Fig. 8: Role of the acetylation program in modulating insulin secretion in response to energy status. | Cell Death & Disease

Fig. 8: Role of the acetylation program in modulating insulin secretion in response to energy status.

From: The pivotal role of protein acetylation in linking glucose and fatty acid metabolism to β-cell function

Fig. 8

a Under fed condition, high glucose reduces AMPK activity, resulting in decreased phosphorylation of ACC and increased production of malonyl-CoA (Mal-CoA), which blocks fatty acyl-CoA (FA-CoA) entrance into mitochondria for β-oxidation via inhibiting CPT-1. On the other hand, high glucose decreases the expression or activity of SIRT3, leading to increased acetylation of ECHA and reduced mitochondrial β-oxidation. Thus, phosphorylation and acetylation programs cooperatively increase cytosolic lipid signaling molecules to promote insulin secretion in islet β-cell. b During fasting, activation of AMPK phosphorylates and inhibits ACC, resulting in reduced Mal-CoA and increased entry of substrates into mitochondria for β-oxidation. Low glucose also increases the expression or activity of SIRT3, which deacetylates ECHA and promotes fatty acid β-oxidation. The two signaling pathways cooperatively decrease lipid signaling molecules for insulin secretion

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