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The polypeptide distribution of lipoprotein density fractions isolated from normal human serum by rate zonal ultracentrifugation was investigated by polyacrylamide gel electrophoresis and qualitative and quantitative immunochemical methods. In very-low-density lipoproteins all known apoA and apoC peptides were present in amounts similar to these preparations from fixed-angle rotors. Low-density apolipoproteins consisted primarily of apoB (98%) but some small amounts of apoAIII and apoCIII were also present. No region of 100% apoB, uncontaminated by A and C peptides could be isolated by subfractionation of the low-density peak. There were marked differences in the protein part of the high-density lipoprotein subtractions 2 and 3, as compared to these subfractions separated in the angle-head rotor. The weight ratio apoAI: apoAII was found to be approximately three times as high for subfraction 2 as for subfraction 3. In addition, apoAIII was detectable only in subfraction 3. Of the known apoC peptides, apoCII was present in both fractions only in trace amounts, while the concentration of apoCI was in the order of 1% and that of apoCIII1 and of apoCIII2 in the order of 1.5%. Apolipoprotein B was not detectable in subfraction 2. Two density regions were found with small amounts of lipoproteins consisting only of apoAI polypeptides. A peak corresponding to subfraction 1 of the high-density lipoprotein from fixed-angle rotor preparations could not be detected in the eluate of zonal rotors after 24-h runs; the low-density lipoprotein peak was symmetrical in all experiments. Lipoproteins present in the bottom fraction amounted to about 2.5–4% of the total lipoprotein content. The only apolipoprotein found in this fraction was apoAI.

In this study, we have investigated the effects of alimentary lipemia in 15 normotriglyceridemic individuals on high density lipoproteins2 (HDL2) with respect to structure, composition, and substrate efficacy for hepatic lipase in vitro. In the study subjects, HDL2 levels ranged widely from 4.7 to 151.7 mg/dl plasma. HDL2 were isolated in the postabsorptive (pa) state and in the postprandial (pp) state, i.e., 7 h after ingestion of a standard fatty meal. In going from the pa state to the pp state, HDL2 exhibited higher flotation rates and lower densities due to a decreased proportion of protein (38.7----36.2%) and a higher abundance in phospholipid (32.5----34.9%). There was a variable increase in triglyceride at the expense of cholesteryl esters; this increase was correlated positively with the magnitude of pp lipemia (r = 0.69, P less than 0.01) and inversely with HDL2 levels (r = -0.72, P less than 0.01). Hdl2 fractions were incubated with human hepatic lipase in vitro. Product lipoproteins formed from lipolysis of pa-HDL2 and triglyceride-poorer pp-HDL2 were reduced in phospholipid content (by 25 and 50%, respectively) but remained in the size and density range of native HDL2. By contrast, a major fraction of triglyceride-richer pp-HDL2 was converted to particles with density, size, and apoprotein composition of native HDL3. Changes consistent with these findings in vitro were observed in vivo also, where 15 h postprandially, individuals with high-level lipemia showed a decrease in HDL2 and rise in HDL3, while those with lower-level lipemia did not. This study indicates that the magnitude of postprandial lipemia determines the proportion of triglyceride in pp-HDL2, which in turn determines whether or not HDL2 are converted to HDL3 by hepatic lipase action.

The effect of calcium infusion on the intravenous glucose tolerance was tested in hypocalcaemic patients suffering from renal insufficiency. It was shown that the delayed glucose disappearance rate in uraemics could be improved (p < 0.005) by the infusion of calcium gluconolactobionate despite the fact that the serum concentrations of potassium, urea nitrogen, and the blood pH were not altered. The basal insulin concentration was significantly depressed by the calcium infusion (p < 0.02). The serum calcium concentration was significantly correlated to the glucose assimilation coefficient in the uraemic patients (p < 0.01). — 3 hypocalcaemic patients without renal failure had a normal glucose tolerance and a normalization of the serum calcium concentration had no discernable effect. — A slight but significant decrease of the serum calcium concentration (p < 0.01) by EDTA-Na2 in normocalcaemic patients did not change the intravenous glucose tolerance. — It is concluded that hypocalcaemia may be one of the causes for the abnormal glucose tolerance in chronic renal failure.