Analysis Of Serum Lipoproteins Research Articles

Effects of antibiotic, acidifier, and probiotic supplementation on mortality rates, lipoprotein profile, and carcass traits of broiler chickens

Antimicrobial resistance is a significant issue, therefore it's relevant to assess the effects of antibiotics, acidifiers, and probiotic supplementation finding a good alternative to reduce the use of antibiotics in broiler production in rural areas of Bangladesh. Using randomized control trial, this 28-day study evaluated 360 Hubbard Classic broiler chicks divided into four groups: oxytetracycline-treated, acidifier-treated, Lactobacillus-based probiotic-treated, and control (no antibiotics, acidifiers, or probiotics). Each group was replicated three times with 30 birds each with adlibitum feeding. Body weight and feed intake were recorded weekly, and on 28th day, carcass traits and blood lipoprotein levels were evaluated. Results showed that in first and fourth weeks, the body weight gain significantly varied in probiotics and acidifier-treated birds than the control group (P < 0.001). The probiotic group had gained considerable increase in body weight (185.0 g vs 161.7 g and 1745.0 g vs 1592.7 g) than the control group. Notably, in the first week, the feed conversion ratio for the probiotic group was 0.76, but the antibiotic group's was 0.96 (P < 0.001). The weights of the drumstick (88.33 g) and liver (61.0 g) having probiotic supplements were substantially higher than those in the control group (77.0 g and 51.33 g, respectively) (P < 0.001). According to serum lipoprotein analysis, the probiotic and acidifier groups exhibited lower LDL levels (71.1 mg/dl and 69.8 mg/dl, respectively) and higher triglyceride levels (122.9 mg/dl and 135.4 mg/dl). These findings highlight the potential of probiotics and acidifiers as effective antibiotic alternatives, promoting carcass traits and lowering LDL levels in broilers in Bangladesh.

Albino mice with the point mutation at the tyrosinase locus show high cholesterol diet-induced NASH susceptibility

Non-alcoholic fatty liver disease (NAFLD) constitutes a metabolic disorder with high worldwide prevalence and increasing incidence. The inflammatory progressive state, non-alcoholic steatohepatitis (NASH), leads to liver fibrosis and carcinogenesis. Here, we evaluated whether tyrosinase mutation underlies NASH pathophysiology. Tyrosinase point-mutated B6 (Cg)-Tyrc-2J/J mice (B6 albino) and C57BL/6J black mice (B6 black) were fed with high cholesterol diet (HCD) for 10 weeks. Normal diet-fed mice served as controls. HCD-fed B6 albino exhibited high NASH susceptibility compared to B6 black, a phenotype not previously reported. Liver injury occurred in approximately 50% of B6 albino from one post HCD feeding, with elevated serum alanine aminotransferase and aspartate aminotransferase levels. NASH was induced following 2 weeks in severe-phenotypic B6 albino (sB6), but B6 black exhibited no symptoms, even after 10 weeks. HCD-fed sB6 albino showed significantly higher mortality rate. Histological analysis of the liver revealed significant inflammatory cell and lipid infiltration and severe fibrosis. Serum lipoprotein analysis revealed significantly higher chylomicron and very low-density lipoprotein levels in sB6 albino. Moreover, significantly higher small intestinal lipid absorption and lower fecal lipid excretion occurred together with elevated intestinal NPC1L1 expression. As the tyrosinase point mutation represents the only genetic difference between B6 albino and B6 black, our work will facilitate the identification of susceptible genetic factors for NASH development and expand the understanding of NASH pathophysiology.

The thyroid receptor modulator KB3495 reduces atherosclerosis independently of total cholesterol in the circulation in ApoE deficient mice.

BackgroundThyroid hormones (TH) regulate cholesterol metabolism but their use as lipid-lowering drugs is restricted due to negative cardiac effects. TH mimetic compounds modulating TH receptor β (THRβ) have been designed as potential drugs, reducing serum cholesterol levels while avoiding apparent deleterious cardiac effects. ObjectiveUsing ApoE deficient mice, we examined whether KB3495, a TH mimetic compound, reduces atherosclerosis and if there is a synergistic effect with atorvastatin. The effect of KB3495 was investigated after 10 and 25 weeks.ResultsKB3495 treatment reduced atherosclerotic plaque formation in aorta and decreased the cholesteryl ester (CE) content by 57%. Treatment with KB3495 was also associated with a reduction of macrophage content in the atherosclerotic plaques and reduced serum levels of IL-1β, TNFalpha, IL-6, Interferon γ, MCP-1 and M-CSF. Serum lipoprotein analysis showed no change in total cholesterol levels in ApoB-containing lipoproteins. KB3495 alone increased fecal BA excretion by 90%. The excretion of neutral sterols increased in all groups, with the largest increase in the combination group (350%). After 25 weeks, the animals treated with KB3495 showed 50% lower CE levels in the skin and even further reductions were observed in the combination group where the CE levels were reduced by almost 95% as compared to controls. ConclusionKB3495 treatment reduced atherosclerosis independently of total cholesterol levels in ApoB-containing lipoproteins likely by stimulation of sterol excretion from the body and by inhibition of the inflammatory response.

