In overweight or obese individuals, increased liver fat oxidation occurs when glucose intolerance persists. Long-chain fatty acids from exogenous or endogenous sources are activated to Long-chain fatty acids from exogenous or endogenous sources are activated to acyl-CoA molecules by fatty acid-CoA ligase and then transported into the mitochondria for ?-oxidation (Birt et al., 2020).

Long-chain fatty acids from exogenous or endogenous sources are activated to acyl-CoA molecules by fatty acid-CoA ligase and then transported into the mitochondria for ?-oxidation (Birt et al., 2020).

In overweight or obese individuals, increased liver fat oxidation occurs when glucose intolerance persists, which can lead to hepatic steatosis (Kozakowski et al., 2019). This occurs due to elevated levels of plasma free fatty acids, as well as increased expression of lipogenic enzymes (Mann et al., 2018). This increase in fat oxidation results in elevated levels of ketone bodies, which can lead to hepatic steatosis and increased risk of fatty liver diseases (Gülseren et al., 2016). The long-chain fatty acids are broken down into acetyl-CoA molecules, which enter into the tricarboxylic acid cycle and are further oxidized to produce ATP, NADH, and FADH2 (Gülseren et al., 2016). These molecules are then used to synthesize glucose in the liver, which further contributes to hepatic steatosis (Kozakowski et al., 2019). In addition, increased fat oxidation can lead to decreased gluconeogenesis, resulting in decreased glucose uptake from the bloodstream and increased levels of free fatty acids in the bloodstream (Mann et al., 2018). This further exacerbates the problem of hepatic steatosis and increases the risk of fatty liver diseases. Cont….

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