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B Teng

Publications and source records attributed to B Teng.

At least 37 records · Page 2Linked to original sources
PubMed1990

Apolipoprotein B messenger RNA editing is developmentally regulated in pig small intestine: nucleotide comparison of apolipoprotein B editing regions in five species.

Apolipoprotein B (apo B) mRNA undergoes a posttranscriptional tissue-specific editing reaction which changes codon 2153 from glutamine (CAA) in apoB-100 mRNA to an in-frame stop codon (UAA) in apoB-48 mRNA. Small intestinal apo B mRNA was found to be predominantly (greater than 90%) unedited in fetal (40-day gestational age) piglets but greater than 95% edited in neonatal, suckling and adult animals. By contrast, both fetal, neonatal and adult pig liver contained greater than 99% unedited, apo B-100 mRNA. The nucleotide sequence spanning the edited region in apo B mRNA was found to be highly conserved. We speculate that the regulation of apo B mRNA editing may be developmentally modulated in pig small intestine.

Aging↗
PubMed1990

Apolipoprotein B messenger RNA editing is developmentally regulated and widely expressed in human tissues.

Apolipoprotein B (apoB) messenger RNA (mRNA) undergoes posttranscriptional (C to U) editing, producing tissue-specific forms of apoB from the unedited (apoB100) and edited (apoB48) transcripts. ApoB mRNA editing is developmentally regulated in human fetal small intestine, producing parallel changes in the synthesis and secretion of apoB100 and apoB48. Neither fetal nor adult liver contained detectable levels (less than 1%) of edited apoB mRNA. By contrast, apoB mRNA is incrementally edited during development in several extraintestinal fetal tissues. These tissues demonstrated significant differences, however, in both the extent and developmental profile of apoB mRNA editing. Additionally, while apoB100 synthesis and secretion was demonstrated in these tissues, apoB48 synthesis was confined to the small intestine. Thus, although the molecular mechanism underlying this process remains unclear, the capacity to edit apoB mRNA is widely distributed among both fetal and adult tissues. We speculate that the asynchronous and developmentally modulated induction of apoB mRNA editing may provide a novel mechanism for regulating lipoprotein biogenesis in both the developing fetus and adult human.

Adult↗
PubMed1988

Adipose tissue glyceride synthesis in patients with hyperapobetalipoproteinemia.

Adipose tissue was obtained at thoracotomy in five control patients with valvular heart disease, all of whom were free of coronary artery disease and all of whom were normolipidemic with normal low density lipoprotein apolipoprotein B levels, and eight patients with coronary artery disease, all of whom had hyperapobetalipoproteinemia. In both groups, the rates at which linoleic acid and palmitic acid were incorporated into diglyceride and triglyceride were determined in vitro. The data indicate that fatty acid incorporation into adipose tissue glycerides was twice as rapid in controls as in patients with hyperapobetalipoproteinemia. By contrast there was no difference between the groups in the rate of net lipolysis of adipocyte glyceride. The data at hand do not establish the mechanism responsible for the difference in synthesis between normal subjects and patients with hyperapobetalipoproteinemia, but this may explain the delayed chylomicron triglyceride clearance previously observed in the disorder.

Adipose Tissue↗
PubMed1987

Kinetics of LDL subfractions.

After injecting 125I- or 131I-labeled lipoproteins, plasma was subjected to discontinuous density gradient centrifugation, which separates low-density lipoproteins (LDL) into three subfractions. Analysis of changes in apolipoprotein B-specific activity with time showed that light LDL is normally the product of intermediate-density lipoprotein and the precursor of heavy LDL, which is subsequently converted to heavier LDL. In hyperapobetalipoproteinemia these relationships are maintained but there is overproduction of light and heavy LDL secondary to increased synthesis of very low-density lipoprotein. In familial hypercholesterolemia, light LDL is produced normally but its conversion into heavy LDL is reduced and independent synthesis of the latter is apparent. These observations suggest that the LDL receptor normally plays a role in the conversion of light into heavy LDL. They also provide an explanation for previously documented differences in LDL composition between hyperapobetalipoproteinemia, in which there is a relative increase in cholesterol-depleted heavy and heavier subfractions, and familial hypercholesterolemia, in which there is a relative increase in the cholesterol-enriched light subfraction.

