Total and high molecular weight adiponectin levels in mice with altered GH signaling

• Published in: The FASEB journal Vol. 24; no. S1; p. 547.1
• Main Authors: Lubbers, Ellen, Miles, Donald Bailey, List, Edward O., Kopchick, John J., Berryman, Darlene E.
• Format: Journal Article
• Language: English
• Published: Federation of American Societies for Experimental Biology 01-04-2010
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.24.1_supplement.547.1

Adiponectin, which negatively correlates to fat mass and insulin resistance, associates into high molecular weight (HMW) and low molecular weight forms. The HMW form possesses the predominate insulin sensitizing bioactivity, yet most mouse studies have reported only total levels. This study evaluates total and HMW adiponectin concentrations in giant bovine GH transgenic (bGH), dwarf GH receptor gene disrupted (GHR−/−), dwarf GH antagonist (GHA) transgenic mice fed either a high fat (HF) or low fat (LF) diet as compared to littermate controls. The bGH and GHR−/− strains represent opposites in GH signaling, with GHR−/− mice being highly insulin sensitive, obese and long‐lived in the absence of GH signaling and with bGH mice being insulin resistant, lean and short‐lived with excess GH signaling. GHA mice have repressed GH signaling are dwarf and obese, like GHR−/− mice, but do not have increased longevity or improved insulin sensitivity. GHR−/− mice on a HF and LF diet and GHA females have increased HMW, total and HMW/total adiponectin levels. Total adiponectin levels are increased in GHA males and decreased in bGH males, but there is no difference in HMW or HMW/total ratio as compared to littermate controls. The increase in total, HMW, and HMW/total adiponectin levels in the long‐lived male GHR−/− mice suggests that elevated adiponectin concentrations could contribute to their improved lifespan.
Research was supported via funds from NIDDK (DK064905, DK075436), NIA (AG031736, AG19899), State of Ohio's Eminent Scholar Program that includes a gift from Milton and Lawrence Goll, DiAthegen, Diabetes Research Initiative at Ohio University, and AMVETS.
Grant Funding Source: DEB was supported in part by funds from NIDDK (DK064905) and NIA (AG031736). EOL is supported by funds from NIA (AG031736) and NIDDK (DK075436). JJK is supported by funds from NIA (AG19899 and AG031736), NIDDK (DK075436), the State of Ohio's Eminent Scholar Program that includes a gift from Milton and Lawrence Goll, and a grant from DiAthegen LLC. All work was further supported by the Diabetes Research Initiative at Ohio University and by a grant from AMVETS.