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Remote modulation on HGP by ATMs. In the fed state, ATMs in response to insulin and LPS produce IL-10 to control gluconeogenesis-mediated HGP. In overnutrition state, ATMs secret large amounts of IL-6 and TNF-α, which link WAT inflammation with lipolysis, resulting in exacerbated HGP through interfering with insulin action or supplying precursors to stimulate aberrant gluconeogenesis. Lipid-associated ATMs play either protective or detrimental roles in controlling aberrant HGP.
