Fig. 9: Schematic models illustrating dynamic gene expressions during induction of adipogenic differentiation and roles of stomatin in promoting fatty acid uptake and lipid droplet enlargement in adipocytes. | Nature Communications

Fig. 9: Schematic models illustrating dynamic gene expressions during induction of adipogenic differentiation and roles of stomatin in promoting fatty acid uptake and lipid droplet enlargement in adipocytes.

From: Stomatin modulates adipogenesis through the ERK pathway and regulates fatty acid uptake and lipid droplet growth

Fig. 9: Schematic models illustrating dynamic gene expressions during induction of adipogenic differentiation and roles of stomatin in promoting fatty acid uptake and lipid droplet enlargement in adipocytes.The alternative text for this image may have been generated using AI.

a Dynamics expression patterns of stomatin, adipogenic genes C/EBPĪ², C/EBPĪ“, C/EBPĪ±, and PPARĪ³ along the adipogenic differentiation process are depicted. Stomatin progressively increases during adipogenesis and may participate in modulation of other adipogenic gene. By inhibiting pERK, stomatin activates PPARĪ³, as a prelude to adipogenesis. Stomatin may also directly activate PPARĪ³ pathway through currently unknown mechanisms. b Stomatin and calveolin-1 are known to associated with lipid raft (shadowed red). Stomatin proteins are present on the surfaces of LDs, together with perilipin. Stomatin can promote enlargement of LDs through facilitating LD-LD fusion (a ā†’ b ā†’ c). The presence of LCFAs outside the cell, through currently unknown mechanisms, relocates stomatin proteins from LDs to lipid rafts on the plasma membrane (1ā†’2), where they interact with CD36 and possibly other FABPs, to promote uptake of LCFAs (3), resulting in increase of intracellular triglycerides, which are transported and stored in LDs (4).

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