Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPERLIPEMIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMedDate not supplied

Induction of hyperlipemia by carbohydrate-rich fractions isolated from crude papain.

A hyperlipemia was obtained in rabbits injected intravenously with two carbohydrate-rich fractions isolated from crude papain dialyzate. The fractions have an approximative molecular weight of 15,000 and 5,000 daltons and contains 35% and 15% of sugars respectively. The hyperlipemia appears 20 hours after the injection and consists in a hypertriglyceridaemia as suggested by the enrichment of serum in very light lipoproteins of density about 1.006. Concomittantly a decrease of the post-heparin lipase activity (PHLA) of the plasma was observed. After a few days the hyperlipemia disappears and the PHLA returns to a normal value. It is suggested that the hypertriglyceridaemia can be due to an inhibitory effect of the injected fractions on the removal action of the lipases which are released into the blood by an heparin injection.

Animals↗
PubMed1989

[Experimental and clinical studies of the effect of dahuang zhechong wan on hyperlipemia].

Experimental and clinical researches were done for the purpose of that to treat the hyperlipemia with Dahuang Zhechong Wan (DHZCW). The patients of primary hyperlipemia were divided into two groups. One group was treated with DHZCW, the other with inositol nicotinate as control. DHZCW could reduce the serum total cholesterol (0.05 less than P less than 0.2), triglyceride (P less than 0.05), the blood viscosity (P less than 0.01), reductive viscosity (P less than 0.001) and fibrinogen (0.05 less than P less than 0.2). No significant change of the other item of hemorheology, HDL-c and the subfraction were observed. No significant differential effect between those two groups. The experimental hyperlipidemic model was made by feeding cholesterol and axungia on rabbits. The results showed that DHZCW could reduce the serum total cholesterol (P less than 0.05), triglyceride (P less than 0.05), beta-LP (P less than 0.01), the blood viscosity (P less than 0.05) and plasma viscosity (P less than 0.05), but no significant effect on HDL-c and its subfraction, ESR, index of erythrocytic deformation and hematocrit. DHZCW could change the viscosity of blood of hyperlipemia and reduce the total cholesterol, triglyceride and fibrinogen of the blood. It might have some beneficial effects on atherosclerosis and prevent ischemic cardiovascular and cerebrovascular diseases.

Adult↗
PubMed1985

[Lipoproteins, post-heparin lipoprotein lipase and hepatic triglyceride lipase in patients with and without severe hyperlipemia caused by alcoholism].

Because of the high incidence for development of a secondary hyperlipemia during chronic alcohol intake, this study was performed to look for a possible reason, why some patients produce severe hyperlipemia and other ones not. 15 male patients with chronic alcoholism (group I) who produce under influence of alcohol a secondary type-V hyperlipoproteinemia (type-V HLP) were compared with 15 male controls. Additionally, 8 male patients with chronic alcoholism (group II) who were normolipemic under alcohol abuse, and 7 male patients (group II) who had also produced type-V HLP under chronic alcohol abuse, but were teetotal since at least 6 months, were investigated. In comparison with controls, patients of group I showed significantly (p less than 0.01) increased plasma concentrations of very low-density lipoproteins (VLDL) and significantly decreased plasma concentrations of low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3 (all p less than 0.01). Furthermore, the activities of postheparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) were significantly decreased (both p less than 0.01). In patients of group III, the plasma concentrations of lipoproteins did not differ significantly from controls, but the activity of LPL was also significantly impaired (p less than 0.01), whereas the activity of HTGL was distinctly (p less than 0.01) increased. No significant difference between patients of group II and controls could be demonstrated. It is concluded that severe alcohol intake strongly impairs LPL in patients with chronic alcoholism. The pronounced increase of HTGL in patients of group III seems to protect these individuals from producing severe hyperlipemia under the influence of alcohol.

Adult↗
PubMed1972

Physiological fatty liver and hyperlipemia in the fetal guinea pig: chemical and ultrastructural characterization.

