Biomedical subjects

B Teng

Publications and source records attributed to B Teng.

40 records · Page 3Linked to original sources

PubMed1978

Low density lipoprotein. A metabolic pathway for return of cholesterol to the splanchnic bed.

The mechanism(s) by which cholesterol returns to the splanchnic bed from peripheral tissues are not well understood. To study this phenomenon in fasting man, lipoproteins were isolated from plasma obtained from hepatic vein and aorta. Cholesterol content of each lipoprotein class was determined and arteriovenous (AV) differences could be calculated for each patient. The results in the first 24 patients indicated splanchnic secretion of very low density lipoprotein cholesterol (mean AV difference - 3 mg/100 ml, P < 0.01), but not significant AV difference for total cholesterol, high density lipoprotein cholesterol, or low density lipoprotein (LDL) B protein. In contrast, for LDL (d 1.006-1.063 g/ml), there was significant uptake of cholesterol across the AV bed +8 mg/100 ml, P < 0.0002). In a further 15 patients, similar samples were obtained and intermediate density lipoprotein isolated at d 1.006-1.019 g/ml and LDL at 1.019-1.063 g/ml. The AV difference previously noted could now be localized to the 1.019-1.063 cholesterol ester moiety (+8 mg/100 ml, P < 0.0005). In the final 14 patients, the LDL cholesterol AV difference was again confirmed and shown to be unrelated to heparin. As well, there was secretion of triglyceride in the hepatic vein LDL. These quantitative data obtained in man raise the possibility that LDL rather than high density lipoprotein transports cholesterol ester to the splanchnic bed.

Apolipoproteins↗

PubMed1977

Predictable changes in low density lipoprotein composition after acute myocardial infarction.

Acute changes in low density lipoprotein cholesterol levels may be due to both a change in the number of LDL particles/ml of plasma and an alteration in the amount of cholesterol per LDL particle. Since LDL cholesterol levels are known to alter abruptly after myocardial infarction, the composition of LDL was determined in nine patients who suffered an uncomplicated transmural myocardial infarction. In six of these, LDL cholesterol levels fell whereas in three LDL cholesterol rose during the first nine days in hospital. The contents of B protein, free cholesterol, phospholipid, cholesterol ester and triglyceride in LDL were determined in the initial sample and the subsequent sample showing the greatest changes in LDL cholesterol level. The proportion of the LDL molecule contributed by B protein, free cholesterol and phospholipid did not differ significantly between the two samples. In contrast, when LDL cholesterol fell, the decrease in the proportion of cholesterol ester was disproportionately greater than in triglyceride. The opposite was observed when LDL cholesterol rose. This inverse relation between changes in LDL cholesterol ester and triglyceride could be expressed by Y = -1.02 X -0.17 (r = -0.94). These data are consistent with a pseudomicellar model of LDL in which the surface components are present in fixed amounts but the interior shell of cholesterol ester and triglyceride varies in an inverse relation depending on the absolute LDL concentration.

Cholesterol↗

PubMed1975

Determination of B protein of low density lipoprotein directly in plasma.

Quantitation of the apoprotein constituents of lipoproteins has extended our knowledge of plasma lipid transport. Previously, B protein content of low density lipoprotein could be measured by radial immunodiffusion only after ultracentrifugation. However, if performed in 1.5% agarose gel with standards and measured at 18 hr rather than at equilibrium, low density lipoprotein B protein can be measured directly in plasma, eliminating the need to separate very low density lipoprotein.

Apoproteins↗

PubMedDate not supplied

Hyperapobetalipoproteinemia. Plasma lipoprotein responses to oral fat load.

To better define lipid transport in patients with hyperapobetalipoproteinemia (HyperapoB), the response to an oral fat load was studied in six normotriglyceridemic patients with the disorder. Plasma triglycerides; Sf greater than 400, and Sf 20 to 400 triglycerides; Sf greater than 20 B100; total HDL and HDL subfractions (HDL2 and HDL3) were measured serially for a 7-hour period after an oral fat load and changes in these parameters were compared to those observed in six normolipidemic controls. In addition, plasma triglyceride levels and HDL2 and HDL3 cholesterol were also determined in seven patients with Type IV hyperlipoproteinemia: three with normal LDL apo B levels and four with HyperapoB. When the two normotriglyceridemic groups were compared, the patients with HyperapoB had significantly higher fasting levels of SF greater than 400 lipoproteins and higher fasting VLDL and LDL levels than the normal patients. After the fat load, Sf 20 to 400 triglycerides and Sf greater than 20 B100 levels increased in both groups. Plasma triglycerides rose to a higher level in the HyperapoB patients than in the normal group, but more strikingly, remained elevated in the HyperapoB patients, an elevation due principally to a persistant increase in Sf greater than 400 triglycerides. On the other hand, HDL2 cholesterol dropped substantially in the HyperapoB patients but not in the normal patients. Finally, in the hypertriglyceridemic group, after the fat load, HDL2 cholesterol levels did not change in the patients with normal LDL apo B levels but did decrease in those with elevated plasma LDL apo B.

Adult↗