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Carbohydrate diet-induced changes in very low density lipoprotein composition and structure
Diabetes
|December 1, 1978
Summary
High carbohydrate diets alter very low-density lipoprotein (VLDL) particles in rats. The liver is a primary source of these diet-induced VLDL changes, affecting triglyceride and apoprotein composition.
Area of Science:
- Lipid metabolism
- Nutritional biochemistry
- Atherosclerosis research
Background:
- High carbohydrate diets are known to influence plasma lipoprotein profiles.
- Very low-density lipoprotein (VLDL) particles are central to triglyceride transport.
- The liver's role in producing diet-altered VLDL requires clarification.
Purpose of the Study:
- To determine if the liver is the source of diet-induced VLDL changes.
- To characterize the composition and structure of VLDL secreted by the liver under high carbohydrate conditions.
- To investigate the impact of diet on hepatic VLDL secretion and postsecretory processing.
Main Methods:
- Rats were fed high carbohydrate or control diets.
- Plasma and liver VLDL composition was analyzed using radioimmunoassay, chromatography, and electrophoresis.
- In vitro liver perfusion was used to study VLDL secretion.
- Lipid and apoprotein levels (ApoA-I, ApoB, ApoC, ARP) were quantified.
Main Results:
- High carbohydrate feeding led to larger, triglyceride-enriched VLDL particles in plasma and liver perfusates.
- Hepatic VLDL secretion increased in triglyceride content but not in absolute apoprotein B secretion.
- Alterations in apoprotein composition, particularly increased ApoC and shifts in ApoC-III isoforms, were observed in both plasma and hepatic VLDL.
- Discrepancies in apoprotein composition between plasma and perfusate VLDL suggest postsecretory modifications.
Conclusions:
- The liver is a significant source of the altered VLDL particles observed in plasma following high carbohydrate diets.
- Diet-induced changes in hepatic VLDL composition are largely mirrored in the circulation.
- Postsecretory processing and metabolism play a role in the final composition of circulating VLDL, particularly concerning apoprotein content.