Effects of short-term high carbohydrate, fat-free diet on plasma levels of Apo C-II and Apo C-III and on the Apo C subspecies in human plasma lipoproteins

Falko, James M.; Schonfeld, Gustav; Witztum, Joseph L.; Kolár, J; Salmon, P.

doi:10.1016/0026-0495(80)90110-9

Cited by 47 publications

(17 citation statements)

References 20 publications

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“…In rats fed a high carbohydrate diet, the relative proportions of apo C-III-0 increased, whereas apo C-III-3 fell in plasma VLDL (10). And in humans fed a high-carbohydrate fat-free diet for 7 d there was an increase of apo C-III-0 relative to the other C-peptides on VLDL (11).…”

Section: Introductionmentioning

confidence: 94%

An abnormal triglyceride-rich lipoprotein containing excess sialylated apolipoprotein C-III.

Holdsworth¹,

Stocks²,

Dodson³

et al. 1982

J. Clin. Invest.

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AB S T R A C T An abnormal triglyceride-rich lipoprotein has been isolated from some patients with chronic renal failure or severe hypertriglyceridemia. The abnormal lipoprotein was characterized by an increased content of apolipoprotein (apo) C-III-2 (57.5% of total apo C-III peptides compared with 35.5% for controls, P < 0.001) as characterized by isoelectric focusing and scanning densitometry. As determined by a substrate competition assay, the abnormal lipoprotein was a less efficient substrate for purified bovine milk lipoprotein lipase than control lipoproteins. Neuraminidase digestion of abnormal or control lipoprotein resulted in a reduction of the apo C-III-2 band with a corresponding increase in the region of apo C-III-0, which suggests that the increased content of apo C-III-2 in the abnormal is due to excessive sialylation of the C-III peptide. Limited incubation of the abnormal lipoproteins with neuraminidase caused a partial loss of sialic acid and resulted in a triglyceride-rich lipoprotein with a normal C-III-2:C-III-1 ratio. This preparation displayed normal substrate interaction with lipoprotein lipase. Three severely hypertriglyceridemic patients with the abnormal lipoprotein showed a marked reduction in serum triglyceride concentration, which is associated with a reversion to a normal C-peptide profile after dietary therapy. The results suggest that the extent of sialylation of the apo C-III peptide carried on triglyceride-rich lipoproteins may be critical for their interaction with lipoprotein lipase.

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Section: Introductionmentioning

confidence: 94%

An abnormal triglyceride-rich lipoprotein containing excess sialylated apolipoprotein C-III.

Holdsworth¹,

Stocks²,

Dodson³

et al. 1982

J. Clin. Invest.

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“…For instance, high carbohydrate diets, which have been associated with reductions in total and LDL cholesterol 2425 have also resulted in increases in VLDL 2425 and decreases in HDL cholesterol. 24 In addition, obese subjects who are hyperinsulinemic have increases in total cholesterol, VLDL cholesterol, and LDL cholesterol with lower HDL cholesterol concentrations than normal-weight controls. 12 Thus, although the present study was a short-term one and involved a nonphysiologic administration of insulin, we observed an antiatherogenic influence of insulin on lipoprotein cholesterol distribution in normal human subjects.…”

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confidence: 99%

Insulin-mediated increases in the HDL cholesterol/cholesterol ratio in humans.

