Acacb, also known as acetyl-coenzyme A carboxylase β, is the rate-limiting enzyme in fatty acid oxidation [4]. It plays a crucial role in fatty acid metabolism pathways. Continuous fatty acid oxidation in Acacb knock-out mice increases insulin sensitivity, highlighting the importance of genetic models in studying its function [4].

In Caucasian diabetic patients, the rs2268388 polymorphism in the ACACB gene is associated with diabetic nephropathy, with the C allele showing a decreased susceptibility risk compared to the T allele [1]. In metastatic colorectal cancer, ACACB is a key metabolism-related biomarker, and its high expression can lead to decreased sensitivity to cetuximab, potentially through affecting EGFR phosphorylation and the mTOR/Akt signaling pathway [2]. In mice, cardiac-specific deletion of Acc2 (a form of Acacb) increases fatty acid oxidation, preventing high-fat diet-induced cardiomyopathy by regulating parkin-mediated mitophagy [3].

In conclusion, Acacb is essential in fatty acid oxidation and is involved in important biological processes and disease conditions. Studies using gene knockout mouse models have revealed its role in diabetes-related nephropathy, metastatic colorectal cancer, and diet-induced cardiomyopathy, contributing to our understanding of these diseases and potentially guiding future therapeutic strategies.