Animals↗
PubMed1986

Metabolic basis of hyperapobetalipoproteinemia. Turnover of apolipoprotein B in low density lipoprotein and its precursors and subfractions compared with normal and familial hypercholesterolemia.

The turnover of apolipoprotein B (apo B) in very low density, intermediate density, and low density lipoproteins (VLDL, IDL, and LDL) and in the light and heavy fractions of LDL was determined in seven patients with hyperapobetalipoproteinemia (hyperapo B), six normolipidemic subjects, and five patients with heterozygous familial hypercholesterolemia (FH). After receiving an injection of 125I-VLDL, hyperapo B patients were found to have a higher rate of synthesis of VLDL-apo B than controls (40.1 vs. 21.5 mg/kg per d, P less than 0.05) but a reduced fractional catabolic rate (FCR) (0.230 vs. 0.366/h, P less than 0.01). After receiving an injection of 131I-LDL, hyperapo B patients had higher rates of LDL-apo B synthesis than controls (23.1 vs. 13.0 mg/kg per d, P less than 0.001), as did FH patients (22.7 mg/kg per d). The FCR of LDL was similar in hyperapo B patients and controls (0.386 vs. 0.366/d) but was markedly decreased in FH patients (0.192/d). Most subjects exhibited precursor-product relationships between VLDL and IDL, and all did between IDL and light LDL; an analogous relationship between light and heavy LDL was evident in most hyperapo B patients and controls but not in FH patients. Simultaneous injection of differentially labeled LDL fractions and deconvolution analysis showed increased light LDL synthesis with normal conversion into heavy LDL in hyperapo B, whereas in FH conversion of light LDL was reduced and there was independent synthesis of heavy LDL. These data show that the increased concentration of LDL-apo B in hyperapo B is solely due to increased LDL synthesis, which is secondary to increased VLDL synthesis; in contrast, in FH there is both an increase in synthesis of LDL (which is partly VLDL-independent) and reduced catabolism.

Apolipoproteins B↗
PubMed1986

Genetic analysis of plasma sitosterol, apoprotein B, and lipoproteins in a large Amish pedigree with sitosterolemia.

We previously reported the finding of phytosterolemia, xanthomatosis, and hyperapobetalipoproteinemia (hyperapoB) in five siblings in a large Amish pedigree ascertained through a 13-year-old boy who died suddenly from advanced coronary atherosclerosis. Here, we present further analyses of the plasma levels of the plant sterol, sitosterol, of low density (beta) lipoprotein (LDL) sterol, and of LDL B protein. Of 254 relatives and spouses of the proband, 90.5% were examined. A series of genetic models were explored using a pedigree analysis where parameters reflecting frequency, transmission, and penetrance of putative genotypes were examined simultaneously using a maximum likelihood approach. Segregation analysis of the sitosterol levels showed that the phenotype of sitosterolemia was controlled by a rare autosomal recessive gene. There was also significant familial correlation in plasma sitosterol levels that was attributed to a polygenic component under a mixed model but could also be due to shared environments such as diets. The recessive model was supported by our finding that the plasma sitosterol levels in the parents and in six children born to three of the five sitosterolemics were less than 1 mg/dl, well within the normal range. The phenotype of hyperapoB is based on an elevated level of LDL B protein in the presence of a normal LDL cholesterol level (low LDL sterol to LDL B ratio). For both LDL sterol and LDL B, a polygenic model showed a slightly greater improvement in ln likelihood than did the Mendelian single locus model when both were compared to a sporadic model. Similar results were obtained for sterol levels of high density (alpha) lipoprotein (HDL) sterol. When segregation analysis was performed using the ratio of LDL sterol to LDL B, the Mendelian single locus model gave a slightly better fit to the data than did the polygenic model. While the analyses presented here provided unequivocal evidence for the recessive phenotype of phytosterolemia, we also identified a possible single gene factor that could account for the major portion of the strong familial aggregation in the ratio of LDL sterol to LDL B, and to a lesser extent LDL B. However, there is clear evidence of familial aggregation for these traits in this pedigree beyond that due to Mendelian components.

Adolescent↗
PubMed1985

Modulation of apolipoprotein B antigenic determinants in human low density lipoprotein subclasses.

