When alcohol is present, it is utilized for energy first, even before CHO's. And that's why the CHO's get stored as glycogen reserves or TAGs in muscle and adipose tissue, via insulin (as the EtOH is being used for energy).
This is the Atkin's theory and this is what I was thinking at first. But then what is the difference between eating a loaf of bread a day and drinking alcohol? Your body would utilize both first, but eating bread does not cause dyslipidemia. This theory also explains why you get fat (how fat gets stored) but not how it is liberated into the bloodstream.
I understand how alcohol causes fatty liver (listed below as a refresher for anyone who is interested) but I'm not sure how alcohol causes an increase in
circulating lipids. I've looked in several books including biochem and Robbins without finding a direct explanation. Maybe it's so obvious they figure it doesn't need explaining.
😕
My thought was that EtOH causes hyperlipidemia because it causes fats to be broken down in the periphery (thus increasing their levels) while simulaneously preventing the liver from producing less lipoproteins that can transport them to the liver for processing. The only problem I can see with this is the fact that most of the fat broken down in the periphery is carried to the liver by
albumin , which although produced in the liver is not a lipoprotein.
Liver's handling of EtOH:
ETOH is oxidized to acetaldehyde by EtOH dehydrogenase (forming 1 molecule of NADH), then to
acetate (which provides the C atoms for building cholesterol) by aldehyde dehydrogenase (forming a 2nd molecule of NADH). This results in a massive increase in the cytosolic concentration of NADH which favors the conversion
pyruvate & oxaloacetate (both intermediates in gluconeogenesis) to
lactate and malate, respectively. This diverts these molecules into other pathways rather than to forming more glucose leading to a hypoglycemic state that is accented by fasting.
Hepatocellular steatosis results from:
1) shunting of normal substrates (pyruvate & oxaloacetate) away from catabolism and toward lipid biosynthesis, owing to generation of NADH. (An increase in NADH relative to NAD+ favors lipid synthesis).
2) impaired assembly & secretion of lipoproteins (acetaldehyde binds to tubulin and prevents the function of microtubules resulting in decreased transport of lipoproteins from the liver).
3) increased peripheral catabolism of fats.
4) decreased oxidation of fatty acids.
).
