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Biomedical subjects

E J Schaefer

Publications and source records attributed to E J Schaefer.

334 records · Page 19Linked to original sources
PubMedDate not supplied

Effect of dietary fat saturation and cholesterol on LDL composition and metabolism. In vivo studies of receptor and nonreceptor-mediated catabolism of LDL in cebus monkeys.

The mechanism(s) by which polyunsaturated fats reduce low density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B were investigated in 20 cebus monkeys (Cebus albifrons) fed diets containing corn oil or coconut oil as fat (31% of calories) with or without dietary cholesterol (0.1% by weight) for 3 to 10 years. Coconut-oil feeding compared to corn-oil feeding resulted in significant increases in levels of plasma total cholesterol (176%), very low density lipoprotein (VLDL)-LDL cholesterol (236%), high density lipoprotein (HDL) cholesterol (148%), apo B (78%), and apo A-I (112%). The addition of dietary cholesterol to corn oil compared to corn oil alone resulted in smaller, but significant, increases in levels of total cholesterol (44%), HDL cholesterol (40%), and apo A-I (33%). Although the increases in VLDL-LDL cholesterol were of similar magnitude (52%), they barely failed to reach statistical significance (p less than 0.08), while the changes in apo B levels were negligible. The addition of dietary cholesterol to coconut oil, compared to coconut oil alone, resulted in no significant changes in lipoprotein cholesterol or apoproteins, although levels of VLDL-LDL cholesterol and apo B values increased 22% and 16%, respectively. Although hepatic free cholesterol content was not altered by diet, coconut-oil compared to corn-oil feeding resulted in significant increases in hepatic cholesteryl esters (236%) and triglycerides (325%), the latter increasing still further when dietary cholesterol was added to coconut oil (563%). To further assess the effects of these dietary changes on LDL metabolism, radioiodinated normal and glucosylated LDL kinetics were performed. The production rate of LDL apo B was not altered by diet. With corn-oil feeding, 63% of LDL catabolism was via the receptor-mediated pathway. Coconut-oil compared to corn-oil feeding resulted in a 50% decrease in receptor-mediated LDL apo B fractional catabolic rate (FCR) and a 27% reduction in nonreceptor-mediated LDL apo B FCR. The addition of dietary cholesterol to corn oil, compared to corn oil alone, resulted in no significant effect on LDL apo B catabolism. The addition of dietary cholesterol to coconut oil, compared to coconut oil alone, was associated with no significant change in nonreceptor catabolism of LDL apo B but with a 58% decrease in receptor-mediated catabolism of LDL (p less than 0.059). The diet-induced alterations of LDL catabolism were significantly correlated with hepatic lipids, which were enriched in saturated fatty acids.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗
PubMedDate not supplied

Relations of body habitus, fitness level, and cardiovascular risk factors including lipoproteins and apolipoproteins in a rural and urban Costa Rican population.

Increased general and abdominal obesity has been independently associated with diabetes, increased risk of stroke, and coronary artery disease (CAD). It is more prevalent in developed countries and in urban areas of nonindustrialized nations than in less developed and rural areas. To evaluate the associations between general and abdominal obesity (as determined by total body fat, waist to hip ratio, umbilical to triceps ratio, and umbilical to subscapular ratio) with glucose, plasma lipoproteins, apolipoprotein (apo) A-I and B concentrations, and low density lipoprotein (LDL) particle size (LDL 1-7), we randomly selected 222 men and 243 women from rural and urban areas of Puriscal, Costa Rica. Abdominal obesity, as assessed by the waist to hip ratio, was independently and significantly associated with higher triglyceride levels (p less than 0.01) and with lower high density lipoprotein cholesterol levels (p less than 0.05) in men and women and with higher glucose levels (p less than 0.05) and smaller LDL particle size (p less than 0.01) in women. Abdominal obesity, as assessed by the umbilical to subscapular ratio, was independently and significantly associated with higher total cholesterol (p less than 0.005) and apo B (p less than 0.01) levels. Umbilical to triceps ratio was positively associated with blood pressure in men. Urban men had increased general and abdominal obesity (p less than 0.0001), number of cigarettes smoked per day (p less than 0.0001), and diastolic blood pressure (p less than 0.05) and had a decreased fitness level (p less than 0.0001) as well as higher (p less than 0.05) plasma glucose, triglyceride, and total cholesterol concentrations and lower (p less than 0.05) apo A-I and HDL cholesterol levels compared with rural men. The differences between rural and urban women were not as striking. Urban women had increased general and abdominal obesity, glucose, and apo B levels (p less than 0.05) and a decreased fitness level (p less than 0.0001). Our data indicate that general and abdominal obesity, increased cigarette smoking, diastolic blood pressure, and decreased fitness level are more prevalent in an urban than in a rural area in Costa Rica, particularly in men. The higher prevalence of such risk factors in the urban area is associated with a more atherogenic plasma lipoprotein profile.