To investigate the effect of low density lipoprotein (LDL) heterogeneity on the conformation of LDL apolipoprotein B (apo-B), the immunoreactivities of 6 monoclonal antibodies against LDL apo-B were measured in 3 LDL subfractions isolated by equilibrium density gradient ultracentrifugation. To ensure a broad range of LDL particles, the LDL subfractions were prepared from normal subjects and patients with hyperapobetalipoproteinemia. With 3 of the antibodies, 1D1, 5E11, and 3A10, LDL fractions 1 (the most buoyant), 2 (the intermediate), and 3 (the densest) were equally immunoreactive and competed similarly with reference whole LDL. In contrast, with 3 other antibodies, 2D8, 3F5, and 4G3, fraction 1 was significantly more reactive than fraction 3; that is for each in turn, 290, 250, and 150% more of the densest LDL protein was required to achieve the same displacement as with fraction 1. Further, the immunoreactivities of the 3 LDL fractions with antibodies 2D8, 3F5, and 4G3 were negatively correlated with their LDL cholesterol to LDL protein ratio with r values of 0.727, 0.898, and 0.870, respectively, suggesting that as LDL particle size decreases, the conformation of the LDL apo-B changes progressively. It is of interest that the antigenic determinants recognized by 3F5 and 4G3 are close to the LDL receptor recognition site on LDL apo-B. Therefore, it is possible that the reduced immunoreactivity of these determinants in dense LDL may be the in vitro correlate of the reduced fractional catabolics rate of dense LDL compared to buoyant LDL previously observed in vivo.

Antibodies, Monoclonal↗
PubMed1985

Familial aggregation and early expression of hyperapobetalipoproteinemia.

Family history is an important predictor of coronary risk. However, this relation, in large part, is not explained by the known risk factors such as systemic hypertension or hyperlipidemia. In the present study, plasma lipid, lipoprotein lipid, and plasma low-density lipoprotein (LDL) apoB levels were measured in 66 offspring (myocardial infarction [MI] offspring) of 24 families in which an index parent had premature coronary artery disease and hyperapobetalipoproteinemia. These results were compared to those obtained in 207 control children and young adults. Univariate analysis revealed that plasma LDL apoB and all other lipid and lipoprotein levels except high-density lipoprotein cholesterol were significantly higher in the MI offspring. Multivariate analysis showed plasma LDL apoB and LDL cholesterol best differentiated the MI offspring from control children and young adults. Of the 66 children, 22 had hyperapobetalipoproteinemia, of whom only 7 had clearly abnormal LDL cholesterol or plasma triglyceride levels. Thus, a substantial portion of children born to a parent with premature coronary artery disease and hyperapobetalipoproteinemia have the same disorder of lipoprotein metabolism.

Adolescent↗
PubMed1985

Surface morphology of Asian cadaveric hips.

The joint surfaces of 60 hips obtained from the cadavers of elderly Asians were studied to determine the incidence, the grade and the distribution of both non-progressive (age-related) and progressive degenerative changes. It was observed that in the Asian population of 40 to 90 years of age, non-progressive changes were common, being seen in 66% of the acetabular specimens and 50% of the femoral heads. Only one specimen of the 60 showed unexplained progressive degenerative change. We conclude that primary osteoarthritis of the hip is rare in Asians.

Acetabulum↗
PubMed1985

Gait analysis in cerebral palsy.

Ambulation problems in cerebral palsy have been very difficult to analyse because it is the central control system rather than the motor system that is at fault. Until recently, decisions regarding surgical management has been made on clinical grounds, which by and large, have been subjective. Attempts to remedy this situation has resulted in the setting up of Gait Analysis Laboratories to provide a more objective method of evaluation of disorders of human motion. We have recently been using an opto-electronic computer-based gait analysis system to analyse normal as well as abnormal gait. Gait analysis can provide information regarding movements of both lower limbs in three planes, ground reaction forces, joint torque and dynamic electromyography. Children with various types of Cerebral Palsy have been assessed. The results of four clinical gait assessment cases are presented and discussed. Information provided by the Gait Analysis Laboratory has introduced more objectivity in pre-operative planning for these children.