During its prolonged period of gestation, the fetal guinea pig gradually develops a striking hyperlipemia (plasma triglycerides ca. 500-1500 mg/dl) and fatty liver (hepatic triglycerides ca. 25% of wet weight). The parenchymal cells of the liver contain not only many fat droplets in the cytoplasm, but also large numbers of osmiophilic particles, interpreted as precursors of plasma lipoproteins, within profiles of the cisternae and secretory vesicles of the Golgi apparatus. Similar particles are found in intercellular spaces, in the space of Disse, and in the hepatic sinusoids. Near the end of gestation, these particles enlarge to the size range characteristic of chylomicrons secreted from the intestinal mucosa after ingestion of fat. At the same time, the hyperlipemia increases and is characterized by the accumulation of particles resembling chylomicrons morphologically and chemically. The results are interpreted as evidence of intense hepatic synthesis and secretion of very low density lipoproteins which may be related to the extensive transplacental transport of free fatty acids known to occur in this species. After birth, the hyperlipemia subsides rapidly and the hepatic steatosis more gradually. The blood plasma of the guinea pig fetus also contains moderate amounts of low density and high density lipoproteins. The latter decrease to barely detectable levels during the first 2 wk of postnatal life. Comparably low levels of high density lipoproteins are found in nonpregnant and pregnant adults.

Aging↗
PubMed1976

Altered insulin and glucagon secretion in treated genetic hyperlipemia: a mechanism of theraphy?

The influence of Halofenate therapy on insulin and glucagon secretion was examined in the Zucker rat with genetic endogenous hyperlipemia. Coincident with the lipid lowering effects of Halofenate, the net change in the basal bihormonal axis favored glucagon, with the I/G molar ratio (Insulin/Glucagon) decreasing from 2.72 +/- 0.53 to 0.96 +/- 0.20 during treatment with this drug. Following arginine stimulation the I/G ratio remained reduced at 0.87 +/- 0.13 in Halofenate treated animals, contrasting with the statistically greater ratio of 2.5 +/- 0.55 in control animals. The Halofenate induced state of reduced insulin:glucagon was associated with hypolipemia, postarginine hyperglycemia, and hyperketonemia,-three metabolic parameters characteristic of glucagon excess relative to insulin. It is suggested that the lipid-lowering action of Halofenate in genetic hyperlipemia may reflect the altered bihormonal axis induced by the drug.

Animals↗
PubMed1989

Postprandial hyperlipemia inhibits platelet aggregation without affecting prostanoid metabolism.

The objective of this work was to characterize changes in platelet aggregability during postprandial hypertriglyceridemia with special emphasis on arachidonic acid metabolism. Ten healthy young men consumed 100 g fat after a fasting period of 12 hr. In-vitro platelet aggregation induced by ADP and collagen was measured at 0, 3, 5, and 9 hours after the fat intake. The major arachidonic acid metabolites, 12-hydroxyeicosatetraenoic acid (12-HETE), thromboxane A2 (TXA2), prostaglandin F2 alpha (PGF2a), and prostaglandin E2 (PGE2) produced during collagen-induced platelet activation were quantified by gas chromatography/mass spectrometry. A significant decrease in platelet aggregability induced by both ADP and collagen was detected during the postprandial hyperlipemia. No significant changes could be found in the prostanoid pattern of collagen activated platelets. There was no correlation between the degree of the inhibition of platelet aggregation and the relative or absolute increase of triglyceride-levels in the plasma during the postprandial hyperlipemia.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed2000

Hyperglycemia, hyperlipemia, and periodic paralysis: a case report of new side effects of clozapine.

1. This case report of a Chinese male schizophrenic patient describes new side effects that have not been documented previously for patients treated with clozapine. At certain doses of clozapine, the patient showed direct adverse reactions, which include a combination of hyperglycemia, hyperlipemia, and periodic paralysis. 2. In a four-year study of this patient who had no previous episodes of diabetes in his or his family history, the authors found that these symptoms disappeared upon withdrawal of clozapine and relapsed with re-treatment of the drug. This study indicates that hyperglycemia, hyperlipemia, and periodic paralysis may need to be monitored on patients treated with clozapine.

