Table 1.

The impact of advanced glycation end products (AGEs) on adipose tissue.

Process	Experimental Model	Effect of AGE–RAGE Pathway Activation	Mechanism	References
Adipogenesis	Human MSCs	↓ differentiation potential towards adipocytes		[10]
	ASCs from diabetic osteoporotic and control C57BL/6 mice	↓ proliferation ↓ differentiation potential of ASCs	↓ Wnt signaling pathway ↑ methyltransferase genes	[34]
	Senescent murine preadipocytes	↑ senescent preadipocytes differentiation	↓ p53 protein	[35]
Browning and thermogenesis	RAGE−/− mice RAGE−/− murine adipocytes	↓ thermogenesis	↓ PKA-mediated phosphorylation of HSL and p38 MAPK	[24]
	Mice on an HFD	↓ browning ↓ thermogenesis		[39]
Lipolysis	RAGE−/− mice	↓ lipolysis ↑ weight gain	↓ PKA-mediated phosphorylation of HSL	[24]
Lipogenesis	DIO mice receiving a RAGE inhibitor	↑ lipogenesis	↑ TLR receptors ↓ PI3K protein kinase B pathway	[46] [48]
Insulin sensitivity	RAGE−/− mice	↓ insulin sensitivity	↓ PI3K protein kinase B pathway ↑ DIAPH1 expression ↑ metabolic inflammation	[13,50] [51] [50]
Adipokine secretion	3T3-L1 adipocytes	↓ leptin secretion	↑ ROS synthesis ↓ PPAR-γ expression	[16] [63]
	RAGE−/− mice	↓ adiponectin secretion	↑ ROS synthesis ↑ metabolic inflammation ↓ NADPH oxidase	[57] [67]

↓, decrease; ↑, increase; ASCs, adipose-derived stem cells; DIAPH1, diaphanous 1 protein; DIO, diet-induced obesity; HFD, high-fat diet; HSL, hormone-sensitive lipase; MAPK, mitogen-activated protein kinase; NADPH, nicotinamide adenine dinucleotide phosphate; PKA, protein kinase A; PI3K, phosphoinositide 3-kinase; PPAR-γ, peroxisome proliferator-activated receptor-γ; RAGE, receptor for advanced glycation end products; ROS, reactive oxygen species.