Adolescent↗
PubMed1985

Effect of dietary treatment on the plasma levels of lipids, lipoprotein cholesterol and LDL B protein in children with type II hyperlipoproteinemia.

These data confirm the effectiveness of therapeutic diets in children with type II hyperlipoproteinemia in conventional terms. However, the decrease in LDL cholesterol was not accompanied by a significant decrease in LDL B (suggesting only a small change in the number of LDL particles in plasma), and a fall in HDL cholesterol occurred, with no significant improvement in the LDL to HDL cholesterol ratio. These findings indicate that further research is needed to develop diets with more optimal effects. Finally, our hypothesis that such diets may produce an LDL particle of altered composition, needs to be confirmed using additional physical-chemical measurements of the size, composition and molecular weight distribution of LDL in plasma before and after dietary intervention.

Adolescent↗
PubMed1983

Composition and distribution of low density lipoprotein fractions in hyperapobetalipoproteinemia, normolipidemia, and familial hypercholesterolemia.

Hyperapobetalipoproteinemia is defined as the combination of a normal low density lipoprotein (LDL) cholesterol in the face of an increased LDL apolipoprotein B (apoB) protein. To examine the physical basis for the apparent disproportion between LDL cholesterol and apoB characteristic of this syndrome, we used density gradient ultracentrifugation to isolate LDL fractions from 10 normal subjects, from 20 patients with hyperapobetalipoproteinemia (10 normotriglyceridemic and 10 hypertriglyceridemic), and from 7 patients with familial hypercholesterolemia. In familial hypercholesterolemia, more LDL was in fraction 1--"light" LDL--and this LDL was relatively enriched in cholesterol and poor in protein. By contrast, it was fraction 2--"heavy" LDL--that differed in hyperapobetalipoproteinemia, being denser, depleted of cholesterol (particularly cholesteryl ester), and relatively enriched in apoB. These findings were more pronounced in the hypertriglyceridemic patients than in the normotriglyceridemic patients with hyperapobetalipoproteinemia. Thus this study confirms that considerable heterogeneity exists between LDL subfractions within individuals but, in addition, indicates there are also marked--and apparently characteristic--differences in LDL composition amongst normal subjects and patients with hyperapobetalipoproteinemia or familial hypercholesterolemia.

Apolipoproteins↗
PubMed1982

Association of hyperapobetalipoproteinemia with endogenous hypertriglyceridemia and atherosclerosis.

Researchers disagree on whether plasma triglyceride levels are an independent risk factor for atherosclerotic coronary artery disease. We hypothesized that patients with endogenous hypertriglyceridemia would differ: Some would have normal values of plasma low-density lipoprotein (LDL) B protein; others, despite their normal level of LDL cholesterol, would have increased levels of LDL B protein. We believe the latter patients--those with hyperapobetalipoproteinemia--would be the ones at risk for atherosclerosis. We studied two populations. Group 1, consisting of 162 patients with type IV lipoprotein patterns, was divided into two groups. One subgroup (A), which included 38 patients with elevated plasma LDL B atherosclerotic disease than the other subgroup (B) of 36 patients with normal levels of plasma LDL B protein (10 patients versus two, p less than 0.02). Group 2 consisted of 100 patients who had had myocardial infarction. Eighty-one percent of the 47 hypertriglyceridemic and 70% of the 53 normotriglyceridemic patients had elevated plasma LDL B protein levels (129 mg/dL or greater)--a proportion significantly higher than that in Group 1 (p less than 0.001). Thus, an elevated plasma level of LDL B protein not only identifies subgroups of patients with type IV lipoprotein patterns, but also may be an important marker for atherosclerotic disease.

Adult↗
PubMed1981

Hyperapobetalipoproteinaemia in two families with xanthomas and phytosterolaemia.

