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Sunday, April 18, 2010

Ketones, Anaplerosis & Insulin

Acetoacetate and β-hydroxybutyrate in combination with other metabolites release insulin from INS-1 cells and provide clues about pathways in insulin secretion

Putting this here for my own orgnization


The synergistic insulin release by compounds that can be metabolized to mitochondrial acetyl-CoA, such as KIC, β-hydroxybutyrate, or acetoacetate, in combination with methyl succinate that can be metabolized to mitochondrial oxaloacetate, suggests that acetyl-CoA and oxaloacetate condense in the citrate synthase reaction to form citrate. Numerous compounds can be formed from citrate, and citrate can carry acetyl-CoA and oxaloacetate out of the mitochondria to the cytosol. Many compounds, including most short-chain acyl-CoAs, can be formed from acetyl-CoA in the cytosol. KIC and β-hydroxybutyrate can also be directly converted to acetoacetate and acetyl-CoA in the mitochondria. Acetoacetate can be exported to the cytosol and converted to acetoacetyl-CoA to form several other short-chain acyl-CoAs. The results support the idea that anaplerosis is important for insulin secretion and suggest that multiple short-chain acyl-CoAs may be some of the products of anaplerosis in the β-cell.

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