Gene/Protein Disease Symptom Drug Enzyme Compound
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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The long term efficacy of granulated guar gum, 15-30 g per day, was studied in 23 patients with severe hypercholesterolaemia (serum cholesterol concentration between 8.0 and 14.3 mmol/l). Originally, 29 patients participated in the study. Two patients dropped out because of gastrointestinal side effects, two others were not willing to complete the study without any given reason, and two discontinued the study because of hospitalization. A 1-month placebo period preceded the guar gum treatment, and another 1-month placebo period followed after 50 weeks of active treatment. The serum total cholesterol concentration (mean +/- SEM) was reduced from 10.0 +/- 0.4 mmol/l to 8.2 +/- 0.3 mmol/l (P less than 0.001) after 8 weeks and to 9.0 +/- 0.4 mmol/l (P less than 0.001) after 50 weeks on guar gum. During the second placebo period serum cholesterol returned to the pretreatment level. After 34 weeks of active treatment the serum LDL-cholesterol concentration had fallen by 15% and that of apoprotein B by 14% from the baseline. The changes in lipid and lipoprotein levels were independent of the initial values and the type of hypercholesterolaemia. Serum triglycerides, HDL-cholesterol, body weight and blood pressure showed no significant changes during the trial. Of the study subjects, 20 reached the maximum intended dose of 30 g per day guar gum between 8 and 14 weeks and thereafter 11 subjects continued the dose of 30 g/day while 12 subjects reduced the dose to 15-25 g/day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long term treatment of severe hypercholesterolaemia with guar gum. 285 Aug 7

25 of a group of 87 White men had Msp 1 restriction site polymorphism within an Alu sequence 3' to the human apo AII gene. Homozygosity for the polymorphism in 8 men was associated with a significant increase in serum apo AII levels (35.4 +/- 1.70 mg/dl, mean +/- SEM) and altered HDL composition, compared with heterozygotes (31.7 +/- 1.29; n = 17) and normal subjects (29.4 +/- 0.64; n = 62). This is the first account of a common variant of an HDL apoprotein gene that affects HDL composition. In view of its association with a high apo AII concentration homozygosity may protect against atherosclerosis.
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PMID:High-density lipoprotein composition is altered by a common DNA polymorphism adjacent to apoprotein AII gene in man. 285 63

High density lipoprotein (HDL) kinetics were studied by injecting [3H]apoprotein A-I (apoA-I)/HDL into 12 subjects with normal glucose tolerance and 12 patients with noninsulin-dependent diabetes mellitus (NIDDM). The results indicate that the mean fractional catabolic rate (FCR) of apoA-I/HDL was significantly faster [0.63 +/- 0.07 (+/- SEM) vs. 0.39 +/- 0.02 1/day; P less than 0.001] and the apoA-I/HDL synthetic rate greater (29.4 +/- 2.9 vs. 22.9 +/- 1.3 mg/kg X day; P less than 0.02) in patients with NIDDM than in normal subjects. Furthermore, there were statistically significant inverse relationships between apoA-I/HDL FCR and plasma levels of both HDL cholesterol (r = -0.71; P less than 0.001) and apoA-I (r = -0.63; P less than 0.001). In addition, the increase in apoA-I/HDL FCR was directly related to fasting plasma glucose (r = 0.78; P less than 0.001) and insulin (r = 0.76; P less than 0.001) concentrations. These data support the view that the decrease in plasma HDL cholesterol and apoA-I levels commonly found in patients with noninsulin-dependent diabetes is due to an increase in the catabolic rate of apoA-I/HDL secondary to the defects in carbohydrate metabolism present in these patients.
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PMID:High density lipoprotein (HDL) metabolism in noninsulin-dependent diabetes mellitus: measurement of HDL turnover using tritiated HDL. 311 4