Gray matter volumetric MRI differences late-preterm and term infants

Gray matter develops rapidly during the third trimester of pregnancy, which is a critical period for lipid deposition. We measured brain volume in term and late-preterm infants to determine if it is related to disabilities in late-preterm infants. In addition, we measured serum lipid concentrations to investigate the relationship between brain volume and lipid nutrition. Magnetic resonance imaging scans were obtained in 16 late-preterm and 13 term infants. We measured cerebrum, gray matter, and white matter volumes. We performed serum cholesterol, triglyceride (TG), and lipoprotein analyses in cord blood by high-performance liquid chromatography using gel permeation columns to assess lipid nutritional levels. The gray matter volume and percent cerebrum volume of gray matter were significantly smaller in late-preterm infants (p<0.001). Head circumference and cerebrum and white matter volume did not differ between the two groups. Gray matter volume correlated positively with gestational age (r=0.647, p<0.001), head circumference (r=0.688, p<0.001), and high-density lipoprotein (HDL)-TG levels (r=0.496, p=0.006). Late-preterm infants had a normal head circumference and a lower gray matter volume than term infants. Gestational age and head circumference were significantly associated with gray matter volume. Only HDL-TG levels were significantly associated with gray matter volume. HDL-TG might contribute to the transport of fatty acids and gray matter development during the postnatal period. Thus, delayed gray matter development may partly contribute to neurodevelopmental disabilities in late-preterm infants.

Free fatty acids and acute coronary syndromes--the history

While it has been known for >40 years that elevation of plasma-free fatty acids (FFAs or non-esterified fatty acids, NEFA) occurs within 1 or 2 h of the onset of an acute coronary syndrome (ACS) and that the greater the increase in plasma FFA the greater the incidence of serious ventricular arrhythmias, no account exists as to how this was discovered and developed. It was derived from analysis of serum lipoproteins. In 1949, Cohn and colleagues, using elaborate low temperature fractionation, reported that almost all the plasma lipids circulate in combination with proteins, particularly the α- and β-globulin fractions1; these were therefore termed α- and β-lipoproteins.2 A more simple method of analysis is zone electrophoresis of serum lipoproteins in a starch block.3 Using lipid stains, it was possible to identify cholesterol-carrying β-lipoproteins [low-density lipoproteins (LDL)] and α-lipoproteins [or high-density lipoproteins (HDL)]. But these methods required many milliliters of serum, so we developed a micro method applying 0.15 ml of serum to Whatman filter paper using sudan IV or oil red O as the lipid stain. The precise analytical method based on cholesterol elution from the electrophoretic bands reacting to protein staining with bromophenol blue was described in detail in 1954.4 It provided the basis of our report in 1955 that, compared with age-matched …

Microminipig, a Non-rodent Experimental Animal Optimized for Life Science Research: Novel Atherosclerosis Model Induced by High Fat and Cholesterol Diet

Atherosclerotic lesions were observed in male and ovariectomized female Microminipig (MMP) fed a high fat and cholesterol diet with sodium cholate (HFCD/SC) for 3 months. HFCD/SC induced hypercholesterolemia accompanied by an increase in serum total cholesterol (T-Cho), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and cholesterol ester (CE). Unlike the mouse or rabbit, a dominant LDL-C fraction in the intact MMP, similar to that in humans, was observed by serum lipoprotein analysis. HFCD/SC increased body weight gain. At the end of the experiment, computed tomography scans of conscious animals showed that HFCD/SC had decreased liver attenuation values (Hounsfield unit) and increased subcutaneous and abdominal fat, suggesting the induction of fatty liver and obesity. HFCD/SC induced atherosclerotic lesions in systemic arteries, including the external and internal iliac arteries, abdominal aorta, coronary artery, and cerebral arterial circle. Atherosclerosis and pathological findings induced by HFCD/SC in MMP were similar to those in humans. The MMP is a potentially suitable tool for investigating human atherosclerosis.

