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The lipogenesis (higher) and glucose uptake (lower) in EAT differ from those of other VATs in response to insulin, which contributes to local insulin resistance in coronary arteries due to a pro-inflammatory environment as indicated by the expression of innate immune regulators of inflammation, such as receptor for advanced glycation end product (RAGE), high mobility group box 1 protein (HMGB1), TLR4 and MyD88 (myeloid differentiation primary response 88) and reduced glucose transporter 4 (GLUT4), adiponectin and glyoxalase 1 (GLO1) [118,120,121]
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