A PPARγ–FGF1 axis is required for adaptive adipose remodelling and metabolic homeostasis

Adipose tissue inflammation and ectopic lipid accumulation [Review]

“…These findings suggest that reduced lipid storage in obese adipose tissue may contribute to ectopic lipid accumulation in non-adipose tissues such as the liver, skeletal muscle, and pancreas, where lipotoxicity impairs their metabolic functions [10,[71][72][73]. Although the molecular mechanisms underlying adipose tissue fibrosis are still largely unknown, recent evidence suggests that a PPARγ-fibroblast growth factor 1 (FGF1) axis is required for obesity-induced adipose tissue remodeling [74]. Collectively, obesityinduced metabolic problems may become overt, in addition to the dysregulation of adipocytokine production, when adipose tissue cannot fully meet demands for additional lipid storage.…”

Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis

“…In this regard, Khan et al 6 reported that mice lacking collagen VI, which is expressed abundantly in adipose tissue, exhibit the uninhibited adipose tissue expansion and substantial improvement in insulin sensitivity on a high-fat diet (HFD). Although recent evidence suggests a role for obesity-induced hypoxic state 7,8 , the molecular mechanisms underlying adipose tissue fibrosis are still largely unknown.…”

Glucose tolerance in obese men is associated with dysregulation of some angiogenesis-related gene expressions in subcutaneous adipose tissue

“…Thus, CYR61 and PDGFC play an important role in proliferation and angiogenesis [18,20]. Fibroblast growth factor proteins (FGF1 and FGF2), which also known as acidic and basic fibroblast growth hormones, are mitogenic signaling molecules that have roles in angiogenesis and function as a modifier of endothelial cell migration and proliferation, but FGF2 mainly induces lymphangiogenesis [21][22][23]. Moreover, FGF1 is required for adaptive adipose remodeling and metabolic homeostasis and FGF2 prevents cancer cells from endoplasmic reticulum stress-mediated apoptosis [21,23].…”

“…Fibroblast growth factor proteins (FGF1 and FGF2), which also known as acidic and basic fibroblast growth hormones, are mitogenic signaling molecules that have roles in angiogenesis and function as a modifier of endothelial cell migration and proliferation, but FGF2 mainly induces lymphangiogenesis [21][22][23]. Moreover, FGF1 is required for adaptive adipose remodeling and metabolic homeostasis and FGF2 prevents cancer cells from endoplasmic reticulum stress-mediated apoptosis [21,23]. Biological effect of the fibroblast growth factors is realized through the fibroblast growth factor receptors, some of which are related to VEGF signaling pathway [24,25].…”

“…An important role in the control of angiogenesis also play cysteine-rich angiogenic inducer 61 (CYR61), brain-specific angiogenesis inhibitor 2 (BAI2), platelet derived growth factor C (PDGFC), fibroblast growth factors and their receptors, and some transcription factors like hypoxia inducible factor 1a (HIF1A), endothelial PAS domain protein 1 (EPAS1/HIF2A), and E2F8 (transcription factor of E2F family) [18][19][20][21][22][23][24][25]. Thus, CYR61 and PDGFC play an important role in proliferation and angiogenesis [18,20].…”