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In PDE3B KO mice, White Adipose Tissue (WAT) Exhibits Characteristics of “Good Fat,” i.e., Brown Adipose Tissue (BAT): II. Alterations in Angiogenesis and cAMP‐and AMP Kinase‐signaling
Author(s) -
Khan Faiyaz Ahmad,
tang Yan,
Chung Youn Wook,
ZmudaTrzebiatowska Emilia,
Hockman Steve,
Gavrilova Oksana,
Berger Karin,
Degerman Eva,
Manganiello Vincent
Publication year - 2009
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.23.1_supplement.856.13
Subject(s) - endocrinology , medicine , insulin resistance , white adipose tissue , adipocyte , adipose tissue , lipolysis , beta oxidation , type 2 diabetes , brown adipose tissue , biology , chemistry , diabetes mellitus , metabolism
Obesity is a major risk factor for type 2 diabetes and cardiovascular disease. WAT affects body fat and energy utilization via storage and turnover/hydrolysis of triglycerides. In addition, WAT regulates and integrates physiological pathways, including energy utilization, glucose, insulin sensitivity, and inflammation. WAT also contributes to metabolic dysregulation that characterizes insulin resistance and obesity‐related metabolic and cardiovascular complications. Aquirement of BAT characteristics by WAT, with enhanced intra‐adipocyte FAO (fatty acid oxidation), represents a potential new strategy in treatment of obesity and diabetes. In PDE3B KO mice, epididymal WAT (EWAT) exhibits characteristics of BAT, including increased mitochondrial biogenesis, increased vascularization and expression of angiogenic genes, modification of proteins regulating cAMP signaling and lipolysis, and alterations in AMP kinase signaling, resulting in increased fatty acid oxidation. Compared to WT mice, O2 consumption was increased in vitro in BAT and EWAT isolated from KO mice, and in intact KO mice treated with B‐3 adrenergic receptor agonist. Although PDE3B KO mice show signs of insulin resistance, most likely due to dysregulation of hepatic glucose production, they are lean and not diabetic, perhaps because, in PDE3B KO mice, "good fat" compensates for insulin resistance.