Leptin in Human Energy and Neuroendocrine Homeostasis
Status:
Terminated
Trial end date:
2013-07-01
Target enrollment:
Participant gender:
Summary
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.
Phase:
N/A
Details
Lead Sponsor:
Columbia University Michael Rosenbaum
Collaborators:
Columbia University National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)