Adult↗
PubMed2002

Endothelial cell response to hyperlipemia. Activation-dysfunction-injury, the protective role of simvastatin.

Experiments on hypercholesterolemic rabbits and hamsters (HH) showed that hyperlipemia induces initial activation of endothelial cells (EC) expressed by modulation of constitutive functions: increased transcytosis of low-density lipoproteins (LDL) and enhanced synthesis of basal lamina. Accumulated LDL appears in the meshes of basal lamina as modified and reassembled lipoproteins (MRL) that, together with hyperlipemia, triggers EC dysfunction. This induces monocyte recruitment, adhesion, diapedesis and residence within the subendothelium where upon activation become macrophages, take up MRL and turn into foam cells. With time, EC overlaying atheroma alter their nonthrombogenic surface and become loaded with lipid droplets, resulting as marks of EC injury. Simvastatin administration to HH increased the antioxidant potential of the serum, diminished transcytosis of lipoproteins (Lp) and restored the endothelium-dependent relaxation.

Animals↗
PubMed1987

Albumin synthesis, albuminuria and hyperlipemia in nephrotic patients.

Hyperlipemia is a common manifestation of the nephrotic syndrome. Serum lipid concentrations have been observed by others to be negatively correlated with serum protein concentration. Hyperlipemia has been postulated to result from a coordinate increase in the synthesis of both albumin and lipoproteins, as well as from their decreased catabolism. Simultaneous measurements of serum lipid concentration and the rate of albumin synthesis have not been previously reported. We measured the rate of albumin synthesis, urinary albumin loss, serum albumin, protein, cholesterol and triglyceride concentration in 13 nephrotic patients. Changes in the rate of albumin synthesis and in urinary albumin excretion were induced in eight patients by alteration in dietary protein intake. The resultant changes in serum triglyceride and cholesterol were analyzed by multiple regression analysis. The rate of albumin synthesis measured while patients were eating a low protein diet was 12.61 +/- 1.20 g/1.73 m2/day, well within normal limits, yet both serum triglyceride and cholesterol concentrations were markedly elevated (265 +/- 65 mg/dl and 325 +/- 44 mg/dl, respectively). Albumin synthetic rate increased to 17.60 +/- 1.25 g/1.73 m2/day when dietary protein intake was increased, while serum triglyceride and cholesterol concentrations changed little; triglyceride concentration was 306 +/- 75 mg/dl and cholesterol 376 +/- 55 mg/dl. Serum cholesterol concentration, by multiple regression analysis, was dependent only upon the renal clearance of albumin P less than 0.0001, and changes in serum cholesterol concentration was dependent only upon changes in the renal clearance of albumin, P less than 0.001. Serum cholesterol concentration was completely independent of the rate of albumin synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Mechanisms of decreased bradykinin- induced vasodilation in experimental hyperlipemia-hyperglycemia: contribution of nitric oxide and Ca2+-activated K+ channels.

