PMID- 214369
OWN - NLM
STAT- MEDLINE
DCOM- 19790221
LR  - 20190515
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 27
IP  - 12
DP  - 1978 Dec
TI  - Carbohydrate diet-induced changes in very low density lipoprotein composition and 
      structure.
PG  - 1215-29
AB  - High carbohydrate (CHO) diets cause accumulation in plasma of larger, 
      triglyceride (TG)-enriched very low density lipoprotein (VLDL) particles. In man, 
      the composition of the VLDL is changed by such diets as well. The source of the 
      altered VLDL particles is presumed to be the liver, but the intestine is known to 
      secrete VLDL, and VLDL is also altered during its postsecretory catabolism. To 
      ascertain that the liver is a source of "diet-induced VLDL," we fed rats CHO and 
      control diets and we examined plasma levels of lipids chemically and apoproteins 
      A-I (ApoA-I) and B (ApoB) by specific radioimmunoassay (RIA). VLDL (d less than 
      1.006) and VLDL density subfractions were isolated and their composition studied 
      by RIA, column chromatography, isoelectric focusing (IEF), and polyacrylamide gel 
      electrophoresis. Livers from control and CHO-fed rats were perfused in vitro. 
      Whole perfusates and perfusate VLDL were studied similary. In the CHO-fed rats, 
      plasma TG increased, cholesterol and ApoA-I remained unchanged, and ApoB fell. 
      The VLDL isolated were TG enriched and less dense. Although total VLDL-protein 
      rose, the proportion of VLDL-protein that was ApoB and arginine-rich protein 
      (ARP) fell, while ApoC rose. The ApoB content varied directly with density of 
      particles. ARP subunits were not changed, but relative proportions of ApoC-III0 
      rose from 39 to 46 per cent of dye uptake on IEF gels and ApoC-III3 fell from 34 
      to 26 per cent. Thus, CHO feeding produced altered plasma VLDL in the rat. The 
      perfused livers of the CHO-fed rat secreted more TG, but absolute secretory rates 
      for cholesterol, ApoB, and ApoA-I were unchanged. The VLDL isolated from 
      perfusates were larger, TG-enriched, and less dense. Although VLDL-protein rose, 
      the proportion that was ApoB fell; both ApoC and ARP rose, ARP subunits were 
      unchanged, while ApoC-III0 rose from 29 to 37 per cent and ApoC-III3 fell from 48 
      to 42 per cent. In contrast to plasma, ApoC content was not increased relative to 
      ARP. As in plasma, content of ApoB varied with particle density. Thus, CHO 
      feeding induced changes in hepatic perfusate VLDL structure and composition that 
      in general paralleled those changes seen in plasma. This strongly suggests that 
      the action of diet on the liver is responsible for many of the changes seen in 
      plasma VLDL. On the other hand, the discrepancy between the VLDL-ApoC content and 
      subunit proportions of plasma and perfusate suggests that the discrepancy is due 
      to postsecretory processing. Similarly, the failure to see decreases in absolute 
      hepatic ApoB secretion, while plasma ApoB levels fell, suggests that the 
      postsecretory metabolism of ApoB-containing lipoproteins is also altered by diet. 
      In addition, the failure to see increases in hepatic VLDL-ApoB secretory rates at 
      a time when VLDL-TG and VLDL-protein increased suggests that there is no tight 
      coupling between the secretion of ApoB and lipids.
FAU - Witztum, J L
AU  - Witztum JL
FAU - Schonfeld, G
AU  - Schonfeld G
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Apoproteins)
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Lipoproteins, VLDL)
RN  - 0 (Triglycerides)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Animals
MH  - Apoproteins/analysis/*blood
MH  - Cholesterol/blood
MH  - Dietary Carbohydrates/*administration & dosage
MH  - Lipoproteins, VLDL/analysis/*blood
MH  - Liver/analysis
MH  - Male
MH  - Radioimmunoassay
MH  - Rats
MH  - Triglycerides/blood
EDAT- 1978/12/01 00:00
MHDA- 1978/12/01 00:01
CRDT- 1978/12/01 00:00
PHST- 1978/12/01 00:00 [pubmed]
PHST- 1978/12/01 00:01 [medline]
PHST- 1978/12/01 00:00 [entrez]
AID - 10.2337/diab.27.12.1215 [doi]
PST - ppublish
SO  - Diabetes. 1978 Dec;27(12):1215-29. doi: 10.2337/diab.27.12.1215.