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Effect of exogenous leptin on thrombotic and metabolic profiles of FVB/B6 lipodystrophic mice
Author(s) -
Kadouh Hoda C.,
Yang Soo Jin,
IglayReger Heidi B.,
Bodary Peter F.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1183.4
Subject(s) - medicine , endocrinology , leptin , insulin resistance , lipodystrophy , triglyceride , adipokine , adipose tissue , insulin , chemistry , cholesterol , obesity , immunology , human immunodeficiency virus (hiv) , antiretroviral therapy , viral load
The adipokine leptin appears to play a pro‐thrombotic role in mice, a function that has not been examined in lipodystrophic animals. This study was designed to examine the thrombotic and metabolic effects of leptin administration in a mouse model of lipodystrophy. Eight‐week‐old, male FVB(AZIP/F1)/B6 mice (Transgenic, Tg and Wild‐type, Wt) received recombinant mouse leptin (Tg‐T, n=4; Wt‐T, n=4) or vehicle (Tg‐C, n=3; Wt‐C, n=5) via osmotic pumps over 12 days. Tg mice had a prolonged time to occlusive thrombosis compared to Wt mice (p<0.05), and leptin therapy had no effect on this trait. At baseline/control, Tg mice were heavier than Wt mice (p<0.05), had larger livers (p<0.0001), higher serum insulin (p<0.01) and plasma and liver triglyceride (p<0.01 and p<0.05, respectively), and undetectable leptin (p<0.0001). Tg‐T mice lost weight (p<0.05) and had smaller livers (p<0.05), higher leptin levels (p=0.01) and reduced insulin levels (p<0.05), compared to Tg‐C mice. Elevated HOMA‐IR scores in Tg‐C mice (p<0.05) verified insulin resistance, ameliorated by leptin therapy. These findings confirm the hepatomegaly, insulin resistance and hyperlipidemia seen in lipodystrophic mice and the effectiveness of leptin therapy while also suggesting that lipodystrophy, at least in the AZIP/F1 mouse, exerts an anti‐thrombotic phenotype independent of the lack of leptin. Funding source: American Diabetes Association.