As a cofactor in the biosynthesis of carnitine, vitamin C may have a role in enhancing PPAR-alpha-dependent fatty acid oxidation

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From the publication:

Ascorbic acid is a known cofactor in the biosynthesis of carnitine, a molecule that has an obligatory role in fatty acid oxidation […] Ascorbic acid supplementation increased the mRNA levels of PPARα and its target enzymes involved in fatty acid β-oxidation in visceral adipose tissues. Consistent with the effects of ascorbic acid on visceral obesity, ascorbic acid not only inhibited hepatic steatosis but also increased the mRNA levels of PPARα-dependent fatty acid β-oxidation genes in livers. Similarly, hepatic inflammation, fibrosis, and apoptosis were also decreased during ascorbic acid-induced inhibition of visceral obesity. In addition, serum levels of alanine aminotransferase, aspartate aminotransferase, total cholesterol, and LDL cholesterol were lower in HFD-AA-fed mice than in those of HFD-fed mice.

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A few bullet points:

  • Reduced visceral obesity
  • Reduced hepatic inflammation
  • Increased expression of PPAR-a
  • Improved markers of liver health and cholesterol

Related: studies in humans have shown reduced vitamin C status directly impacts fat oxidation in response to exercise.