retinol-palmitate and Hyperlipidemias

Topics: Apolipoprotein B-100; Apolipoprotein B-48; Apolipoproteins B; Arteriosclerosis; Biomarkers; Blood Chemical Analysis; Breath Tests; Cholesterol; Coronary Disease; Diterpenes; Electrophoresis, Polyacrylamide Gel; Humans; Hyperlipidemias; Lipoproteins; Receptors, LDL; Retinyl Esters; Triglycerides; Vitamin A

Postprandial lipaemia, whether measured using levels of triglyceride of retinyl palmitate, is more severe in patients with coronary heart disease; however, little improvement in the discrimination between individuals with and without coronary heart disease can be made using postprandial measurements rather than measuring levels of high-density-lipoprotein2 cholesterol of apolipoproteins B. Retinyl palmitate levels occasionally reveal differences not apparent from triglyceride measurements. Elevated fasting and postprandial triglyceride levels may produce clinical disease partly by enhancing coagulation and by interfering with fibrinolysis.

Topics: Anticarcinogenic Agents; Clinical Trials as Topic; Coronary Disease; Diterpenes; Eating; Factor VII; Fasting; Humans; Hyperlipidemias; Lipoproteins; Retinyl Esters; Risk Factors; Triglycerides; Vitamin A

Exacerbated postprandial lipid responses are associated with an increased cardiovascular risk. Dietary proteins influence postprandial lipemia differently, and whey protein has a preferential lipid-lowering effect. We compared the effects of different whey protein fractions on postprandial lipid and hormone responses added to a high-fat meal in type 2 diabetic subjects.. A total of 12 type 2 diabetic subjects ingested four isocaloric test meals in randomized order. The test meals contained 100 g of butter and 45 g of carbohydrate in combination with 45 g of whey isolate (iso-meal), whey hydrolysate (hydro-meal), α-lactalbumin enhanced whey (lac-meal) or caseinoglycomacropeptide enhanced whey (CGMP-meal). Plasma concentrations of triglyceride, retinyl palmitate, free fatty acid, insulin, glucose, glucagon, glucagon-like peptide 1 and glucose-dependent insulinotropic peptide were measured before and at regular intervals until 8-h postprandially.. We found no statistical significant differences between meals on our primary variable triglyceride. The retinyl palmitate response was higher after the hydro-meal than after the iso- and lac-meal in the chylomicron-rich fraction (P=0.008) while no significant differences were found in the chylomicron-poor fraction. The hydro- and iso-meal produced a higher insulin response compared with the lac- and CGMP-meal (P<0.001). Otherwise no significant differences in the hormone responses were found in the incremental area under the curve over the 480-min period.. A supplement of four different whey protein fractions to a fat-rich meal had similar effects on postprandial triglyceride responses in type 2 diabetic subjects. Whey isolate and whey hydrolysate caused a higher insulin response.

Topics: Aged; Area Under Curve; Cardiovascular Diseases; Caseins; Chylomicrons; Diabetes Mellitus, Type 2; Dietary Fats; Dietary Proteins; Dietary Supplements; Diterpenes; Female; Glycopeptides; Humans; Hyperlipidemias; Hypolipidemic Agents; Insulin; Lactalbumin; Male; Middle Aged; Milk Proteins; Postprandial Period; Protein Hydrolysates; Retinyl Esters; Triglycerides; Vitamin A; Whey Proteins

Exaggerated and prolonged postprandial lipemia is potentially atherogenic and associated with type 2 diabetes. Limited data exist regarding the influence of dietary protein on postprandial lipemia in type 2 diabetes. We investigated, over 8-h, the acute effects of casein alone or in combination with carbohydrate on postprandial lipid and incretin responses to a fat-rich meal in type 2 diabetes.. Eleven type 2 diabetic subjects ingested four test meals in random order: an energy-free soup plus 80 g of fat (control-meal); control-meal plus 45 g carbohydrates (CHO-meal); control-meal plus 45 g of casein (PRO-meal); and PRO-meal plus 45 g carbohydrates (CHO+PRO-meal). Triglyceride and retinyl palmitate responses were measured in plasma and in a chylomicron-rich and chylomicron-poor fraction. We found no significant differences in triglyceride responses to PRO- and CHO+PRO-meal compared to the control-meal. However, the addition of casein to the CHO-meal reduced the raised triglyceride response in the chylomicron-rich fraction. Retinyl palmitate responses did not differ significantly between meals in the chylomicron-rich fraction, whereas the PRO-meal increased retinyl palmitate in the chylomicron-poor fraction. PRO- and PRO+CHO-meal increased insulin and glucagon compared to the control-meal. PRO+CHO-meal increased the glucose-dependent insulinotropic peptide response while no change in glucagon-like peptide-1 responses was detected.. The data presented suggest that casein per se did not modulate the postprandial triglyceride response in type 2 diabetes. When added to carbohydrate, casein suppressed the triglyceride response in the chylomicron-rich fraction, increased insulin and glucagon but did not affect the incretin responses.