The long-term effects of fructose as a natural sweetener in the physiologic meals of ambulatory obese patients with type II diabetes remain uncertain. An outpatient 12-week study was therefore conducted to evaluate the metabolic effects of crystalline fructose (60 g) supplementation of the diet of nine patients with type II diabetes (Group A, mean age 57 +/- 2 years, seven women and two men). Their results were compared with age-, sex-, and weight-matched patients with type II diabetes who were similarly studied but without fructose supplementation of their usual meals (Group B). The mean +/- SEM fasting serum glucose (224 +/- 24 versus 204 +/- 14 mg/dl) and glycosylated hemoglobin (11.57 +/- 0.49 versus 10.20 +/- 0.60 percent) values progressively decreased (p less than 0.05, week 12 versus week 0) in Group A. In contrast, both parameters increased in Group B when compared with the week 0 values, but differences were not statistically significant. Levels of fasting serum triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol remained unchanged at week 12 compared with week 0 in Group A. However, the mean apoprotein A1 concentrations increased significantly at weeks 4 and 12 in Group A, whereas only transient changes occurred in apoprotein B100 values. Levels of mean fasting serum triglycerides increased at weeks 4 (15 percent) and 12 (38 percent) in Group B; however, no significant changes occurred in the rest of the lipid, lipoprotein, and apoprotein A1 and B100 levels. Metabolic by-products of fructose such as serum lactic acid and uric acid levels remained essentially unchanged in both groups at the end of the study. In addition, no significant weight changes were observed in either group. The fructose supplementation was well tolerated without significant adverse effects. Thus, this study demonstrates that addition of moderate amounts of fructose as a natural sweetener in the physiologic mixed meal does not appear to have deleterious effects on glycemic control and lipid and lipoprotein metabolism in ambulatory obese patients with type II diabetes and poor metabolic control. Rather, a slight improvement in glycemic control and alterations in the apoprotein compositions in favor of decreased risk for coronary artery disease may occur.
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PMID:Metabolic effects of fructose as a natural sweetener in the physiologic meals of ambulatory obese patients with type II diabetes. 361 27

Very low density lipoprotein (VLDL) and low density lipoprotein (LDL) apoprotein (apo)-B turnover rates were measured simultaneously by injecting 131I-labeled VLDL and 125I-labeled LDL into fasting baboons (Papio sp.) selectively bred for high serum cholesterol levels and having either low or high LDL levels. The radioactivities in VLDL, intermediate density lipoprotein (IDL), LDL apoB, and urine were measured at intervals between 5 min and 6 days. Kinetic parameters for apoB were calculated in each baboon fed a chow diet or a high cholesterol, high fat diet (HCHF). VLDL apoB residence times were similar in the two groups of animals fed chow; they were increased by HCHF feeding in high LDL animals, but not in low LDL animals. Production rates of VLDL apoB were decreased by the HCHF diet in both high and low LDL animals. Most of the radioactivity from VLDL apoB was transferred to IDL. However, a greater proportion of radioactivity was removed directly from IDL apoB in low LDL animals than in high LDL animals, and only about one-third appeared in LDL. In high LDL animals, a greater proportion of this radioactivity was converted to LDL (61.4 +/- 7.2% in chow-fed animals and 49.2 +/- 10.9% in animals fed the HCHF diet; mean +/- SEM, n = 5). Production rates for LDL apoB were higher in high LDL animals than those in low LDL animals on both diets. The HCHF diet increased residence times of LDL apoB without changing production rates in both groups. VLDL apoB production was not sufficient to account for LDL apoB production in high LDL animals, a finding that suggested that a large amount of LDL apoB was derived from a source other than VLDL apoB in these animals.
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PMID:Metabolism of apoprotein B in selectively bred baboons with low and high levels of low density lipoproteins. 373 33

Men have lower high density lipoprotein (HDL) and higher low density lipoprotein (LDL) levels than women. To dynamically evaluate the role of endogenous testosterone on the lipoprotein profile, eight normal men received a long-acting gonadotropin releasing hormone analog (LHRHA) for 10 weeks by SC injection. Plasma testosterone levels were acutely lowered below 1 ng/ml after 4 weeks of LHRHA treatment and remained depressed at this level for the duration of administration of the analog. There were prompt increases in total cholesterol [baseline vs. peak (milligrams per dl) mean +/- SEM, 177 +/- 18 vs. 208 +/- 22; P less than 0.005], apoprotein B (apo B; 69 +/- 12 vs. 97 +/- 13; P less than 0.05), HDL-cholesterol (23 +/- 2 vs. 33 +/- 2; P less than 0.005), and apo A-I (80 +/- 7 vs. 112 +/- 5; P less than 0.005), but not in apo A-II (40 +/- 3 vs. 40 +/- 4; P = NS) levels. The peaks occurred after 10 weeks of treatment and were followed by a fall in these values after discontinuing LHRHA. These changes were largely prevented in a second study (six men) in which LHRHA was administered together with im testosterone enanthate, which was given every 2 weeks. These results show that suppression of endogenous testosterone leads to increases in HDL and LDL, demonstrating that testosterone has an important effect on lipoprotein metabolism and plays a key role in defining the lipoprotein profile in men.
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PMID:Suppression of plasma testosterone leads to an increase in serum total and high density lipoprotein cholesterol and apoproteins A-I and B. 391 67