The death of a 13-year-old boy from coronary atherosclerosis prompted the study of an Amish family. Five of his twelve sibs had tendon and tuberous xanthomas, and increased plasma plant sterols, particularly beta-sitosterol. The plasma level of the major apoprotein of low density lipoprotein (LDL), the B protein, was very high (mean 173 mg/dl) in these five sibs, while the LDL cholesterol level was moderately increased (209 mg/dl). Four other sibs and both parents had an increased LDL B protein level with a normal or mildly raised plasma total and LDL cholesterol level (hyperapobeta-lipoproteinaemia). Evidence for coronary artery disease was found in both parents and three xanthomatous sibs. The original family with beta-sitosterolaemia and xanthomatosis, described in 1974, was re-examined. The proband and her sister had persistent phytosterolaemia and normocholesterolaemia but increased LDL B protein levels. Both parents, two uncles, and three of four grandparents had increased LDL B protein levels and normal total and LDL cholesterol levels. The proband's father had atypical angina pectoris. People with the full syndrome (phytosterolaemia, xanthomas, and hyperapobetalipoproteinaemia) are most probably homozygous for a mutant allele. An increased LDL B protein level permits the identification of heterozygotes in these families, even though in the fasting state they show no phytosterolaemia. The homozygote and probably the heterozygote are at increased risk for cardiovascular atherosclerotic disease.

Adolescent↗
PubMed1980

Transfer of cholesterol esters between human high density lipoproteins and triglyceride-rich lipoproteins controlled by a plasma protein factor.

A protein factor from the d greater than 1.25 g/ml plasma fraction controls the transfer of cholesterol esters between high density lipoproteins and very low density lipoproteins. This transfer is time-dependent, and follows saturation kinetics relative to the concentration ratio of acceptor to donor lipoproteins. Although the process is reversible, the transfer rates are faster from high density to very low density lipoproteins and result in a net increase of cholesterol esters in the very low density lipoproteins. Under the same conditions, there is also a net mass transfer of cholesterol esters from high density lipoproteins to chylomicrons. This constitutes the first demonstration of cholesterol ester mass transfer between isolated lipoproteins and contrasts with the equilibrium of cholesterol esters between HDL and LDL which we previously demonstrated [4]. The apparent maximum transfer rate of cholesterol esters from high density to very low density lipoproteins was calculated to be about 80 nmoles cholesterol esters/h/ml plasma, which is very similar to the initial rate of reaction of lecithin:cholesterol acyltransferase in plasma. It is concluded that cholesterol ester formation in high density lipoproteins and their transfer to triglyceride-rich lipoproteins may be closely coupled.

Adult↗
PubMed1980

Association of coronary atherosclerosis with hyperapobetalipoproteinemia [increased protein but normal cholesterol levels in human plasma low density (beta) lipoproteins].

Most patients with coronary artery disease do not have elevated plasma or low density lipoprotein (LDL) cholesterol. To test whether the protein moiety of LDL, LDL B, might be a parameter to identify ischemic heart disease, the plasma cholesterol, triglyceride, LDL cholesterol, and LDL B were measured in 100 consecutive patients undergoing cardiac catheterization. On the basis of coronary angiography, these patients were divided into two groups: group I, 31 patients without, and group II, 59 patients with significant coronary artery disease. Although cholesterol, triglyceride, and LDL cholesterol levels were all significantly higher in group II, discriminant analysis indicated that LDL B concentrations most clearly separated the two groups. In group I (noncoronary), LDL B was 82 +/- 22 mg/100 ml, whereas in group II, LDL B was 118 +/- 22 mg/100 ml. The B protein level in group I was similar to other normal groups studied (35 asymptomatic male physicians, 83 +/- 11 mg/100 ml; 90 normolipidemic medical students, 72 +/- 17 mg/100 ml). The results therefore indicate that not only does LDL B better separate coronary and noncoronary groups than other lipid parameters studied, but also, among those with coronary artery disease, there exists a group with normal LDL cholesterol but with levels of LDL B protein similar to those observed in type II hyperlipoproteinemia. The explanation for the altered LDL composition observed in this group remains to be elucidated.

Apolipoproteins↗
PubMed1978

Cholesterol ester exchange between human plasma high and low density lipoproteins mediated by a plasma protein factor.

Although unesterified cholesterol and phospholipids exchange freely, a protein factor from the d greater than 1.25 g/ml plasma fraction was found to be necessary for cholesterol esters to transfer from HDL to LDL. This transfer was reversible, time-dependent and a function of the concentration of the d greater than 1.25 fraction, but independent of lecithin : cholesterol acyltransferase reaction. The transfer represented an equilibration of molecules, but no net mass transfer of cholesterol esters could be demonstrated from HDL to LDL.

Blood Proteins↗