The metabolic syndrome — a neuroendocrine disorder?

Björntorp, Per; Rosmond, Roland

doi:10.1017/s0007114500000957

Cited by 247 publications

(180 citation statements)

References 26 publications

(20 reference statements)

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“…Em humanos, a obesidade parece ser seguida de vários sinais de disfunções hipotalâmicas similares aos observados em roedores, mas usualmente em menor grau (9). De fato, já foi demonstrado que a obesidade é caracterizada por uma produção aumentada de cortisol, combinada a uma elevada taxa de turnover, a qual resulta num cortisol circulante normal e, freqüentemente, em níveis baixos pela manhã (13 (17).…”

Section: A Síndrome Metabólica E O Eixo Adenocorticotróficounclassified

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Aspectos neuroendócrinos da síndrome metabólica

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Guedes

2003

Arq Bras Endocrinol Metab

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Arq Bras Endocrinol Metab vol 47 nº 4 Agosto 2003 410 RESUMOA síndrome metabólica (SM) é caracterizada por alterações no metabolismo glicídico, obesidade, hipertensão e dislipidemia. Estas alterações metabólicas interrelacionam-se com diversos eixos endócrinos controlados pelo hipotálamo e pela hipófise. A obesidade central parece relacionar-se a uma hiperativação do eixo hipotálamo-hipófise-adrenal, como também do sistema nervoso simpático, que poderia levar a um quadro de hipercortisolismo sub-clínico e hipertensão arterial. A SM é também um estado de hipo-somatotropismo relativo relacionado à gordura visceral. Além disso, níveis elevados de ácidos graxos livres e a hiperinsulinemia, secundários à resistência insulínica, estão relacionadas a um bloqueio do eixo somatotrófico. Em homens, a SM relaciona-se a um hipogonadismo tanto por diminuição de gonadotrofinas como por inibição direta da produção de testosterona. Já nas mulheres, existe um excesso de produção de androgênios, principalmente relacionado à hiperinsulinemia, aumento da atividade da aromatase e da liberação de LH. Desta forma, a SM é um estado relacionado a importantes modificações nos mecanismos de feedback responsáveis pelo correto funcionamento dos eixos neuroendócrinos. The metabolic syndrome (MS) is characterized by alterations in carbohydrate metabolism, obesity, hypertension and dislipidemia. These metabolic alterations interfere with some endocrine axes controlled by the hypothalamus and the pituitary. Central obesity might be associated to a state of subclinical hypercortisolism and hypertension, secondary to an activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. MS is also a state of relative hyposomatotropism, probably related to visceral fat. Furthermore, high levels of free fat acids and hyperinsulinemia, secondary to insulin resistance, can contribute to a blockade of the somatotropic axis. In men, MS is related to a state of hypogonadism caused by impairment in gonadotropin secretion and testosterone production. Women exhibit excessive androgen production, secondary to hyperinsulinemia, high levels of LH and to an increase in aromatase activity. In summary, MS is a condition linked to important modifications in feedback mechanisms responsible for the correct functioning of the neuroendocrine axes.

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Section: A Síndrome Metabólica E O Eixo Adenocorticotróficounclassified

“…A dosagem do cortisol salivar se enquadra nas necessidades de avaliação do eixo HHA, pois possibilita a coleta de amostras repetidas durante o dia, sob diversas circunstâncias, além de estar medindo o cortisol livre circulante (13,18). Utilizando esta técnica em homens obesos, Rosmond e cols.…”

Section: A Síndrome Metabólica E O Eixo Adenocorticotróficounclassified

Aspectos neuroendócrinos da síndrome metabólica

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2003

Arq Bras Endocrinol Metab

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“…[8][9][10] The determinants of abdominal obesity appear to be more complex than those for overall obesity. Hormonal and other neuroendocrine actions have been shown to affect the abdominal adipocytes differently than the peripheral adipocytes.…”

Section: Introductionmentioning

confidence: 99%

“…Hormonal and other neuroendocrine actions have been shown to affect the abdominal adipocytes differently than the peripheral adipocytes. 10 There also appear to be genetic effects that differ from those of overall obesity. 11,12 The determinants of hypertension may include genetic factors, overweight and obesity (particularly abdominal obesity), dietary salt intake, and social and psychological factors.…”

Section: Introductionmentioning

confidence: 99%

Genetic and environmental influences on body fat and blood pressure in African-American adult twins

et al. 2005

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Objective: African Americans have a particularly high prevalence of excessive body fat and high blood pressure. Genetic and environmental influences may be implicated for both of these risk factors. We investigated the potential for common genetic and environmental influences on body fat (waist circumference (WC), body mass index (BMI)) and blood pressure measures (systolic and diastolic pressure (SBP, DBP)) among African-American male and female subjects. Research methods and procedures: Measurements were taken as part of the Carolina African-American Twin Study of Aging (CAATSA). The CAATSA sample contains 217 same-sex African-American male and female twins with average age of 47 years. This analysis included 39 monozygotic male pairs (MZ), 43 dizygotic male pairs (DZ); 63 MZ female pairs, and 72 DZ female pairs. Maximum likelihood quantitative genetic analyses were used. Results: The total genetic variance for SBP was 22% in male subjects and 40.1% in female subjects. Of this total variance, 3.1% was in common with BMI in male subjects and 6% was in common with BMI in female subjects. After controlling for the effects of BMI, WC had less than 1% of its variance in common with SBP in male and female subjects. For DBP, the total genetic variance was 16.9% in male and 38.7% in female subjects. Of this total variance 6.1% was in common with BMI in male subjects and 3.7% was in common in female subjects. Again, WC had less than 1% of its genetic variance in common with DBP in both male and female subjects. The environmental variance common among these measures was also very small. The remaining variance was primarily accounted for by genetic and environmental effects unique to each measure as well as age. Discussion: Based on the very small common genetic variance for BMI, SBP, and DBP as well as WC and the blood pressure measures, our results suggest that searching for common genes among these measures may be inconclusive.

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“…Chez les patients obèses, la sécrétion du cortisol et sa clairance sont augmentées, avec pour conséquence des concentrations circulantes normales, voire diminuées [5]. L'augmentation de la sécrétion du cortisol peut être expliquée soit par une stimulation chronique des facteurs centraux de régulation [6], soit par une diminution du rétrocontrôle négatif des glucocorticoïdes [7]. L'augmentation de la clairance du cortisol est probablement consécutive à une augmentation de l'activité 5α-réductase et à une diminution de l'activité 11β-déshydro-génase dans le foie [8].…”

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