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Dynamics of Leptin and Endocrine Function

3 marzo 2008 aggiornato da: National Institute of Mental Health (NIMH)

This is a study investigating the hormones and substances important to the stress response. The hormone that is most directly responsible for stress response is called corticotropin-releasing hormone (CRH). CRH is produced in the hypothalamus of the brain and causes the pituitary gland to produce another hormone called ACTH. The hormone ACTH then acts on the adrenal glands causing them to produce the hormone cortisol.

Unfortunately, CRH levels are unable to be measured in simple blood samples. However, substances like cortisol and leptin can provide information as to the activity of the hypothalamus.

The hormone leptin is associated with the regulation of body weight and the normal maintenance of bodily functions (homeostasis). It is found in fat cell (adipocyes) and communicates the nutritional status of the body to the brain (central nervous system). Research using animals has shown that defects in the communication between leptin and the brain causes obesity (the state of being overweight). It has also been noted that obese humans tend to have high levels of leptin.

By studying patients with abnormal genes responsible for leptin production, researchers have found that a least one leptin gene must be intact for the normal secretion of hormones to proceed. These results show that the hormone leptin is produced outside of the brain in fat cells and acts directly on the function of the hypothalamus within the brain. Researchers believe that leptin plays a key role in the normal release of hormones from the HPA axis.

Researchers intend on continuing to study the role of leptin in fat distribution, and the activity of the HPA axis in normal volunteers. In addition, this study will focus on the role of leptin in depression, because depression is characterized by changes in food intake, body weight, and neuroendocrine function. Data gathered from this study will provide a better understanding of the causes and medical consequences of major depression.

Panoramica dello studio

Stato

Completato

Descrizione dettagliata

Our group has tested the hypothesis that the molecules involved in the neurobiology of the stress response are key elements in the pathophysiology, treatment, and medical consequences of major depressive disorder. Leptin is implicated in the regulation of adipose tissue, body weight and homeostasis. In the first three years of this protocol we accomplished the following: (1) discovered leptin pulsatility; (2) showed that is secreted in a highly organized manner in men and women; (3) showed for the first time in humans an inverse relation between rapid fluctuations in plasma leptin concentrations in healthy volunteers and those of adrenocorticotropic hormone (ACTH) and cortisol; (4) demonstrated a complex relation between the minute-to-minute dynamics of leptin and those of luteinizing hormone and estradiol; (5) showed a striking correlation between the 24-h dynamics of leptin and those of TSH and GH; (6) demonstrated highly significant correlation between hourly fluctuations of leptin levels and those of psychometric variables such as sadness, social withdrawal, and carbohydrate craving, and (7) showed that women produce twice as much leptin per secretory event than men. By studying patients with a leptin gene mutation we showed that at least one intact copy of the leptin gene is required for the regulation of TSH function and GH architecture in humans. These results indicate that leptin, a peripherally secreted molecule, appears to modulate the secretion of hypothalamic hormones. We have therefore proposed that hypothalamic neuroendocrine transduction, a key function of the CNS, may be regulated by leptin, a peripheral pulsatile signal of nutritional status. We would like to continue and expand our studies on the interactions of leptin, fat distribution, and the pituitary-adrenal axis in normal volunteers and also in patients with depression, because depression is characterized by alterations in food intake, body weight, and neuroendocrine function. Leptin profoundly affects the regulation of these three parameters. Leptin also increases insulin resistance, being therefore a risk factor for coronary artery disease, which is more prevalent and associated with higher mortality in depressed patients than in the general population. The data to be generated by this study will provide a better understanding of pathophysiology and medical consequences of major depression.

Tipo di studio

Osservativo

Iscrizione

230

Contatti e Sedi

Questa sezione fornisce i recapiti di coloro che conducono lo studio e informazioni su dove viene condotto lo studio.

Luoghi di studio

    • Maryland
      • Bethesda, Maryland, Stati Uniti, 20892
        • National Institute of Mental Health (NIMH)

Criteri di partecipazione

I ricercatori cercano persone che corrispondano a una certa descrizione, chiamata criteri di ammissibilità. Alcuni esempi di questi criteri sono le condizioni generali di salute di una persona o trattamenti precedenti.

Criteri di ammissibilità

Età idonea allo studio

  • Bambino
  • Adulto
  • Adulto più anziano

Accetta volontari sani

Sì

Sessi ammissibili allo studio

Tutto

Descrizione

Depressed patients must have a history of past major depression of at least four months duration, or a history of two or more briefer episodes. Must be overweight.

Must not need a hospital admission as part of their treatment.

Overweight normal volunteers.

No subjects on chronic medication which cannot be washed out for one month.

No subjects with any serious medical illness.

No women who are pregnant, trying to become pregnant, or sexually active and not using effective contraception.

No patients with HIV infection.

No subjects who cannot discontinue use of alcohol/tobacco.

Piano di studio

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Come è strutturato lo studio?

Collaboratori e investigatori

Qui è dove troverai le persone e le organizzazioni coinvolte in questo studio.

Pubblicazioni e link utili

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Studiare le date dei record

Queste date tengono traccia dell'avanzamento della registrazione dello studio e dell'invio dei risultati di sintesi a ClinicalTrials.gov. I record degli studi e i risultati riportati vengono esaminati dalla National Library of Medicine (NLM) per assicurarsi che soddisfino specifici standard di controllo della qualità prima di essere pubblicati sul sito Web pubblico.

Studia le date principali

Inizio studio

1 marzo 1996

Completamento dello studio

1 giugno 2002

Date di iscrizione allo studio

Primo inviato

3 novembre 1999

Primo inviato che soddisfa i criteri di controllo qualità

3 novembre 1999

Primo Inserito (Stima)

4 novembre 1999

Aggiornamenti dei record di studio

Ultimo aggiornamento pubblicato (Stima)

4 marzo 2008

Ultimo aggiornamento inviato che soddisfa i criteri QC

3 marzo 2008

Ultimo verificato

1 giugno 2002

Maggiori informazioni

Queste informazioni sono state recuperate direttamente dal sito web clinicaltrials.gov senza alcuna modifica. In caso di richieste di modifica, rimozione o aggiornamento dei dettagli dello studio, contattare register@clinicaltrials.gov. Non appena verrà implementata una modifica su clinicaltrials.gov, questa verrà aggiornata automaticamente anche sul nostro sito web .

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