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Sponsor study identifier
Secondary identifiers
observational
230
1 country
1
Study Start
March 1996
Date type not reportedThis date has not been verified as actual or estimated.
Primary Completion
Not reported
Date not reportedStudy Completion
June 2002
Date type not reportedThis date has not been verified as actual or estimated.
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.
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
June 2002
Date type not reportedThis date has not been verified as actual or estimated.
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Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
March 1996
Date type not reportedThis date has not been verified as actual or estimated.
November 3, 1999
Actual (reported)November 4, 1999
Actual (reported)June 2002
Date type not reportedThis date has not been verified as actual or estimated.
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National Institute of Mental Health (NIMH)
Bethesda, Maryland, 20892, United States
Behan DP, Linton EA, Lowry PJ. Isolation of the human plasma corticotrophin-releasing factor-binding protein. J Endocrinol. 1989 Jul;122(1):23-31. doi: 10.1677/joe.0.1220023.
Campbell EA, Linton EA, Wolfe CD, Scraggs PR, Jones MT, Lowry PJ. Plasma corticotropin-releasing hormone concentrations during pregnancy and parturition. J Clin Endocrinol Metab. 1987 May;64(5):1054-9. doi: 10.1210/jcem-64-5-1054.
First Submitted
November 3, 1999
First Posted
November 4, 1999
Study Start
March 1996
Date type not reportedThis date has not been verified as actual or estimated.
Study Completion
June 2002
Date type not reportedThis date has not been verified as actual or estimated.
Gold PW, Goodwin FK, Chrousos GP. Clinical and biochemical manifestations of depression. Relation to the neurobiology of stress (1). N Engl J Med. 1988 Aug 11;319(6):348-53. doi: 10.1056/NEJM198808113190606. No abstract available.
Last Updated
March 4, 2008
Record last verified: 2002-06
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Source: ClinicalTrials.gov.
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