Common complications of diabetes are accelerated atherosclerosis and vascular disturbances. We investigated whether the simultaneous insult of hyperlipemia-hyperglycemia affects the reactivity of the resistance arteries to bradykinin (BK), and if so, what are the mechanisms responsible for this disturbance. Experiments were conducted on male Golden Syrian hamsters rendered hyperlipemic (H) by a fat-rich diet, diabetic (D) by streptozotocin injection, or simultaneously hyperlipemic-diabetic (HD). Normal age-matched animals were used as controls (C). At 24 weeks after the induction of disease(s) the vascular reactivity of the mesenteric resistance arteries to BK (10(-8)-10(-4) M) was assayed by the myograph technique. To explore the role of nitric oxide (NO) in modulating the endothelium-dependent BK-induced relaxation, two experimental approaches were employed: (i) in vivo administration of L-arginine (622.14 mg/kg bw) to H, D, and HD hamsters (for 12 weeks); (ii) in vitro blockage of nitric oxide synthase by N(omega)-nitro- L-arginine methyl ester (10(-4) M). To evaluate the contribution of Ca2+-activated K+ channel(s) to BK-induced relaxation, the resistance arteries were exposed to 10(-3) M tetraethylammonium. Comparatively, the endothelium-independent relaxation was assayed using sodium nitroprusside (10(-8)-10(-4) M). The results showed that compared to the H and D groups, the HD hamsters exhibited the most reduced vasodilation of the resistance arteries to BK (34.09 +/- 1.5%). The diminished vasodilation was found to be due to a dual mechanism: an L-arginine:NO pathway and a NO-independent process, mediated via Ca2+-activated K+ channels. In vivo administration of L-arginine had favourable effects especially in the HD group, which manifested (i) an; 30% improvement of attenuated BK relaxation, (ii) an increase in sensitivity of the response to BK, (iii) a 3-fold diminishment of plasma hyperglycemia. Collectively, these data explain in part, the mechanisms and possible ways to correct the arterial endothelial dysfunction when diabetes is complicated with hyperlipemia.

Animals↗
PubMed1956

The pathogenesis of hyperlipemia induced by means of surface-active agents. I. Increased total body cholesterol in mice given triton WR 1339 parenterally.

Mice rendered hyperlipemic by means of intravenous or subcutaneous injections of triton WR 1339 were found to have an increase in the total amount of cholesterol in their bodies. This observation indicates that the injected surface-active agent affects the metabolism of cholesterol and brings about hyperlipemia by augmenting the synthesis of lipides, or by interfering with their degradation or excretion, or by some combination of these factors. The implications of the findings for the pathogenesis of the hyperlipemia induced by triton are discussed further in the accompanying paper (16).

Animals↗
PubMed1961

Triton hyperlipemia in dogs. II. Atheroscieross, diffuse lipidosis, and deletion of fat stores produced by prolonged administration of the non-tonic surface-active agent.

Fourteen dogs, fed a regular diet and given 250 mg/kg of triton (a non-ionic surface-active agent) intravenously every 4th day, exhibited a progressively severe hyperlipemia. Serum triglycerides were the first to increase. Cholesterol, mostly in the free form, and phospholipids showed elevation only at a later stage and increased at almost identical rates. The plasma-free fatty acid concentration was from 2 to 3 times above normal. With establishment of sustained hyperlipemia, there was reduction, followed by total disappearance, of the high density D 1.063 to 1.21 lipoprotein. Most of the cholesterol and phospholipids (70 to 75 per cent of the total) were found in the D 1.006 to 1.063 lipoprotein class, the remainder in the D < 1.006 class. Triglycerides were almost evenly distributed between these two classes. The concentration of the serum lipoprotein proteins was within normal limits. All of the animals died within from 4 to 5 months after receiving the first injection of triton. Autopsy findings consistently showed: (a) numerous lipidladen macrophages in the liver, spleen, and lymph nodes; (b) significant depletion of all fat stores; (c) presence of lipids, either free or engulfed in macrophages (foam cells), in the subintima of the coronary arteries, aorta, and pulmonary arteries, indicating an early stage of atherosclerosis. Concurrent daily administration of heparin (5 mg per kilogram of body weight) did not substantially change the course of the disease. Withdrawal of triton from animals that had been receiving the detergent for from 3 to 4 months, elicited a slow return to normal of the lipid pattern. In two dogs killed when normolipemia was reestablished, all tissues were normal with the minor exception of a few hepatic macrophages still laden with sudanophilic material. It is postulated that the primary action of the injected triton was on the lipid moieties of plasma lipoproteins with formation of complexes, which, as foreign bodies, were preferentially taken up by the cells of the reticuloendothelial system. Depletion of fat stores was probably secondary to increased lipid mobilization, as an attempt by these tissues to supply energy to the parenchymal cells unable to utilize triton-bound lipids.