Abolished synthesis of cholic acid reduces atherosclerotic development in apolipoprotein E knockout mice

To investigate the effects of abolished cholic acid (CA) synthesis in the ApoE knockout model [apolipoprotein E (apoE) KO],a double-knockout (DKO) mouse model was created by crossbreeding Cyp8b1 knockout mice (Cyp8b1 KO), unable to synthesize the primary bile acid CA, with apoE KO mice. After 5 months of cholesterol feeding, the development of atherosclerotic plaques in the proximal aorta was 50% less in the DKO mice compared with the apoE KO mice. This effect was associated with reduced intestinal cholesterol absorption, decreased levels of apoB-containing lipoproteins in the plasma, enhanced bile acid synthesis, reduced hepatic cholesteryl esters, and decreased hepatic activity of ACAT2. The upregulation of Cyp7a1 in DKO mice seemed primarily caused by reduced expression of the intestinal peptide FGF15. Treatment of DKO mice with the farnesoid X receptor (FXR) agonist GW4064 did not alter the intestinal cholesterol absorption, suggesting that the action of CA in this process is confined mainly to formation of intraluminal micelles and less to its ability to activate the nuclear receptor FXR. Inhibition of CA synthesis may offer a therapeutic strategy for the treatment of hyperlipidemic conditions that lead to atherosclerosis.

Analysis of cholesterol levels in lipoprotein(a) with anion-exchange chromatography

We previously established an analysis method for determining the cholesterol levels of five major lipoprotein classes [HDL, LDL, intermediate density lipoprotein (IDL), VLDL, and chylomicrons] in serum by an anion-exchange (AEX)-HPLC method, but lipoprotein(a) [Lp(a)], a well-known risk factor for atherosclerotic diseases, was not determinable. Therefore, we established new AEX-HPLC separation conditions for analyzing the cholesterol levels of six lipoprotein classes, including Lp(a). Serum lipoproteins were separated by HPLC with a diethylaminoethyl-ligand nonporous polymer-based column by elution with a stepwise gradient of the sodium perchlorate concentration. In this improved method, HDL, LDL, IDL, VLDL, chylomicrons, and Lp(a) were each eluted from the column. The cholesterol levels of the eluted lipoproteins were measured enzymatically by a postcolumn reaction. The within-day assay and between-day assay coefficients of variation for the lipoprotein cholesterol levels were in the ranges of 0.29-11.86% and 0.57-11.99%, respectively. The Lp(a) cholesterol levels determined by AEX-HPLC were significantly correlated with the amounts of Lp(a) protein measured by an immunoturbidimetry method available commercially (r = 0.9503, P < 0.0001). Taken together, this AEX-HPLC method may be effectively applied to the analysis of serum lipoproteins with high levels of Lp(a).

Very low-density lipoprotein in the cord blood of preterm neonates

Human fetuses have markedly low levels of serum lipids and a unique lipoprotein profile with respect to quality, with low-density lipoprotein (LDL)–like particle as the dominant cholesterol carrier. However, little is known about triglyceride (TG) distribution. In addition, lipid metabolism is important in lung development, with indications that TG from very low-density lipoprotein (VLDL) is essential for surfactant synthesis. We investigated TG distribution in preterm neonate cord blood and the relationship of VLDL-TG levels with respiratory distress syndrome (RDS). The study included 103 appropriate-for-gestational-age neonates (61 males). We performed serum lipoprotein analyses in cord blood by high-performance liquid chromatography with gel permeation columns. Term neonates had low cord blood TG concentrations distributed equally to the LDL and VLDL fractions. However, preterm neonates had even lower TG concentrations, with VLDL as the dominant carrier. The LDL-TG and high-density lipoprotein–TG concentrations in cord blood increased gradually with gestational age, but cord blood VLDL-TG concentrations increased dramatically from 32 to 34 weeks of gestational age. Neonates with RDS exhibited no RDS-specific lipoprotein profile; however, most were born before the timing of the dramatic VLDL-TG increase. Our results suggest that 34 weeks of gestation is a critical period for TG metabolism, indicating the need for evaluation of the lipid nutritional state in preterm neonates.

