRODUCTIONStudies from our laboratory have demonstrated that dietary intake exerts an important effect on sympathetic nervous system (SNS)' activity in the rat. Norepinephrine (NE) turnover techniques have shown that fasting suppresses SNS (1), whereas overfeeding sucrose has been shown to stimulate sympathetic activity in heart (2) and other tissues of the rat (3). An important role for carbohydrates in the relationship *between dietary intake and SNS activity has been inferred from data indicating that hypoglycemia (4, 5) and 2-deoxy-D-glucose administration (6) suppress sympathetic activity, whereas hyperinsulinemia, in the absence of hypoglycemia, has a stimulatory effect (7,8) (-50 MCi/ml) with isotonic saline and inje...

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Section: Discussionmentioning

confidence: 99%

Effect of dietary fat on sympathetic nervous system activity in the rat.

Schwartz¹,

Young²,

Landsberg³

1983

J. Clin. Invest.

129

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“…18 Inexiste um consenso se as alterações encontradas nos valores de noradrenalina e seus metabólitos na AN indicam aumento ou diminuição da atividade da noradrenalina nesta doença. [19][20][21] A mesma indefinição existe para a 5-HT e seus metabólitos na AN. As concentrações séricas de 5-HT encontraram-se elevadas.…”

Section: Somáticosunclassified

Etiologia dos transtornos alimentares: aspectos biológicos, psicológicos e sócio-culturais

Morgan

Vecchiatti

Negrão

2002

Rev. Bras. Psiquiatr.

105

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Os transtornos alimentares possuem uma etiologia multifatorial, composta de predisposições genéticas, socioculturais e vulnerabilidades biológicas e psicológicas. Entre os fatores predisponentes, destacam-se a história de transtorno alimentar e (ou) transtorno do humor na família, os padrões de interação presentes no ambiente familiar, o contexto sociocultural, caracterizado pela extrema valorização do corpo magro, disfunções no metabolismo das monoaminas centrais e traços de personalidade. A dieta é o comportamento precursor que geralmente antecede a instalação de um transtorno alimentar. Contudo, a presença isolada da dieta não é suficiente para desencadear o transtorno alimentar, tornando-se necessária uma interação entre os fatores de risco e outros eventos precipitantes. Por último, o curso transitório ou crônico de um transtorno alimentar está relacionado à persistência de distorções cognitivas, à ocorrência de eventos vitais significativos e a alterações secundárias ao estado de desnutrição. Resumo Descritores Abstract Keywords IntroduçãoOs transtornos alimentares (TA) têm uma etiologia multifatorial, ou seja, são determinados por uma diversidade de fatores que interagem entre si de modo complexo, para produzir e, muitas vezes, perpetuar a doença. Classicamente, distinguem-se os fatores predisponentes, precipitantes e os mantenedores dos TA.

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“…Fasting induced suppression of sympathetic activity and NE turnover was decreased in rats (Young and Landsberg, 1977). In patients with anorexia nervosa, blood pressure and pulse rate, plasma NE and 24 h urinary excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid were reduced during the emaciation phase (Gross et al, 1979). Although the reduction of urinary MHPG, a major metabolite of brain NE, might be related to psychotic depression associated with this disorder (Halmi et al, 1979), most of these abnormalities in CA metabolism were thought to be caused by starvation.…”

Section: Resultsmentioning

confidence: 99%