Sadur¹,

Eckel²

1983

Arteriosclerosis

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The role of insulin in the regulation of lipoprotein cholesterol distribution was studied in 18 human volunteers who were of normal weight, normolipemic, and glucose-tolerant. We used the euglycemic clamp technique and made comparisons with six saline-infused controls. While total cholesterol and low density lipoprotein cholesterol levels fell similarly by 6 hours in both groups (p = NS), there was a greater decrease in triglyceride levels (p < 0.02) but less decrease in high density lipoprotein cholesterol levels (p < 0.02) in the insulin-infused group. These changes resulted in both a higher high density lipoprotein cholesterol/total cholesterol ratio (p = 0.01) and a higher high density lipoprotein cholesterol/low density cholesterol ratio (p = 0.02) in the insulin-infused group. The timing of this effect of insulin implies a mechanism unrelated to high density lipoprotein turnover. Thus, insulin infusion during euglycemia appears to alter cholesterol distribution favorably in normal subjects. T he role of insulin in the regulation of lipoprotein cholesterol metabolism is unclear. In vivo, diseases at the extremes of serum insulin concentration have been associated with alterations in lipoprotein cholesterol distribution. In obesity, a state where serum insulin is high, there are increases in total, very low density lipoprotein (VLDL), and low density lipoprotein (LDL) cholesterol and a decrease in high density lipoprotein (HDL) cholesterol.12 Type I diabetes mellitus, where serum insulin is low, is associated with altered lipoprotein metabolism which normalizes with improved glycemic control.3 " 5 In fact, some studies have demonstrated increased levels of HDL cholesterol, 67 HDL cholesterol/total cholesterol, or HDL cholesterol/LDL cholesterol ratios 8 in insulin-treated diabetics. Although the lipoprotein alterations seen in the insulinopenic patient could have resulted from insulin deficiency alone, a direct effect of insulin on lipoprotein cholesterol metabolism has not been proven because other metabolic alterations are also corrected (e.g., ketonemia). Thus, a method to examine the insulin effect in a more direct manner would be beneficial. In the present study, the euglycemic clamp technique has provided a tool for assessment of the effect of insulin on lipoprotein cholesterol distribution in human subjects. MethodsThe study group included 18 subjects who received intravenous insulin and glucose. Each person was average in height and within 20% of ideal body weight according to the Metropolitan Life Insurance Company Standards. 9 The body mass index (wt/ht 2 ) was 2.06 x 10" 3 ± 0.05 kg/cm 2 (x ± SEM). The subjects ranged in age from 20 to 45 years, x = 29.2 ± 1.4 years. There were 15 women and three men. The control group, composed of four women and two men, received intravenous infusions of 0.9% (normal) saline at approximately 100 to 150 ml/hr. They were also normal in height and weight with a body mass index of 2.17 x 10~3 ± 0.05 kg/cm 2 and with an age range of 23 to 40 years, x = 29.0 ± 2.5 year...

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“…Earlier studies have showed that the total absence of apoC or defects in its structure severely hamper the lipolysis of TG-enriched lipoproteins (TRLs), contributing to the development of hypertriglyceridemia in humans 24) . On the other hand, it has been reported that transgenic mice overexpressing human apoC were hypertriglyceridemic 25) , and hypertriglyceridemia is regularly accompanied by a several-fold increase in apoC plasma levels [26][27][28] . In comparison with numerous studies of the functional properties of apoC , only modest attention has been paid to the roles of apoC in lipoprotein metabolism.…”

Section: Discussionmentioning

confidence: 99%

Influence of ApolipoproteinCII Concentrations on HDL Subclass Distribution

Tian

Xu²,

et al. 2009

JAT

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Aim:To demonstrate the interrelationship between plasma apolipoprotein(apo)C concentrations and the pattern of high-density lipoprotein (HDL) subclass distribution. Methods: ApolipoproteinA-contents of plasma HDL subclasses were quantified by 2-dimensional gel electrophoresis associated with immunodetection in 504 Chinese subjects. Results: Compared with subjects in the lowest tertile of the apoC group, the contents of pre 1-HDL, HDL3b, and HDL3a were significantly higher than HDL2a and HDL2b in subjects in the middle and highest tertiles of the apoC group. Moreover, regardless of whether apoB100 increased, pre 1-HDL contents increased, but HDL2b fell when apoC rose while, at any apoC levels, HDL2b rose with the elevation of apoA-. Additionally, a reduction in pre 1-HDL (from 131.9 to 90.6 mg/L) but an increase in HDL2b (from 269.1 to 382.7 mg/L) with a rise in the apoC /C value (between 0.8 and 5.6) were also observed. Conclusion:The particle size of HDL become smaller with the increase of apoC levels, implying that the efficiency of reverse cholesterol transport (RCT) was impaired and blocked the maturation of HDL. ApoC might be an independent factor affecting the distribution of HDL subclasses. Further, the apoC /C ratio correlated with the size of HDL particles. J Atheroscler

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Effects of short-term high carbohydrate, fat-free diet on plasma levels of Apo C-II and Apo C-III and on the Apo C subspecies in human plasma lipoproteins

Cited by 47 publications

References 20 publications

An abnormal triglyceride-rich lipoprotein containing excess sialylated apolipoprotein C-III.

An abnormal triglyceride-rich lipoprotein containing excess sialylated apolipoprotein C-III.

Insulin-mediated increases in the HDL cholesterol/cholesterol ratio in humans.

Influence of ApolipoproteinCII Concentrations on HDL Subclass Distribution

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