Animals↗
PubMed1975

Inhibition of serum and urine amylase activity in pancreatitis with hyperlipemia.

In 6 of 7 patients with acute pancreatitis and hyperlipemia, inhibition of serum amylase activity was detected by dilution of the serum before assaying for amylase and by correcting for tthe dilution factor. In 4 patients the inhibition phenomenon disappeared within the first few days of hospitalization as the elevated serum triglycerides fell. However, in 2 others there was no relation between triglyceride level and amylase inhibition. Removal of the excess serum lipids by ultracentrifugation did not eliminate the inhibition of amylase activity. Inhibition of amylase activity also occurred in the urine of these patients. No amylase inhibition was demonstrable in lipemic serum from patients without pancreatitis or in pancreatitis serum to which excess lipids were added. The data suggest the presence of a circulating inhibitor of amylase, distinct from the elevated serum lipids, in the serum and urine of patients with acute pancreatitis associated with hyperlipemia. The diagnosis of acute pancreatitis in the patient with abdominal pain and lactescent serum can be facilitated by correcting the serum amylase activity by dilution.

Acute Disease↗
PubMed2004

Foam cells generated by a combination of hyperglycemia and hyperlipemia in rats.

Diabetes is a major risk factor for atherosclerosis, as well as hyperlipemia. Investigators have suggested that denatured lipoprotein in hyperglycemia transforms macrophages into foam cells, which correlates with the development or progression of atherosclerosis. In the present study, we examined the generation of foam cells in rats caused by a combination of hyperglycemia and hyperlipemia. Streptozotocin-induced diabetic male Wister rats were fed a high cholesterol diet (HCD) containing 1% cholesterol and 0.5% cholic acid to maintain a hyperglycemic and hyperlipemic state. Animals fed the HCD for 8 weeks or longer showed a high incidence of foam cell accumulation in the renal glomerulus, intima of aortic arch, splenic red pulp and marginal zone, liver sinusoid and intestinal lamina propria. The foam cells exhibited positive staining for antimonocyte/macrophage antibody and lipids in all these tissues. Anti-rat apolipoprotein B (apo B) antibody revealed that positive staining existed only in the cytoplasm of glomerular foam cells. These results suggest that the origin of these foam cells can be attributed to lipid-laden macrophages. The generation of foam cells in the hyperglycemia-hyperlipidemia supervening rat model presented in the present study might be a useful tool for investigations of the pathogenesis of foam cells.

Animals↗
PubMed1981

Hyperlipemia among 1407 Danish children whose fathers have died from ischemic heart disease before age 45.

1407 children whose fathers had died from ischemic heart disease before age 45 were investigated. 15% had hypercholesterolemia and 8% hypertriglyceridemia at visit 1. At visit 2 and 3 this number of children with hyperlipemia fell to a minimum of 3% and 1.4%, resp. which is around 10 times higher than in a reference population. 1.8% of the children had familial hypercholesterolemia (FH) which is 10-15 times higher than in a reference population. These findings indicate that serum lipids should always be measured in children from such coronary heart risk families, and a decision made whether or not their permanent hyperlipemia should be treated.

Adolescent↗
PubMed1991

Treatment of hyperlipemia in diabetic patients on dialysis with a physiological substance.

