(P31-054-23) High-Fat Diet Alters Thermogenic Gene Expression in Adipocytes Derived From White and Brown Adipose Tissue of Mice in Response to β-Agonists or 18-Carbon Fatty Acids

Objectives: Although activating thermogenic adipocytes is a promising strategy to reduce the risk of obesity and its related metabolic disorders, it is known to be hard to induce thermogenic adipocytes in obesity. Therefore, we aimed to investigate the regulation of adipocyte thermogenesis in diet-induced obesity.

Methods: White and brown primary adipocytes derived from high-fat diet (HFD)-fed mice were treated with β-agonists or 18-carbon fatty acids, and thermogenic gene expression was measured.

Results: Brown adipose progenitor cells derived from HFD-fed mice had less adipogenic capacity than those derived from control diet (CD)-fed mice, and norepinephrine (NE) had less effect on Pgc1a upregulation in white primary adipocytes derived from HFD-fed mice than those derived from CD-fed mice. Regardless which 18-carbon fatty acids were treated, white primary adipocytes derived from HFD-fed mice had higher expression levels of Ucp1, Pgc1a, and Prdm16, and brown primary adipocytes derived from HFD-fed mice had higher expression levels of Pgc1a and Prdm16 compared to their counterparts. Oleic acid (OLA) and γ-linolenic acid (GLA) upregulated Pgc1a expression in white primary adipocytes derived from HFD-fed mice.

Conclusions: These data indicate that in diet-induced obesity, brown adipogenic capacity and NE-induced thermogenesis in white adipocytes are downregulated; however, HFD feeding induces thermogenic gene expression in white and brown primary adipocytes, and OLA and GLA augment the expression levels.

Funding Sources: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (No. 2021R1G1A1092356).