Figure 3.

A brief overview of the molecular mechanisms by which SFRPs regulate lipid metabolism and cardiovascular disease. The figure shows the potential mechanisms by which how SFRPs modulate adipocyte differentiation, obesity and type 2 diabetes mellitus (T2DM). Acaca, acetyl-Coenzyme A carboxylase alpha; Acly, ATP citrate lyase; Akt, AKT serine/threonine kinase 1; Rho, rhodopsin; BMI, body mass index; Chreb, cAMP responsive element binding protein; FABP4, fatty acid binding protein 4; Fasn, fatty acid synthase; Foxo1, forkhead box O1; G6PC, glucose-6-phosphatase, catalytic; hADSCs, adipose mesenchymal stem cells; Hba1c, Glycosylated hemoglobin; IFN-γ, interferon-γ; IL-6, leukotriene-6; IRS1, insulin receptor substrate 1; Lxr-α, LexA regulated function-α; Nmnat, Nicotinamide mononucleotide adenylyltransferase; Nr1h3, nuclear receptor subfamily 1 group H member 3; NRF1/2, nuclear respiratory factor 1/2; Pck1, phosphoenolpyruvate carboxykinase 1, cytosolic; PCP, Pupal cuticle protein; PEPCK, phosphoenolpyruvate carboxykinase; PPARγ, peroxisome proliferator activated receptor-γ; BNP, natriuretic peptides A-like; Scd1, stearoyl-Coenzyme A desaturase 1; SerpinE1, serpin family E member 1; SFRP1, secreted frizzled related protein1; Slc2a2/4, solute carrier family 2 (facilitated glucose transporter), member 2/member4; Srebp1, sterol regulatory element binding protein 1; TCF4, transcription factor 4; TFAM, transcription factor A, mitochondrial; TG, triglyceride; Tgf-β2, transforming growth factor β 2; VEGF, vascular endothelial growth factor.