Topics: Aged; Biomarkers; Blood Glucose; Caseins; Chylomicrons; Cross-Over Studies; Diabetes Mellitus, Type 2; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Diterpenes; Female; Glucagon; Glucagon-Like Peptide 1; Glycated Hemoglobin; Humans; Hyperlipidemias; Hypoglycemic Agents; Incretins; Insulin; Male; Middle Aged; Postprandial Period; Retinyl Esters; Time Factors; Triglycerides; Vitamin A

Premixed insulin analogues reduce postprandial hyperglycemia in patients with Type 2 diabetes in comparison to premixed regular insulin. Insulin also plays an important role in the regulation of postprandial lipid metabolism. It is known that increased levels of postprandial insulin reduce postprandial hyperlipemia but, on the other hand, no information exists with regard to the possible effect of insulin analogues in comparison to human insulin.. 12 subjects (3 men; age 59 +/- 5 years; BMI 30.5 +/- 5.9 kg/m2, duration of diabetes 9 +/- 1 years, HbA1c 8.33 +/- 1.1 %) already on therapy with premixed insulin were treated either with biphasic human insulin (BHI30) or with biphasic insulin aspart (BIAsp30) (1.3 IU fast acting insulin/12 g KH) in the setting of a standardized test meal. Serum levels of glucose, insulin, C-peptide and triglycerides as well as retinylpalmitate in plasma and chylomicron remnants were determined before and up to 8 hours after the meal.. As was to be expected, therapy with BIAsp30 reduced the maximum increase of postprandial glucose from 7.10 +/- 2.00 mmol/l to 5.27 +/- 1.83 mmo/l (p = 0.007) compared to BHI30 insulin. In the same way, the maximum increase of triglycerides (from 2.33 +/- 1.03 to 1.65 +/- 0.69 mmol/l, p = 0.014) was reduced. The AUC 0 - 8 for triglycerides was not significantly influenced (34.20 +/- 19.86 vs. 31.46 +/- 16.21 mmol x 8 h/l) but the incremental area over baseline (AOB 0 - 8) was significantly reduced from 8.02 +/- 4.35 to 6.12 +/- 3.94 mmol x 8 h/l (p = 0.024).. Compared to conventional human premixed insulin the prandial therapy with biphasic insulin aspart results not only in an improvement of glucose tolerance but also in a significant reduction of postprandial hyperlipemia.

Topics: Biphasic Insulins; Chylomicron Remnants; Chylomicrons; Cross-Over Studies; Diabetes Mellitus, Type 2; Diterpenes; Female; Humans; Hyperlipidemias; Hypoglycemic Agents; Insulin; Insulin Aspart; Insulin, Isophane; Male; Postprandial Period; Retinyl Esters; Time Factors; Vitamin A

To assess the usefulness of remnant-like particles (RLPs), which represent potentially atherogenic lipoprotein remnants, as an index of postprandial hyperlipidemia, RLPs and other lipids were measured in 19 healthy adults (23-44 years old) after ingestion of a test meal (fat content, 32.9%). The lipoprotein derivatives, with a marked increase after fat-loading, were triglycerides, retinyl palmitate and RLPs. The retinyl palmitate peak lagged behind the RLP and triglyceride peaks, indicating that it may have different kinetics than RLP and triglyceride. While triglycerides are considered as an index of atherosclerotic risk factor, RLPs also may be a suitable index for evaluating postprandial hyperlipidemia. RLPs remained high even 8 h after fat-loading, suggesting that the postprandial state persists for almost the whole day. Accordingly, it may be important to assess postprandial remnant concentrations.

