Fig. 1: Genetic ablation of ACBP confers resistance against high-fat diet-induced weight gain.
A Schematic representation of whole-body inducible ACBP knockout murine model in regular chow diet (RCD) or high-fat diet (HFD) regime for 4 weeks (ubi = ubiquitin, Acbpf/f = Acbpflox/flox control mice, Acbp KO = Acbpflox/flox; ubiCre mice having received five daily tamoxifen injections to activate Cre and to excise the floxed Acbp exon 2). Both controls and Acbpflox/flox; ubiCre similarly received tamoxifen injections. B Representative immunoblots of ACBP and β-actin from liver and white adipose-tissue (fat) protein lysates in ACBP whole-body knockout (KO) and control (f/f) littermates. C Body weight of ACBP whole-body knockout (KO) and control (f/f) littermates receiving either RCD or HFD regime for 4 weeks. Statistical comparison between the two types of regimes (RCD, HFD) as well as between the two types of genetic backgrounds (f/f, KO) was performed via two-tailed unpaired Student’s t test (ns nonsignificant). Each point represents one mouse. D Schematic representation of adipocyte-specific ACBP knockout murine model in RCD or HFD regime for 4 weeks (Acbpf/f = Acbpflox/flox control mice, Acbp KO = Acbpflox/flox; AdipoQCre-positive mice). E Representative immunoblots of ACBP and β-actin from liver and white adipose-tissue (fat) protein lysates in ACBP adipocyte-specific knockout (KO) and wild-type (f/f) littermates. F Weight measurement in ACBP adipocyte-specific knockout (KO) and control (f/f) littermates receiving either RCD or HFD regime for 4 weeks. Statistical comparison was performed by means of the two-tailed unpaired Student’s t test (ns nonsignificant).