Adult↗
PubMedDate not supplied

Nutrient intake comparisons between Framingham and rural and Urban Puriscal, Costa Rica. Associations with lipoproteins, apolipoproteins, and low density lipoprotein particle size.

To assess cross-cultural relations between dietary intake and plasma lipoproteins, we randomly selected 222 men and 243 women from the urban and rural areas of Puriscal, Costa Rica; related their dietary composition (assessed by a food-frequency questionnaire), fitness level, and body fat to plasma lipids, apolipoproteins, and low density lipoprotein (LDL) particle size; and compared these data with those from a subsample of 280 adults from the Framingham Offspring Study. Total cholesterol and LDL cholesterol levels were significantly (p less than 0.0001) higher in Framingham (207 and 137 mg/dl, respectively) than in Puriscal (184 and 114 mg/dl, respectively) residents. Elevated triglyceride and apolipoprotein (apo) B levels (25% and 16% higher), low HDL cholesterol and apo A-I levels (12% and 29% lower), and smaller LDL particles (17%) were more frequent in Puriscal than in Framingham residents. Urban Puriscal residents had a significantly lower fitness level; increased body fat, total cholesterol, and triglyceride levels; decreased HDL cholesterol in men; and higher apo B levels in women compared with rural Puriscal residents. Body fat, animal fat, and saturated fat intakes were significantly correlated with total cholesterol, LDL cholesterol, and apo B levels in both men and women in Puriscal. Intakes of protein and animal fat were higher among urban (10.7% and 14.1%, respectively) compared with rural (8.9% and 9.9%, respectively) Puriscal residents and in Framingham (16.0% and 20.8%, respectively) compared with Puriscal residents. No significant differences were found in dietary cholesterol. Saturated fat (largely from palm oil in Puriscal) intakes were significantly different among the three groups: rural Puriscal, 10.7% of calories; urban Puriscal, 11.6%; and Framingham residents, 12.9%. These data indicate that the more atherogenic plasma lipid profile among urban compared with Puriscal residents was largely explained by increased adiposity, decreased fitness level, and higher saturated fatty acid intake. Puriscal residents consumed less animal fat and more carbohydrate than did Framingham residents, and these differences were associated with a 21% lower LDL cholesterol level, a 12% lower HDL cholesterol level, a 29% lower apo A-I level, a 25% higher triglyceride level, a 16% higher apo B level, and a 17% smaller LDL particle size. Some of these cross-cultural differences may be due to differences in ethnic background and physical activity as well.

Adipose Tissue↗
PubMedDate not supplied

Prevalence of familial hyperhomocyst(e)inemia in men with premature coronary artery disease.