Topics: Adult; Apolipoproteins; Biomarkers; Blood Glucose; Dietary Fats; Diterpenes; Female; Humans; Hyperlipidemias; Lipoproteins; Male; Postprandial Period; Retinyl Esters; Triglycerides; Vitamin A

The effect of tetrahydrolipstatin (THL), a recently developed pancreatic lipase inhibitor, on fasting plasma lipid levels and postprandial lipoprotein and retinyl palmitate (RP) metabolism was studied in 17 hyperlipidemic subjects, using an oral RP fat load (8 hours, 50 g fat/m2). During therapy with THL, fasting plasma cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoprotein (apo) B concentrations decreased by 8% (P = .006), 9% (P = .002), and 10% (P = .002), respectively. The postprandial plasma triglyceridemia, which was expressed as the area under the 8-hour triglyceride (TG) curve, improved by 27% during THL therapy (P = .04) without changes in fasting plasma TG or high-density lipoprotein (HDL) cholesterol levels. The improved postprandial triglyceridemia was accompanied by a 19% reduction in circulating levels of chylomicrons and chylomicron remnants, determined by the decreased areas under the 8-hour RP curves. The most likely mechanisms involved are decreased formation of chylomicrons by a decrease of intestinal TG absorption as a consequence of THL treatment, as well as reduced delivery of dietary lipid and fatty acids to the liver and subsequent upregulation of hepatic LDL receptors. In agreement with the latter mechanism, the decrease in postprandial lipemia expressed as delta area under the TG curve was significantly related to the decrease (delta) in LDL cholesterol level during THL treatment (r = .81, P = .0001). The present data indicated that pancreatic lipase inhibition improved postprandial lipoprotein metabolism, which in turn resulted in lower plasma total and LDL cholesterol concentrations.

Topics: Administration, Oral; Apolipoproteins B; Cholesterol, HDL; Cholesterol, LDL; Chylomicrons; Diterpenes; Dose-Response Relationship, Drug; Double-Blind Method; Eating; Female; Humans; Hyperlipidemias; Intestinal Absorption; Lactones; Linear Models; Lipase; Lipids; Lipoproteins, LDL; Male; Middle Aged; Orlistat; Pancreas; Retinyl Esters; Triglycerides; Vitamin A

Familial hypobetalipoproteinemia (FHBL) is characterized by inherited low plasma levels of apolipoprotein B (apoB)-containing lipoproteins. In this paper we investigated whether the already described APOB R463W missense mutation, a FHBL mutation able to impair the activity of microsomal triglyceride transfer protein (MTP), may cause intestinal fat accumulation and reduced postprandial lipemia.. Four out of five probands harboring APOB R463W mutation were compared with six healthy controls and six patients with celiac disease (CD). An oral fat load supplemented with retinyl palmitate (RP) was administered and a gastro-duodenal endoscopy with biopsy was performed.. Plasma triglyceride area under curves was significantly reduced in FHBL probands compared to controls and CD patients; the proportion of absorbed RP was similar to that of CD patients. Only the intestinal biopsies of FHBL patients showed lipids accumulating within the duodenal mucosa.. FHBL due to R463W apoB mutation is a cause of intestinal fat accumulation and postprandial lipid absorption impairment.

Topics: Adolescent; Adult; Apolipoproteins B; Carrier Proteins; Child; Diterpenes; Female; Humans; Hyperlipidemias; Hypobetalipoproteinemia, Familial, Apolipoprotein B; Intestinal Mucosa; Intra-Abdominal Fat; Lipid Metabolism; Male; Middle Aged; Mutation, Missense; Postprandial Period; Retinyl Esters; Triglycerides; Vitamin A

The -250G/A promoter polymorphism of the hepatic lipase gene has been associated with changes in the activity of the enzyme. We investigated whether this polymorphism modifies the postprandial response of triacylglycerol-rich lipoproteins (TRL) in young normolipemic males.. Fifty-one healthy apolipoprotein (apo) E3/E3 male volunteers (30 G/G and 21 carriers of the A allele) underwent a vitamin A fat-loading test and blood samples were drawn every hour until the 6th, and every 2h and 30 min until the 11th. Total plasma cholesterol and triacylglycerols (TG), as well as cholesterol, TG and retinyl palmitate (RP) in TRL, isolated by ultracentrifugation, were determined. Carriers of the A allele showed a higher response (P=0.008), a higher area under the curve (AUC; P=0.022) and a lower RP peak time (P=0.029) in small TRL during the postprandial response, as well as a lower peak time in total plasma TG levels (P=0.034) and large TRL-TG (P=0.033) than subjects who were homozygous for the G allele.. Our data indicate that the presence of the A allele in the -250G/A promoter polymorphism of the hepatic lipase gene is associated with a higher postprandial lipemic response.

