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. 2006 Dec 19;2007:53843. doi: 10.1155/2007/53843

Table 1.

Loss-of-function studies on PPARγ cofactors in adipogenesis and energy metabolism

PPARγ cofactor Phenotype in the absence of the cofactor

Cell-based studies Mouse studies

Brg1, hBrm (SWI/SNF components) Blocked adipogenesis (Salma et al. [25])
Reduced presence of Pol II and GTFs on the promoter (Salma et al. [25])
Decreased PPARγ transcription (Salma et al. [25])

TIF2 Increased lipolysis (Picard et al. [50]) Enhanced adaptive thermogenesis (Picard et al. [50])
Protection against obesity (Picard et al. [50])
Increased insulin-sensitivity (Picard et al. [50])
Improved metabolic profile. Increased lipolysis (Picard et al. [50])
Decreased presence of PPARγ

SRC-1 Predisposition to obesity (Picard et al. [50])
Reduced energy expenditure (Picard et al. [50])
Reduced fatty acid oxidation in brown adipose tissue (Picard et al. [50])
Decreased energy expenditure, attenuated fatty acid oxidation (Picard et al. [50])

SRC-1/pCIP double knockout Abrogated preadipocyte differentiation (Wang et al. [51]) Diminished lipid storage in brown fat; increased caloric intake on both chow and high-fat diet due to increased leptin levels; resistance to diet-induced obesity; increased basal metabolic rate and energy expenditure (Wang et al. [51])
Reduced expression of PPARγ-target genes, including UCP-1, due to corepressor recruitment and decreased PPARγ recognition of PPREs (Wang et al. [51])

PGC-1α Impaired induction of thermogenic genes in BAT (Uldry et al. [52]) Reduced mitochFondrial function (Lin et al. [53])
Decreased number and impaired function of mitochondria (Uldry et al. [52]) Resistance to obesity and hyperactivity (Lin et al. [53])

TRAP220/DRIP205/PBP Defective PPARγ-stimulated adipogenesis (Ge et al. [31]) Defective vascular development similar to that seen in PPARγ-null mice (Barak et al. [54]; Zhu et al. [55])

PRIP/NRC/RAP250/TRBP Decreased PPARγ-mediated transcriptional activation (Antonson et al. [56]; Zhu et al. [57])

RIP140 Upregulation of genes involved in energy dissipation (Poweka et al., 2006) Increased oxygen consumption and resistance to high-fat diet-induced obesity (Leonardsson et al. [58])
Increased PGC-1α expression (Poweka et al., 2006) Expression of lipgenic enzymes is decreased. UCP-1 (involved in energy dissipation in BAT) expression is increased (Leonardsson et al. [58])

NCoR and SMRT Increased adipocyte differentiation (Yu et al. [42])

Sirt1 Decreased NCoR levels (Picard et al. [43])