Elevated plasma levels of homocyst(e)ine have been reported to be more prevalent in patients with coronary artery disease (CAD) than in controls. The purpose of this study was to determine whether this elevation was genetic. We determined homocyst(e)ine levels in 176 men with premature CAD (greater than 50% stenosis of a major epicardial coronary artery occurring before the age of 60 years) and in 255 controls free of cardiovascular disease. Homocyst(e)ine levels were higher in the CAD group compared with controls (13.9 +/- 6.7 versus 10.9 +/- 4.9 nmol/ml, p less than 0.001); in addition, 28% of CAD patients had homocyst(e)ine levels above the 90th percentile of controls. Statistical analysis revealed that homocyst(e)ine levels were not related to the presence of hypertension or diabetes, smoking, or plasma levels of lipoprotein cholesterol and apolipoproteins A-I and B. The families of 71 CAD patients were sampled (selected on the basis of availability of relatives) and included 60 spouses and 239 first-degree relatives; 370 subjects were thus sampled. Spearman correlations between probands and spouses (r = 0.264, p = 0.041) and between mean values for parent and offspring (r = 0.356, p = 0.002) for homocyst(e)ine levels indicated that homocyst(e)ine levels are in part genetically determined. In 20 families (28.2%), the proband had homocyst(e)ine levels greater than the 90th percentile; familial segregation was observed in 10 of these kindreds. Therefore, 14% of CAD patients had familial hyperhomocyst(e)inemia. In conclusion, our data suggest that plasma homocyst(e)ine is a risk factor for the development of CAD, independent of other cardiovascular risk factors, and that this elevation is in part genetically determined.

Adolescent↗
PubMedDate not supplied

Effect of corn and coconut oil-containing diets with and without cholesterol on high density lipoprotein apoprotein A-I metabolism and hepatic apoprotein A-I mRNA levels in cebus monkeys.

The mechanism(s) by which diets containing corn or coconut oil (31% of energy as fat) totally free of cholesterol or with 0.1% added cholesterol by weight (0.3 mg/kcal) affect plasma high density lipoprotein cholesterol (HDL-C), apoprotein (apo) A-I levels, apo A-I kinetics, and hepatic apo A-I mRNA concentrations were investigated in 26 cebus monkeys. Coconut oil-fed monkeys had elevated levels of plasma total cholesterol (217%), very low density lipoprotein plus low density lipoprotein cholesterol (331%), HDL-C (159%), and apo A-I (117%) compared with corn oil-fed animals. Although the addition of cholesterol to the corn oil diet significantly increased these parameters, no such effects were seen when cholesterol was added to the coconut-oil diet. Both the type of fat and cholesterol in the diet significantly affected HDL apo A-I metabolism by decreasing apo A-I fractional catabolic rate and increasing apo A-I production rate in the coconut oil-fed groups. The decrease in apo A-I fractional catabolic rate in the coconut oil-fed animals was also associated with an increase in the HDL core lipid to surface ratio. Liver apo A-I mRNA abundance was elevated in the coconut oil-fed groups; however, dietary cholesterol had no affect on these levels. The lack of parallel effects of dietary fat and cholesterol on apo A-I production rate and liver apo A-I mRNA levels suggests that the increase in the apo A-I production rate observed in the coconut oil-fed groups resulted from the fat-induced rise in liver apo A-I mRNA abundance, whereas the cholesterol-induced rise in the apo A-I production rate resulted from a mechanism other than changes in liver apo A-I mRNA levels.

Animals↗
PubMedDate not supplied

Plasma apolipoprotein A-1 absence associated with a marked reduction of high density lipoproteins and premature coronary artery disease.

A 45-year-old woman with corneal opacification and severe coronary artery disease was noted to have the following plasma lipid levels (mg/dl, +/- SD): total cholesterol 111 +/- 13, triglyceride 62 +/- 6, very low density lipoprotein cholesterol 4 +/- 1, low density lipoprotein cholesterol 106 +/- 14, and high density lipoprotein (HDL) cholesterol 1 +/- 1 (normal, 50 +/- 14). Her two offspring and one brother were found to have HDL cholesterol values (mg/dl) of 23, 20, and 20, respectively. The percentage of cholesterol in the esterified form in the patient's plasma was normal at 70%. Lipoprotein electrophoresis showed no alpha lipoprotein band, and no HDL was detectable when plasma was subjected to analytic ultracentrifugation. Only trace amounts of lipids were noted within the HDL density region following preparative ultracentrifugation. Mean plasma apolipoprotein (apo) A-ll, apo B, and apo C-ll plasma levels were 13.8%, 130.6% and 26.6% of normal, respectively. The ratio of apo B to cholesterol within LDL was elevated. Apo A-l, the major HDL protein constituent, was immunologically undetectable in this patient's plasma. A decreased HDL cholesterol concentration has been associated with premature coronary artery disease. These data indicate that plasma apo A-l absence results in a striking reduction in HDL, is associated with premature coronary artery disease, and represents a new distinct disease entity.