Topics: Adult; Alleles; Apolipoprotein B-100; Apolipoprotein B-48; Area Under Curve; Cholesterol; Dietary Fats; Diterpenes; Gene Amplification; Genotype; Humans; Hyperlipidemias; Lipase; Lipoproteins; Liver; Male; Polymorphism, Genetic; Postprandial Period; Promoter Regions, Genetic; Retinyl Esters; Triglycerides; Vitamin A

Dyslipidemia is common among patients receiving antiretroviral therapy for HIV infection. The purpose of this study was to determine whether postprandial lipemia contributes to the dyslipidemia observed in HIV-positive patients taking antiretroviral therapy.. A standardized fat load was administered to 65 subjects (group 1 35 HIV-positive subjects receiving protease inhibitors [PIs]; group 2 20 HIV-positive subjects not receiving PIs; group 3 10 HIV-negative controls). Serum triglycerides, retinyl palmitate, and lipoproteins were measured using enzymatic and nuclear magnetic resonance spectroscopic techniques. Compared with HIV-negative controls, peak postprandial retinyl palmitate and large very low-density lipoprotein (VLDL) levels occurred later in both HIV-positive groups, and a delayed decrease in serum triglycerides was observed. However, postprandial areas under the curve (AUCs) for triglycerides, retinyl palmitate, chylomicrons, and large VLDL were similar. Postprandial AUCs for intermediate-density lipoproteins (IDLs) and low-density lipoproteins (LDLs) were higher in group 1 than groups 2 and 3 (all P<0.035).. Postprandial clearance of triglyceride-rich lipoproteins is delayed in HIV-positive individuals receiving antiretroviral therapy. Compared with HIV-positive individuals not on PIs, those taking PIs do not have increased postprandial triglyceride-rich lipoproteins but do have increased postprandial IDLs and LDLs. An oral fat load was administered to 55 HIV-positive and 10 HIV-negative individuals. Postprandial clearance of triglyceride-rich lipoproteins was delayed in HIV-positive individuals. Compared with HIV-positive subjects not on PIs, those taking PIs do not have increased postprandial triglyceride-rich lipoproteins but do have increased postprandial intermediate-density and low-density lipoproteins.

Topics: Adult; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Apolipoproteins E; Area Under Curve; Blood Glucose; Chylomicrons; Coronary Disease; Dietary Fats; Diterpenes; Female; HIV Infections; HIV Protease Inhibitors; Humans; Hyperlipidemias; Hypertension; Insulin; Lipoproteins; Lipoproteins, IDL; Lipoproteins, LDL; Lipoproteins, VLDL; Male; Postprandial Period; Retinyl Esters; Risk Factors; Smoking; Triglycerides; Vitamin A

In a previous study it was shown that postprandial lipid metabolism is delayed in individuals with intra-abdominal visceral fat accumulation. Population studies have shown that as compared with individuals with apolipoprotein (apo) E3/3, those with phenotype apo E3/4 phenotype have higher plasma and low density lipoprotein (LDL)-cholesterol (C) concentration and increased susceptibility to coronary heart disease. The aim of the present study is to determine how apo E4 affects postprandial lipid metabolism by comparing individuals with apo E3/4 to those with apo E3/3 phenotype matched for abdominal visceral fat. Sixty-two Japanese subjects (41 male, 21 female) [average age 48+/-14 years; mean body mass index (BMI) 25+/-5.6 kg/m2] were recruited for this study. The subjects were divided into two groups: those with apo E3/3 (n=43) and those with apo E3/4 phenotype (n=19), as determined by isoelectric focusing (IEF). Visceral fat accumulation was analyzed as area of fat deposition by computerized tomography at the umbilicus level. After a 12-h overnight fasting, an oral vitamin A and a fatty meal were administered to these subjects. The plasma triglyceride (TG) increased significantly hours after fat loading in both groups but the levels of TG were significantly higher in apo E3/4 than in apo E3/3 phenotype at 2, 4 and 6 h after fat loading. Plasma retinyl palmitate (RP) levels were also significantly higher in individuals with apo E3/4 than in those with apo E3/3 phenotype at 2, 4 and 6 h after fat loading. This investigation was then conducted in both genders separately, and found that these associations were statistically significant in men. Furthermore, after matching men for fasting TG levels, these associations did not persist for plasma TG levels at any time point, while plasma RP levels were still significantly higher in apo E3/4 group at 2 and 6 h after fat loading. These results indicate that in Japanese population especially for men apo E phenotype E3/4 is associated with an impaired postprandial TG-rich lipoprotein metabolism relative to apo E3/3 phenotype when matched for intra-abdominal visceral fat accumulation, which has a substantial effect on the metabolism of plasma TG-rich lipoproteins.

