β-hydroxybutyrate dehydrogenase promotes pancreatic cancer cell proliferation through regulation of the NAD(+)/NADH balance and mitochondrial acetylation

This study examined ketone body metabolism in pancreatic ductal adenocarcinoma (PDAC). Ketone body synthesis metabolism was activated in pancreatic cancer, while exogenous ketone supplementation did not affect PDAC cell proliferation. The enzyme BDH1 was significantly upregulated in human PDAC tissue compared with adjacent normal pancreatic tissue. BDH1 promoted PDAC cell proliferation by maintaining mitochondrial acetylation levels through regulation of the intracellular NAD+/NADH ratio.