Hyperlipemia is a very frequent complication of the diabetic patient on dialysis. There is difficulty of treatment with the diet, because the dietary restriction already imposed on these patients and the secondary effects and toxicity of the available drugs in uremics aggravate the problem. We have treated 22 diabetic patients on dialysis (8 on hemodialysis and 14 on continuous ambulatory peritoneal dialysis) suffering from hyperlipemia with pantethine, a physiological substance and coenzyme A precursor in the Krebs cycle. With the administration of an oral dose of 900 mg/day we obtained a reduction of total cholesterol (275 +/- 72 vs. 231 +/- 54 mg/dl; p less than 0.001), very-low-density lipoprotein (VLDL)-cholesterol (66 +/- 36 vs. 46 +/- 18 mg/dl; p less than 0.01) and triglycerides (332 +/- 182 vs. 227 +/- 90 mg/dl; p less than 0.01) at 2 months. High-density lipoprotein (HDL)-cholesterol did not change, but the total cholesterol/HDL-cholesterol ratio decreased significantly (p less than 0.05). Total cholesterol, VLDL and triglycerides showed a progressive and significant reduction at 4 and 6 months. No changes were observed in serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, uric acid, blood glucose and glycosylated hemoglobin. Gastric discomfort in 2 patients and pruritus in another one were the secondary effects related. Pantethine was shown to be a very effective hypolipemic agent in diabetic patients on dialysis with a great tolerance.

Cholesterol↗
PubMed1986

Increased platelet aggregation during alimentary hyperlipemia in normal and hypertriglyceridemic subjects.

The influence of 2 different fatty meals, rich in either saturated or polyunsaturated fatty acids, on platelet aggregation in 7 normolipemic subjects and in 10 patients with phenotype IV hyperlipemia, was studied. 3 h after ingestion of a saturated- or polyunsaturated-fat-rich meal, plasma triglycerides were similarly increased in both groups. 5 h after ingestion of fat of either origin, the plasma triglyceride level in normal subjects returned almost to the fasting level, whereas in patients with hypertriglyceridemia it was still elevated. Platelet aggregation induced by ADP in platelet-rich plasma significantly increased in the normal group 3 h after both meals, whereas in the patient group it increased only after the saturated-fat-rich meal. These results were not changed 5 h after the meals. Postprandial elevated platelet activity was not correlated with increased plasma triglyceride concentration. No changes were found in washed-platelet aggregation in normal subjects, whereas the patient-derived washed platelets showed increased aggregation after the saturated-fat-rich meal. Plasma chylomicrons prepared from both groups during alimentary hyperlipemia inhibited ADP-induced platelet aggregation as well as thrombin-induced platelet 14C-serotonin release. This study indicates that the intake of fatty meals induces acute disturbance in platelet aggregation, favoring thrombosis. These changes are more comprehensive in hyperlipemic patients and after a saturated-fat-rich meal.

Adult↗
PubMed2003

Pharmacological activity of deep-sea water: examination of hyperlipemia prevention and medical treatment effect.

When normal rabbits were administered various samples of deep-sea water, their biochemical values changed within normal limits, and no differences from distilled water administration (control) group levels were observed. Furthermore, no histopathological changes were observed in internal organs on the 28th day after administration. The serum total cholesterol (T-Cho) and low density lipoprotein cholesterol (LDL-Cho) levels of normal rabbits fed with a 1% cholesterol-containing diet simultaneously administered deep-sea water (desalinated water, hardness 28, 300, and 1200) increased with time up to about 1500 mg/dl. However, the degrees of increase were smaller than those of the control group, which received distilled water. Furthermore, when prepared hyperlipemia rabbits were administered deep-sea water (desalinated water, hardness 28, 300, and 1200), there were no significant changes in aspartate aminotransferase (AST), alanine aminotransferase (ALT), high density lipoprotein cholesterol (HDL-Cho), or triglyceride (TG) levels. On the other hand, T-Cho and LDL-Cho levels were reduced when the rabbits were changed to normal food, and the degree of reduction was more than that of the control group. In the liver and main artery bow, as the hardness of the deep-sea water increased, the accumulation of lipid and permeation of macrophages was reduced. This result was well in agreement with the results of the T-Cho and LDL-Cho levels. From these results, it is clear that deep-sea water controls the increase of serum lipid values (T-Cho and LDL-Cho) of cholesterol-fed rabbits, and promotes the reduction of serum lipid hyperlipemia rabbits. The minerals in deep-sea water greatly influence this effect.

Animals↗