Topics: Adult; Aged; Apolipoprotein A-I; Apolipoprotein E3; Apolipoprotein E4; Apolipoproteins B; Apolipoproteins E; Dietary Fats; Diterpenes; Female; Humans; Hyperlipidemias; Lipids; Lipoproteins; Male; Middle Aged; Phenotype; Postprandial Period; Retinyl Esters; Triglycerides; Vitamin A

Postprandial lipemia after an oral fat challenge was studied in middle-aged men with visceral obesity. The two groups had similar plasma cholesterol levels, but obese subjects had higher levels of plasma triglyceride and reduced amounts of high-density cholesterol. Fasting plasma insulin was fourfold greater in obese subjects because of concomitant insulin resistance, with a calculated HOMA score of 3.1 +/- 0.6 vs. 0.8 +/- 0.2, respectively. Plasma apolipoprotein B(48) (apoB(48)) and retinyl palmitate (RP) after an oral fat challenge were used to monitor chylomicron metabolism. Compared with lean subjects, the fasting concentration of apoB(48) was more than twofold greater in obese individuals, suggestive of an accumulation of posthydrolyzed particles. After the oral lipid load, the incremental areas under the apoB(48) and RP curves (IAUC) were both significantly greater in obese subjects (apoB(48): 97 +/- 17 vs. 44 +/- 12 microg.ml(-1). h; RP: 3,120 +/- 511 vs. 1,308 +/- 177 U. ml(-1). h, respectively). A delay in the conversion of chylomicrons to remnants probably contributed to postprandial dyslipidemia in viscerally obese subjects. The triglyceride IAUC was 68% greater in obese subjects (4.7 +/- 0.6 vs. 2.8 +/- 0.8 mM. h, P < 0.06). Moreover, peak postprandial triglyceride was delayed by approximately 2 h in obese subjects. The reduction in triglyceride lipolysis in vivo did not appear to reflect changes in hydrolytic enzyme activities. Postheparin plasma lipase rates were found to be similar for lean and obese subjects. In this study, low-density lipoprotein (LDL) receptor expression on monunuclear cells was used as a surrogate marker of hepatic activity. We found that, in obese subjects, the binding of LDL was reduced by one-half compared with lean controls (70.9 +/- 15.07 vs. 38.9 +/- 4.6 ng LDL bound/microg cell protein, P = 0.02). Because the LDL receptor is involved in the removal of proatherogenic chylomicron remnants, we suggest that the hepatic clearance of these particles might be compromised in insulin-resistant obese subjects. Premature and accelerated atherogenesis in viscerally obese, insulin-resistant subjects may in part reflect delayed clearance of postprandial lipoprotein remnants.

Topics: Apolipoprotein B-48; Apolipoproteins B; Arteriosclerosis; Body Constitution; Body Mass Index; Cholesterol; Cholesterol, HDL; Chylomicrons; Dietary Fats; Diterpenes; Food; Humans; Hyperlipidemias; Insulin; Insulin Resistance; Kinetics; Lipase; Lipoproteins, LDL; Male; Middle Aged; Obesity; Receptors, LDL; Retinyl Esters; Triglycerides; Viscera; Vitamin A