Suppression of 2,3-Oxidosqualene Cyclase by High Fat Diet Contributes to Liver X Receptor-α-mediated Improvement of Hepatic Lipid Profile

The liver X receptors (LXRs) sense oxysterols and regulate genes involved in cholesterol metabolism. Synthetic agonists of LXRs are potent stimulators of fatty acid synthesis, which is mediated largely by sterol regulatory element-binding protein-1c (SREBP-1c). Paradoxically, an improved hepatic lipid profile by LXR was observed in mice fed a Western high fat (HF) diet. To explore the underlying mechanism, we administered mice normal chow or an HF diet and overexpressed LXRalpha in the liver. The HF diet with tail-vein injection of adenovirus of LXRalpha increased the expression of LXR-targeted genes involved in cholesterol reverse transport but not those involved in fatty acid synthesis. A similar effect was also observed with the use of 22R-hydroxycholesterol, an LXR ligand, in cultured hepatocytes. Consequently, SREBP-1c maturation was inhibited by the HF diet, which resulted from the induction of Insig-2a. Importantly, increased cholesterol level suppressed the expression of 2,3-oxidosqualene cyclase (OSC), which led to an increase in endogenous LXR ligand(s). Furthermore, siRNA-mediated knockdown of OSC expression enhanced LXR activity and selectively up-regulated LXR-targeted genes involved in cholesterol reverse transport. Thus, down-regulation of OSC may account for a novel mechanism underlying the LXR-mediated lipid metabolism in the liver of mice fed an HF diet.

Local and Systemic Responses in Matrix Metalloproteinase 8-Deficient Mice duringPorphyromonas gingivalis-Induced Periodontitis

Periodontitis is a bacterium-induced chronic inflammation that destroys tissues that attach teeth to jaw bone. Pathologically excessive matrix metalloproteinase 8 (MMP-8) is among the key players in periodontal destruction by initiating type I collagen degradation. We studied MMP-8 in Porphyromonas gingivalis-induced periodontitis by using MMP-8-deficient (MMP8(-/-)) and wild-type (WT) mice. Alveolar bone loss, inflammatory mediator expression, serum immunoglobulin, and lipoprotein responses were investigated to clarify the role of MMP-8 in periodontitis and systemic inflammatory responses. P. gingivalis infection induced accelerated site-specific alveolar bone loss in both MMP8(-/-) and WT mice relative to uninfected mice. The most extensive bone degradation took place in the P. gingivalis-infected MMP8(-/-) group. Surprisingly, MMP-8 significantly attenuated (P < 0.05) P. gingivalis-induced site-specific alveolar bone loss. Increased alveolar bone loss in P. gingivalis-infected MMP8(-/-) and WT mice was associated with increase in gingival neutrophil elastase production. Serum lipoprotein analysis demonstrated changes in the distribution of high-density lipoprotein (HDL) and very-low-density lipoprotein (VLDL) particles; unlike the WT mice, the MMP8(-/-) mice underwent a shift toward a smaller HDL/VLDL particle sizes. P. gingivalis infection increased the HDL/VLDL particle size in the MMP8(-/-) mice, which is an indicator of lipoprotein responses during systemic inflammation. Serum total lipopolysaccharide activity and the immunoglobulin G-class antibody level in response to P. gingivalis were significantly elevated in both infected mice groups. Thus, MMP-8 appears to act in a protective manner inhibiting the development of bacterium-induced periodontal tissue destruction, possibly through the processing anti-inflammatory cytokines and chemokines. Bacterium-induced periodontitis, especially in MMP8(-/-) mice, is associated with systemic inflammatory and lipoprotein changes that are likely involved in early atherosclerosis.

An optimized fast-performance liquid chromatography method for analyzing lipoprotein profiles using microliter volumes of serum

Plasma or serum lipoprotein analysis is commonly carried out with a conventional size-exclusion fast-performance liquid chromatography method that requires large sample volumes (1–2 ml). To determine lipoprotein profiles of mice with this method, plasma or serum samples have to be pooled from a group of animals, which often requires sacrificing animals. Here we report an optimized anion-exchange chromatography method with simplified cholesterol collection and detection system. After 5–10 μl serum was injected for anion-exchange chromatography, a stepwise gradient was applied and fractions were collected on a 96-well plate. Cholesterol content in each well was measured using a fluorescence-based detection method. With this method, distinct lipoprotein peaks corresponding to high-density lipoprotein, low-density lipoprotein, and very-low-density lipoprotein, can be easily separated and identified with excellent resolution. The entire high-performance liquid chromatography run takes about 30 min and the results are reproducible with a low variability. The small sample size allows analyzing the lipoprotein profile in a given mouse at a given time point with nonterminal bleeding. The method is simple to set up with commercially available parts and convenient to run.

