Disruption of cardiac growth hormone receptor (GHR) in adult mice decreases fat mass and alters insulin sensitivity

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 780-806-Determinants of Insulin Resistance & Associated Metabolic Disturbances
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-800
Adam Jara*, Xingbo Liu, Chance Michael Benner, Don Sim, Edward Owen List, Darlene E Berryman and John Joseph Kopchick
Ohio University, Athens, OH
GH is a central mediator of metabolism and is necessary for the proper development and maintenance of several tissues, including the heart. Evidence of the profound effect GH has on the heart can be found in patients with diseases that disrupt GH action. In pathological states of acromegaly and GH deficiency, patients exhibit unique cardiac phenotypes of altered structure and function. To better understand the effects that GH action has on cardiac tissue, we have recently developed a tamoxifen-inducible, cardiac-specific GHR disrupted (iC-GHRKO) mouse. Four month old iC-GHRKO mice (n=9) were injected with tamoxifen (80mg/kg) and subjected to insulin tolerance testing at 6 months of age and echocardiography at 7 months of age. Beginning two weeks after tamoxifen injection, and repeated monthly, fasting glucose, body composition, and blood pressure measurements were performed. iC-GHRKO mice showed no difference in basal cardiac function at 7 months of age nor did they demonstrate any difference in longitudinal systolic blood pressure (4-7 months). However, while not statistically significant, fasting glucose was lower in iC-GHRKO mice versus controls at all time points measured (4-7 months). Surprisingly, iC-GHRKO mice were significantly more insulin sensitive at 6 months of age and had less fat mass (4-7 months) versus controls. These data indicate that altered cardiac GH signaling may influence whole body metabolism. Future work will focus on continuing to track these mice throughout age while investigating cardiac and adipose insulin signaling and also exploring the presence of paracrine factors from the heart (cardiokines) which may influence peripheral tissues.

Nothing to Disclose: AJ, XL, CMB, DS, EOL, DEB, JJK

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: AJ is supported by a graduate GMS fellowship from the Bill and Melinda Gates Foundation and by a student enhancement award from Ohio University. CB is supported by the provost undergraduate research fund from Ohio University. EOL, DEB, and JJK are supported by funds from NIA (AG031736), NIDDK (DK075436) and by the Diabetes Institute at Ohio University. JJK also is supported the State of Ohio’s Eminent Scholar Program that includes a gift from Milton and Lawrence Goll and by the AMVETS.