Research

Hormonal

Knocking out ACC2 improves insulin sensitivity in high-fat-fed mice by reducing intracellular diacylglycerol and novel PKC activity, thereby preventing fat-induced insulin resistance.

This mechanism suggests that reducing intracellular fat metabolites (like diacylglycerol) can improve insulin sensitivity even in the presence of high fat intake. This supports the idea that metabolic health is more about where fat is stored and oxidized than just total fat intake.

GoodSupportsHIGH confidence
Acc2-/- mice were protected from fat-induced peripheral and hepatic insulin resistance. These improvements in insulin-stimulated glucose metabolism were associated with reduced diacylglycerol content in muscle and liver, decreased PKCtheta activity in muscle and PKCzeta activity in liver, and increased insulin-stimulated Akt2 activity in these tissues.
Cheol Soo Choi et al. · Proceedings of the National Academy of Sciences · 2007

Why this rating

High-quality mechanistic data using hyperinsulinemic-euglycemic clamps and tissue-specific biochemical assays.

Source

Continuous fat oxidation in acetyl–CoA carboxylase 2 knockout mice increases total energy expenditure, reduces fat mass, and improves insulin sensitivity

Cheol Soo Choi et al. · Proceedings of the National Academy of Sciences · 2007

DOI 10.1073/pnas.0706794104

mechanism_only · n=38Cited 324×
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DOI resolved against Crossref · corpus check 2026-06-10

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