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. Author manuscript; available in PMC: 2023 Mar 1.
Published in final edited form as: J Nutr Biochem. 2021 Dec 20;101:108928. doi: 10.1016/j.jnutbio.2021.108928

Figure 3. Graphical Abstract.

Figure 3.

It is known that genetic variation can alter satiety signaling and hypothalamic inflammation, and that dysfunction in both of these pathways contributes to the development and progression of obesity (solid line). It is also known that hypothalamic inflammation dysregulates satiety signaling (solid line), further contributing to weight gain. What remains to be determined is the extent to which genetic variations in satiety-signaling genes (LEPR, MC4R, ADCY3, FTO, etc) contribute to development of inflammation, and how variations in inflammatory-related genes (SOCS3, JNK, UCP2, etc) might alter satiety signaling (dashed line). Better understanding the connections between these two pathways will reveal new drug targets for obesity treatment, and will allow physicians to gain a wider perspective on how genetic variants will affect metabolic health. Created with BioRender.com.