Postprandial hyperlipidemia is frequently accompanied with intra-abdominal visceral accumulation in human subjects. We have found that the decreased lipoprotein lipase (LPL) mass and activity is negatively associated with the amount of visceral fat accumulation. Here, we studied the postprandial hyperlipidemia using the OLETF rat, a model with visceral obesity, in order to clarify the molecular mechanism causing postprandial hyperlipidemia accompanied with visceral obesity. At the same age of 32 weeks, the OLETF rats showed obviously higher plasma leptin, total cholesterol, triglyceride, and HDL-cholesterol levels than the control LETO rats, although the plasma glucose level was not significantly different. Fat-loading test revealed the delayed metabolism of exogenous fat in the OLETF rats compared to the LETO rats, similar to human subjects with visceral obesity. In the obese rats, plasma levels of LPL mass and activities were 60 and 49% of control rats. The expression of LPL gene was decreased in subcutaneous adipose tissues and skeletal muscle of OLETF rats to 40 and 52% compared to those of LETO rats. In OLETF rats, plasma tumor necrosis factor-alpha (TNF-alpha) and insulin levels were increased to 2.0- and 2.3-folds compared to those in control rats. Furthermore, plasma insulin and TNF-alpha levels in OLETF rats were negatively correlated with the expression levels of LPL gene in subcutaneous fat and muscle. These results indicate that decreased LPL mass and activity in the animal model with visceral obesity is possibly caused by decreased expression of LPL gene in tissues mediated by the increased levels of insulin and TNF-alpha. The different expression of LPL gene in tissues associated with the increased levels of insulin and TNF-alpha possibly elucidate the underlying mechanisms involving the postprandial hyperlipidemia observed in visceral obesity.

Topics: Adipose Tissue; Animals; Blood Glucose; Blotting, Northern; Body Weight; Cholesterol; Cholesterol, HDL; Cloning, Molecular; Disease Models, Animal; Diterpenes; Humans; Hyperlipidemias; Insulin; Leptin; Lipoprotein Lipase; Male; Muscle, Skeletal; Obesity; Rats; Rats, Long-Evans; Retinyl Esters; RNA, Messenger; Time Factors; Tissue Distribution; Triglycerides; Tumor Necrosis Factor-alpha; Vitamin A

Individuals with obesity, in particular those with intra-abdominal visceral fat accumulation, are known to have various complications, such as hyperlipidaemia, impaired glucose tolerance, hyperinsulinaemia and hypertension, leading to the development of coronary heart disease. Post-prandial hyperlipidaemia has repeatedly been shown to be an independent risk factor for coronary heart disease. The aim of the present study was to investigate post-prandial lipoprotein metabolism in subjects with excessive visceral fat accumulation.. Eighty-three patients (52 men, 31 women) [average age 48 +/- 14 years; mean body mass index (BMI) 25 +/- 5 kg m-2] were recruited to the study. Visceral (or subcutaneous) fat accumulation was analysed as areas of fat deposition by computerized tomography at the umbilicus level. After a 12-h overnight fast, oral vitamin A and a fatty meal (40 g m-2 fresh cream containing 50 000 units m-2 vitamin A) were administered to these subjects. The concentration of retinyl palmitate (RP) was measured by high-performance liquid chromatography.. The visceral fat area (V) was positively correlated with plasma triglyceride (TG) 0, 2, 4 and 6 h after fat loading and with plasma RP 0, 4 and 6 h after fat loading. The BMI did not show any correlation with plasma TG and RP at any point. The visceral fat area was positively correlated with the RP area under the curve (AUC) in the serum from the subjects [V vs. RP AUC: n = 83, r = 0.327, P = 0.013]. The BMI of the subjects did not show any correlation with the RP AUC (r = 0.021, P = 0.85).. These results suggest that post-prandial lipid metabolism is impaired in subjects with intra-abdominal visceral fat accumulation, irrespective of BMI, leading to the development and progression of coronary atherosclerosis.

Topics: Abdomen; Adipose Tissue; Adult; Aged; Anticarcinogenic Agents; Apolipoproteins E; Body Mass Index; Dietary Fats; Diterpenes; Female; Humans; Hyperlipidemias; Lipoprotein Lipase; Male; Middle Aged; Obesity; Phenotype; Postprandial Period; Regression Analysis; Retinyl Esters; Triglycerides; Viscera; Vitamin A