Apolipoprotein A-I↗
PubMedDate not supplied

Clinical, biochemical, and genetic features in familial disorders of high density lipoprotein deficiency.

This review assesses current knowledge of the clinical, genetic, and biochemical features of familial high density lipoprotein (HDL) deficiency syndromes. The focus is on HDL deficiency states occurring in the absence of severe hypertriglyceridemia or lecithin/cholesterol acyltransferase deficiency. Specific entities falling within this category include Tangier disease, familial HDL deficiency with planar xanthomas, familial apolipoprotein A-I and C-III deficiency (formerly known as apolipoprotein A-I absence), familial deficiency of apolipoprotein A-I and C-III, fish-eye disease, familial hypoalphalipoproteinemia, and apolipoprotein A-I variants (apo A-I Milano, apo A-I Marburg, apo A-I Giessen, and apo A-I Munster 1-3). Diffuse corneal opacification and premature coronary artery disease are common features in many of these kindreds. No striking clinical abnormalities have been noted in patients with currently known apolipoprotein A-I variants, possibly because these subjects are heterozygotes for their respective defects. The HDL deficiency in many of these disorders has been associated with abnormalities or deficiencies of apolipoprotein A-I. Further research will undoubtedly define the defects in all the disorders that have been described, uncover new mutations, as well as provide additional insights into the precise relationship between HDL deficiency and atherosclerosis.

Adolescent↗
PubMedDate not supplied

Effect of gender, age, and lipid status on low density lipoprotein subfraction distribution. Results from the Framingham Offspring Study.

The presence of low molecular weight low density lipoprotein (LDL) particles in plasma has been associated with premature coronary artery disease. In this study we have examined factors affecting LDL subfraction distribution as determined by 2% to 16% polyacrylamide-agarose gradient gel electrophoresis of whole plasma in a normal, primarily middle-aged, population of adult male and female participants (n = 280, ages 25 to 75 years) in the Framingham Offspring Study. Seven major LDL bands (LDL-1 to LDL-7) were observed in different individuals, with most subjects having either one or two major bands. The presence of low molecular weight LDL (LDL-4 to LDL-7) in plasma as the predominant LDL type was significantly more common in men than in women (43.5% versus 14.8%, p less than 0.001). The presence of low molecular weight LDL was correlated (p less than 0.01) with increased age, plasma triglyceride, total cholesterol, very low density lipoprotein (VLDL) cholesterol, LDL cholesterol (in women only), and apolipoprotein (apo) B concentrations, as well as with decreased high density lipoprotein (HDL) cholesterol and apo A-I levels. Approximately 69% of the variability in LDL subfractions could be accounted for by alterations in plasma triglyceride and HDL cholesterol levels. These data are consistent with the concept that LDL subfraction distribution is influenced by gender and plasma lipoprotein levels and can be determined readily by the use of whole plasma.

Age Factors↗
PubMedDate not supplied

Oxidized low density lipoprotein stimulates prostacyclin production by adult human vascular endothelial cells.

Interactions between vascular endothelium and low density lipoprotein (LDL) have been implicated in the development of atherosclerosis. The effect of normal and oxidized LDL (Ox-LDL) on prostaglandin release by cultured adult human saphenous vein endothelial cells was investigated. Ox-LDL induced a rapid release of prostacyclin (PGI2) to levels which were several-fold higher than those observed with control LDL. PGI2 release was concentration-dependent and was biphasic, with a first peak occurring within 30 minutes (followed by a decrease), and a second peak occurring after several hours of incubation. PGI2 production was inhibited by lipoprotein-depleted serum and by indomethacin, an antagonist of cyclooxygenase activity. These cells produced mainly PGF2 alpha, with some PGE2 and PGI2 when stimulated by the ionophore A23187 at confluency. However, among these prostanoids, mainly PGI2 was produced in response to Ox-LDL. The data indicate that Ox-LDL induces the production of PGI2 by human vascular endothelial cells. Since Ox-LDL is cytotoxic, this phenomenon may be a manifestation of an early response to injury.

Adult↗