CLINICAL TRIALS PROFILE FOR CYTOMEL
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All Clinical Trials for Cytomel
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00208702 ↗ | Thyroid Medication and Antidepressants for Treating Major Depression | Completed | National Institute of Mental Health (NIMH) | Phase 4 | 1996-09-01 | This study will evaluate the effectiveness of treatment with supplemental triiodothyronine (T3, Cytomel) and sertraline (Zoloft), a selective serotonin reuptake inhibitor (SSRI), in improving symptoms of major depressive disorder (MDD). |
| NCT00208702 ↗ | Thyroid Medication and Antidepressants for Treating Major Depression | Completed | Emory University | Phase 4 | 1996-09-01 | This study will evaluate the effectiveness of treatment with supplemental triiodothyronine (T3, Cytomel) and sertraline (Zoloft), a selective serotonin reuptake inhibitor (SSRI), in improving symptoms of major depressive disorder (MDD). |
| NCT00265980 ↗ | Leptin in Human Energy and Neuroendocrine Homeostasis | Terminated | Columbia University | N/A | 2002-07-01 | Previous work in our laboratory, and many others, has shown that body weight is regulated. When anyone, fat or thin, tries to maintain a reduced body weight, many systems affecting energy balance (skeletal muscle, neuroendocrine, and autonomic systems) conspire to slow metabolic rate thus favoring the regain of lost weight. Individuals with leptin deficiency are remarkably similar to weight-reduced individuals. Their metabolism, thyroid hormones, and sympathetic nervous system activity are all low despite their obesity. While administration of leptin to leptin-deficient humans results in substantial weight loss and increases in energy expenditure. However, leptin administration to leptin-sufficient humans at usual body weight has little or no effect on weight unless given in doses 10-20 times what would be considered to be in the normal physiological range. This study examines the hypothesis that leptin is "read" by various systems regulating energy balance as an indicator of how much energy we have stored and that the body perceives the weight-reduced state as a condition of relative leptin insufficiency. Within this model, restoration of leptin to levels present prior to weight loss should relieve much of the metabolic opposition to keeping weight off. Preliminary studies support this hypothesis. |
| NCT00265980 ↗ | Leptin in Human Energy and Neuroendocrine Homeostasis | Terminated | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) | N/A | 2002-07-01 | Previous work in our laboratory, and many others, has shown that body weight is regulated. When anyone, fat or thin, tries to maintain a reduced body weight, many systems affecting energy balance (skeletal muscle, neuroendocrine, and autonomic systems) conspire to slow metabolic rate thus favoring the regain of lost weight. Individuals with leptin deficiency are remarkably similar to weight-reduced individuals. Their metabolism, thyroid hormones, and sympathetic nervous system activity are all low despite their obesity. While administration of leptin to leptin-deficient humans results in substantial weight loss and increases in energy expenditure. However, leptin administration to leptin-sufficient humans at usual body weight has little or no effect on weight unless given in doses 10-20 times what would be considered to be in the normal physiological range. This study examines the hypothesis that leptin is "read" by various systems regulating energy balance as an indicator of how much energy we have stored and that the body perceives the weight-reduced state as a condition of relative leptin insufficiency. Within this model, restoration of leptin to levels present prior to weight loss should relieve much of the metabolic opposition to keeping weight off. Preliminary studies support this hypothesis. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
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