We have studied the effects of melatonin and retinol palmitate (RP) on the nephropathy and oxidative stress induced by a single and high dose of adriamycin (AD) in Wistar male rats. A dose of melatonin (75 microg/kg/day) and a dose of RP (0.25 g oily solution/kg/day, s.c.) were injected 3 and 9 days before and after the administration of AD (25 mg/kg, i.p.), respectively. After the decapitation, samples were taken from the neck vascular trunk in order to determine the triglycerides, total cholesterol, phospholipids, HDL-cholesterol, total proteins, urea, lipoperoxides, and reduced glutathione (GSH). We estimated the lipoperoxide and glutathione (GSH) contents in renal homogenates, and the excretion of proteins in urine over a 24 hr period. The administration of AD caused significant increases in proteinuria and in the other parameters studied [lipids (triglycerides, total cholesterol, phospholipids, and HDL-cholesterol), non-protein nitrogen compounds, and lipoperoxides]. AD increased the lipoperoxide content, but it decreased the GSH content in the kidney. Both melatonin and RP, although melatonin more significantly, decreased the intensity of the changes produced by the administration of AD alone. In fact, melatonin was quite efficient in reducing the formation of lipoperoxides, restoring renal GSH content and decreasing remarkably the severity of proteinuria. These results support the powerful antioxidant action of melatonin at renal level and a lower antioxidant action of retinol. Likewise, these data reinforce the hypothesis which supports the pathogenetic role and the close relation between the oxidative stress and the expression of the nephropathy induced by AD. However, in spite of this obvious antioxidant effect of melatonin in the kidney, additional studies are required to establish accurately the role of this pineal indole in the regulation and dynamics of the antioxidative defense enzyme system, which neutralizes the damaging effect of free radicals, both endogenous and exogenous, in this organ.

Topics: Animals; Diterpenes; Doxorubicin; Glutathione; Hyperlipidemias; Kidney; Kidney Diseases; Lipid Metabolism; Lipid Peroxides; Male; Malondialdehyde; Melatonin; Oxidative Stress; Proteinuria; Rats; Rats, Wistar; Retinyl Esters; Vitamin A

Post-prandial lipaemia was investigated in a group of nine subjects with nephrotic syndrome by following the concentrations of triglyceride and retinyl palmitate in the d < 1.006 g ml-1 fraction of plasma after a standard oral fat load containing vitamin A. Lipoprotein lipase and hepatic triglyceride lipase activities were measured in post-heparin plasma. Subjects with other renal disease but insignificant proteinuria acted as controls. The time course of the lipaemic response was similar in both groups although individual patients demonstrated a prolonged lipaemia. Overall, there were no significant differences in the rise in triglyceride at 6 h (nephrotic--median 2.53 mmol l-1; range 0.87-4.76 vs. control 1.88; 0.38-4.12, P = 0.34), the peak concentration of retinyl palmitate (nephrotic 0.87 mg dl-1; 0.27-2.16 vs. control 0.65; 0.24-1.89, P = 0.97) or the areas under the curve from 0-24 h for triglyceride (nephrotic 10.5 mmol. h l-1; 2.9-43.6 vs. control 9.7; 4.3-27.0, P = 1.0) or retinyl palmitate (5.5 mg.h dl-1; 1.0-23.4 vs. 4.3; 1.5-12.4, P = 0.7). At baseline, the particles in the d < 1.006 g ml-1 fraction of plasma from nephrotic subjects had a higher free cholesterol:phospholipid ratio but this difference was no longer apparent 6 h after the test meal. There were no differences in total heparin-releasable lipase, lipoprotein lipase or hepatic triglyceride lipase activities between the two groups. These data suggest that impaired clearance of chylomicrons is not a major contributor to nephrotic hyperlipidaemia in man.

Topics: Adult; Aged; Chylomicrons; Dietary Fats; Diterpenes; Female; Humans; Hyperlipidemias; Lipase; Lipoprotein Lipase; Lipoproteins; Male; Middle Aged; Nephrotic Syndrome; Retinyl Esters; Triglycerides; Vitamin A

Topics: Cholesterol; Chylomicrons; Coronary Artery Disease; Dietary Fats; Diterpenes; Female; Fenofibrate; Humans; Hyperlipidemias; Lipoproteins; Male; Metabolic Clearance Rate; Middle Aged; Niacin; Retinyl Esters; Triglycerides; Vitamin A

Topics: Acute Disease; Chromatography, High Pressure Liquid; Diterpenes; Hepatitis; Humans; Hyperlipidemias; Hypervitaminosis A; Liver Cirrhosis; Reference Values; Retinyl Esters; Specimen Handling; Vitamin A