This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Growth hormone (GH) secretion is reduced in obesity and reduced GH secretion is associated with increased carotid intima-medical thickness and inflammatory cardiovasculare (CV) risk markers. No studies have assessed whether relative reductions in GH secretion contribute independently to increased CV disease in patients with abdominal obesity. We hypothesize that a relative growth hormone deficiency is seen in relationship to excess visceral adiposity and contributes to increased cardiovascular risk in patients with abdominal obesity, above and beyond traditional risk factors. The following hypotheses will be investigated:1. Relative GH deficiency, as defined by inadequate stimulatory responses of GH, will be highly prevalent among patients with abdominal obesity, in association with excess visceral adiposity, elevated free fatty acids, increased inflammatory markers and altered adipocytokines. 2 Carotid IMT will be increased among patients with abdominal obesity and relative GH deficiency compared to patients with abdominal obesity and adequate GH secretion.
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