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The Essential Role of the L4F‐Adiponectin Regulatory Axis: Leading to Improvements in the Metabolic Profile of Diabetes Mellitus
Author(s) -
Burgess Angela Patricia Haynes,
Peterson Stephen J,
Tsenovoy Peter,
Li Ming,
Kim Dong Hyun,
Abraham Nader G
Publication year - 2008
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.22.1_supplement.1226.43
Subject(s) - medicine , endocrinology , adiponectin , insulin resistance , inflammation , adipose tissue , vasoprotective , insulin , diabetes mellitus , adipogenesis , type 2 diabetes mellitus , nitric oxide
Apolipoprotein A1 mimetic peptide (L‐4F), a natural component of HDL‐ has been shown to have both anti‐atherosclerotic and vasoprotective effects. Therefore, we hypothesized treatment with L4‐F in an obese‐ diabetic mouse model, would lead to improvements in the metabolic consequences of diabetes: inflammation, weight gain, and insulin resistance. L‐4F (1mg/kg.d) was administered to obese‐diabetic mice for 6 weeks. L‐4F improved HO activity and decreased superoxide production ( P <0.001) in ob/ob mice. L‐4F treatment decreased visceral fat content and prevented weight gain ( P <0.02), and decreased inflammatory cytokine IL‐1β (p<0.05) compared to wild type, c‐ob/+. L‐4F treatments also led to increased insulin sensitivity, glucose tolerance and adipose tissue remodeling ( P <0.001). L‐4F inhibited adipogenesis in bone marrow and increased total adiponectin levels ( P <0.02) only in obese mice. Therefore, suggesting a mechanism by which L4‐F increases HO‐1 activity and adiponectin, leading to decreased inflammation, increased insulin sensitivity, maintenance of normal weight, and an overall improvement in the diabetic profile of obese‐diabetic mice. This work was supported by NIH grants DK068134, HL55601 and HL34300 (NGA).