Considering the documented, potentially undesirable influence of various thiazide-type or loop diuretics on serum lipoproteins, we prospectively investigated in 69 men (mean age +/- SEM, 32 +/- 1 years) the metabolic effects of the new diuretic-antihypertensive compound indapamide. Compared to placebo, indapamide (2.5 mg/day) given for 6 to 8 weeks lowered (p less than 0.02 to less than 0.001) blood pressure (supine values from 148/98 +/- 3/2 to 137/93 +/- 3/2) in 29 men with mild to moderate essential hypertension, but not in 40 healthy men. In both groups, significant (p less than 0.05 to less than 0.001) decreases in body weight (-0.8 kg) and plasma potassium (-0.6 mmol/L), and increases in plasma uric acid (+20%), renin activity (+200%), and aldosterone documented good compliance. There were no significant changes in total cholesterol (in all subjects, from 208 +/- 6 to 213 +/- 6 mg/dl), low- or very low-density lipoprotein (VLDL) cholesterol (127 +/- 6 to 129 +/- 6 and 21 +/- 1 to 21 +/- 2 respectively), high-density lipoprotein cholesterol (50 +/- 1 to 51 +/- 1 mg/dl), total triglycerides (Tg) (108 +/- 5 to 112 +/- 6 mg/dl), VLDL-Tg, apoproteins A1 and A2, plasma glucose, epinephrine, norepinephrine, sodium, calcium, magnesium, and creatinine; apoprotein B (84 +/- 2 to 88 +/- 3 mg/dl) and plasma insulin after glucose loading dose tended to be increased minimally. The absence of distinct lipoprotein alterations after short-term indapamide treatment may be of clinical and epidemiological interest.
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PMID:Serum lipoproteins during treatment with the antihypertensive agent indapamide. 407 35

Utilizing the polyvinyl sponge-implant model in the rabbit we have previously demonstrated modification in low density lipoproteins (LDL) of interstitial tissue fluid obtained in association with a cellular inflammatory response. In order to examine the interaction between the inflammatory response and lipoproteins from hypercholesterolemic rabbits, 30 male, New Zealand White rabbits were fed standard chow supplemented with 0.5% cholesterol for 4 weeks prior to sponge implantation. Lipoproteins were prepared from interstitial inflammatory fluid (IF) as well as homologous whole plasma (WP). Total IF cholesterol was positively correlated with plasma cholesterol (459 +/- 43 vs. 1485 +/- 130 mg/dl, means +/- SEM, r = 0.81, P less than 0.01). Distribution of lipoproteins in IF was similar to WP in both particle size and density. Beta-migrating VLDL were the predominant particles in both WP and IF, containing 43.7 +/- 3.4 and 42.2 +/- 5.1% of WP and IF cholesterol, respectively. IF-VLDL were similar to WP-VLDL in lipid and apoprotein composition, morphology and particle size distribution. We conclude from these data that the observed dramatic alterations in lipoprotein distribution in response to a dietary cholesterol challenge in rabbit plasma is essentially unaltered in interstitial inflammatory fluid obtained from these animals.
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PMID:Effect of cholesterol feeding on lipoprotein distribution in interstitial inflammatory fluid of the rabbit. 638 11

Since the fat content of a single meal influences chylomicron size and hence intestinal apoprotein synthesis, we determined the chronic effects of the daily distribution of fat intake on plasma concentrations of total cholesterol (TC), high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C). Eight normal male subjects ingested 100 g of fat (a) as a bolus at the evening meal (SL) or (b) equally distributed over 4 meals (q4h) (DL). Each diet was consumed for 7 days; studies were performed 14 days apart using a crossover design and paired comparisons. Nutrient intake and body weight were held constant. At the end of the DL dietary regimen, fasting plasma concentrations of TC, LDL-C and HDL-C were significantly increased as compared to the SL phase of study (TC: 174 +/- 2.9 (mean +/- SEM) vs 161 +/- 2.7; LDL-C: 108 +/- 3.2 vs 98 +/- 3.3 and HDL-C: 53 +/- 1.1 vs 48 +/- 0.8) (P less than 0.05). The consumption of 100 g/day of fat in several small meals results in a sustained increase in LDL-C and HDL-C. This may be due to increased synthesis of lipoprotein components (e.g. apoprotein A-I) or to altered metabolism of intestinal and hepatic TG-rich lipoproteins dependent on size, number and apoprotein composition.
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PMID:Sustained alterations in lipoprotein cholesterol concentrations dependent on the daily distribution of lipid intake. 668 61

Immune complexes induced the synthesis of apoprotein III, the protein component of tissue thromboplastin (tissue factor), in human monocytes cultured in vitro. The response was maximal (11.1 +/- 1.7 fold increase (mean +/- SEM) when immune complexes were formed at antigen/antibody equivalence. Immune complexes formed with the antigen-binding fragments (F(ab')2) of immunoglobulins induced a 4.7 +/- 1.4 fold activity increase, suggesting that another signal mechanism in addition to the Fc-receptor may be involved.
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PMID:Thromboplastin (factor III) activity in human monocytes induced by immune complexes. 680 71


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