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. 2023 Dec 23;14(1):12. doi: 10.3390/metabo14010012

Figure 5.

Figure 5

Fatty acid oxidation in MASLD. Legend: Illustration of diverse fatty acid sources contributing to cellular oxidation in non-alcoholic fatty liver disease (MASLD). Carnitine palmitoyltransferase 1 (CPT1), a pivotal outer-membrane mitochondrial enzyme, facilitates fatty acid uptake and oxidation through the ß-oxidation pathway. Malonyl-CoA, an intermediate in de novo lipogenesis (DNL), inhibits CPT1, preventing the entry of fatty acids from plasma non-esterified fatty acids (NEFA), diet, triglyceride (TAG) catabolism, and cholesterol ester (CE) hydrolysis into mitochondria for oxidation. This dysregulation results in hepatic lipid accumulation, fostering the progression of liver steatosis and metabolic dysfunction. The red dot (●) represents changes altered during MASLD pathogenesis. Figure abbreviations: 2C—two carbons; ATGL—Adipose triglyceride lipase; CD36—cluster of differentiation 36; CE—cholesterol esters; CPT1—carnitine palmitoyltransferase 1; DGAT—diacylglycerol acyltransferase enzyme; DNL—de novo lipogenesis; FA—fatty acids; HSL—hormone-sensitive lipase; LDL-R—low-density lipoprotein receptor; MTP—mitochondrial trifunctional protein; NCEH—neutral cholesterol ester hydrolase; NEFA—non-esterified fatty acids; SOAT2—sterol O-acyltransferase 2; and TAG—triacylglycerols.