Andre Brooking Negrao

Dr. Andre Brooking Negrao


Research Focus & Metrics

Academic Career Length

33Years (1994-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 1997 in Nature Medicine
Verified
Journal Article
Closed access
JLJulio Licinio
Julio Licinio
CMChristos Mantzoros
Christos Mantzoros
ANAndre Brooking Negrao
Andre Brooking Negrao
GCGiovanni Cizza
Giovanni Cizza
MWMa-Li Wong
Ma-Li Wong
PGPhilip W. Gold
Philip W. Gold

3 March 1998 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
PDF file
JLJulio Licinio
Julio Licinio
ANAndre Brooking Negrao
Andre Brooking Negrao
CMChristos Mantzoros
Christos Mantzoros
VKVirginia Kaklamani
Virginia Kaklamani
MWMa-Li Wong
Ma-Li Wong
PGPhilip W. Gold
Philip W. Gold
Leptin, an adipocyte hormone, is a trophic factor for the reproductive system; however, it is still unknown whether there is a dynamic relation between fluctuations in circulating leptin and hypothalamic—pituitary–ovarian (HPO) axis hormones. To test the hypothesis that fluctuations in plasma leptin concentrations are related to the levels of luteinizing hormone (LH) and estradiol, we sampled plasma from six healthy women every 7 min for 24 h during days 8–11 of the menstrual cycle. Cross-correlation analysis throughout the 24-h cycle revealed a relation between release patterns of leptin and LH, with a lag of 42–84 min but no significant cross-correlation between LH and estradiol. The ultradian fluctuations in leptin levels showed pattern synchrony with those of both LH and estradiol as determined by cross-approximate entropy (cross-ApEn). At night, as leptin levels rose to their peak, the pulsatility profiles of LH changed significantly and became synchronous with those of leptin. LH pulses were fewer, of longer duration, higher amplitude, and larger area than during the day. Moreover, the synchronicity of LH and leptin occurred late at night, at which time estradiol and leptin also exhibited significantly stronger pattern coupling than during the day. We propose that leptin may regulate the minute-to-minute oscillations in the levels of LH and estradiol, and that the nocturnal rise in leptin may determine the change in nocturnal LH profile in the mid-to-late follicular phase that precedes ovulation. This may explain the disruption of hypothalamic—pituitary–ovarian function that is characteristic of states of low leptin release, such as anorexia nervosa and cachexia.

1 August 1998 in American Journal of Psychiatry
Verified
Journal Article
Closed access
FAFernando R. Asbahr
Fernando R. Asbahr
ANAndre Brooking Negrao
Andre Brooking Negrao
VGValentim Gentil
Valentim Gentil
DZDirce M.T. Zanetta
Dirce M.T. Zanetta
JPJosé A. da Paz
José A. da Paz
MKMaria H. Kiss
Maria H. Kiss

1 April 2000 in Biomedicine & Pharmacotherapy
Verified
Journal Article
Closed access
ANAndre Brooking Negrao
Andre Brooking Negrao
PDPatricia A. Deuster
Patricia A. Deuster
PGP.W. Gold
P.W. Gold
ASA. Singh
A. Singh
GCG.P. Chrousos
G.P. Chrousos

1 June 2002 in Molecular Psychiatry
Verified
Journal Article
Closed access
KGK E Gabry
K E Gabry
GCG P Chrousos
G P Chrousos
KRK C Rice
K C Rice
RMR M Mostafa
R M Mostafa
ESE Sternberg
E Sternberg
PGP W Gold
P W Gold

1 December 2002 in Brazilian Journal of Psychiatry
Verified
Journal Article
Open access
PDF file
CMChristina M Morgan
Christina M Morgan
IVIlka Ramalho Vecchiatti
Ilka Ramalho Vecchiatti
ANAndre Brooking Negrao
Andre Brooking Negrao
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.