Abstract
Transcription of acetyl-CoA carboxylase in avian liver is low during starvation or after consumption of a low-carbohydrate, high-fat diet and high during consumption of a high-carbohydrate, low-fat diet. The role of fatty acids or metabolites derived from fatty acids in the nutritional control of acetyl-CoA carboxylase transcription was investigated by determining the effects of long- and medium-chain fatty acids on acetyl-CoA carboxylase expression in primary cultures of chick embryo hepatocytes. Palmitate, oleate, and arachidonate caused a decrease in acetyl-CoA carboxylase activity in hepatocytes incubated with triiodothyronine (T3). The inhibition of acetyl-CoA carboxylase activity caused by arachidonate was accompanied by a similar decrease in transcription of the acetyl-CoA carboxylase gene. In contrast, neither palmitate nor oleate were effective in modulating acetyl-CoA carboxylase transcription. These results are consistent with arachidonate or a metabolite derived therefrom mediating the effects of diets containing high levels of n-6 polyunsaturated fatty acids on acetyl-CoA carboxylase transcription in liver. Hexanoate and octanoate also inhibited acetyl-CoA carboxylase activity in the presence of T3. The magnitude of the hexanoate- or octanoate-induced decrease in acetyl-CoA carboxylase activity was greater than that observed for long-chain fatty acids. Hexanoate and octanoate inhibited acetyl-CoA carboxylase activity at a transcriptional step, and did so within 2 h of addition of fatty acid. Addition of carnitine partially reversed the inhibitory effects of octanoate on acetyl-CoA carboxylase expression, suggesting that a metabolite of octanoate is involved in mediating this response. 2-Bromooctanoate was a more potent inhibitor of acetyl-CoA carboxylase expression than octanoate or hexanoate. We postulate that a metabolite of hexanoate and octanoate, possibly a six or eight carbon acyl-CoA, plays a role in the nutritional regulation of acetyl-CoA carboxylase transcription.
Highlights
Transcription of acetyl-CoA carboxylase in avian liver is low during starvation or after consumption of a lowcarbohydrate, high-fat diet and high during consumption of a high-carbohydrate, low-fat diet
Changes in acetyl-ChA carboxylase concentration caused by nutritional manipulation are accompanied by coniparable alterations in the synthesis rate and mRNA abundance for acetyl-CoA carboxylase, indicab ing that regulation occurs at a pretranslational step [59, 13,14,15,16]
Insulin accelerates the increase in acetyl-coA carboxylase transcription caused by T3 and glucose, whereas glucagon inhibits the stimulatory effect of T3 and glucose by 65%
Summary
Transcription of acetyl-CoA carboxylase in avian liver is low during starvation or after consumption of a lowcarbohydrate, high-fat diet and high during consumption of a high-carbohydrate, low-fat diet. Neither palmitate nor oleate were effective in modulating ac hoxylase transcription These results are cot ardchidonate or a metabolite derived therefrom mediating the effects of diets containing high levels o f n-6 polyunsaturated fatty acids on acetyl-coA carboxylase transcription in liver. Saturated, monounsaturated, and polyunsaturated long-chain fatty acids cause a decrease in the concentration and rate of synthesis of acetyl-CoA carboxylase in rat hepatocyte cultures [19, 20]. This finding coupled with the observation that levels of unesterified long-chain fatty acids in the blood and liver are elevated during starvation or high-fat feeding [21, 22] suggest that these agents may signal alterations in nutritional state to the liver. We postulate that a metabolite derived from these fatty acids plays a role in the nutritional regulation of acetyl-coA carboxylase transcription
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