Heterogeneity of high-density lipoprotein in cord blood and its postnatal change

BackgroundSeveral subclasses of HDL are demonstrated to have different roles in atherosclerosis based on adult studies, but the significance of HDL heterogeneity in the fetus and neonate has not been clarified. It has been described that the cholesterol supply from apoE-rich HDL is essential for central nerve system neuron growth. MethodsSixty-five healthy, term, appropriate for gestational age neonates (38 males and 27 females) were included in the study. Serum lipoprotein analyses were performed by HPLC with gel permeation columns, which classified HDL into 5 subgroups (i.e., very large, large, medium, small, and very small) on the basis of particle size. Apolipoprotein A-I, B, and E were also determined by turbidimetric immunoassay. ResultsCord blood has higher very large and very small HDL-cholesterol levels. Cord blood apolipoprotein E was not uniformly distributed in the HDL subclasses, with a strong association with very large HDL-cholesterol levels (males, r=0.548, p<0.001; females, r=0.631, p<0.01). However, the association disappeared by 1 month of age in males; in females, the association remained during the neonatal period. ConclusionsThese results suggest that HDL may play the role of a dominant cholesterol carrier in the human fetus, and very large HDL-cholesterol have some contribution to the neurodevelopment in the fetus and neonates because of the close relationship with apolipoprotein E levels.

Consumption of Ready-to-Eat Cereals in Relation to Health and Diet Indicators among School Adolescents in Crete, Greece

Background/Aims: We aimed at examining the intake of ready-to-eat cereals (RTEC) among adolescents in Crete, Greece, and investigate relationships with health and diet indicators. Methods: A sample of 392 adolescents (183 boys, 209 girls) aged 15 ± 0.4 years, attending high schools of two major counties in Crete, was studied to determine consumption of RTEC using a frequency questionnaire. Anthropometric measurements were performed and blood was drawn for analysis of serum lipoproteins and blood glucose (BG). The physical fitness was assessed with the 20-meter shuttle run test (SRT) and the amount of time watching television was estimated. Nutrient intakes were calculated through 24-hour dietary recalls. Results: 42% (n = 77) of boys and 43% (n = 90) of girls reported consumption of RTEC at least once per week. Approximately 40% of the male and 47% of the female consumers reported eating RTEC only at meals other than breakfast. RTEC consumption was inversely related to the obesity indices and BG levels, and positively related to the SRT (p < 0.05 in all analyses). RTEC consumers had significantly higher intakes of fibre, magnesium, calcium, iron, folate, and vitamins A, B₂ and B₆ (p < 0.05 in all analyses). Conclusion: Our results demonstrated favourable associations between RTEC intake and health and diet indicators in Greek adolescents, with potential implications for improved health status and chronic disease risk reduction.

Common sequence variations in ABCG8 are related to plant sterol metabolism in healthy volunteers

Polymorphisms in the ATP binding cassette (ABC) transporters ABCG5 and ABCG8 are related to plasma plant sterol concentrations. It is not known whether these polymorphisms are also associated with variations in serum plant sterol concentrations during interventions affecting plant sterol metabolism. We therefore decided to study changes in serum plant sterol concentrations with ABCG5/G8 polymorphisms after consumption of plant stanol esters, which decrease plasma plant sterol concentrations. Cholesterol-standardized serum campesterol and sitosterol concentrations were significantly associated with the ABCG8 T400K genotype, as were changes in serum plant sterol concentrations after consumption of plant stanols. The reduction of -57.1 +/- 38.3 10(2) x micromol/mmol cholesterol for sitosterol in TT subjects was significantly greater compared with the -36.0 +/- 18.7 reduction in subjects with the TK genotype (P = 0.021) and the -16.9 +/- 13.0 reduction in subjects with the KK genotype (P = 0.047). Changes in serum campesterol concentrations showed a comparable association. No association with serum LDL cholesterol was found. Genetic variation in ABCG8 not only explains cross-sectional differences in serum plant sterol concentrations but also determines a subject's responsiveness to changes in serum plant sterols during interventions known to affect plant sterol metabolism.

Glucosyl Hesperidin Lowers Serum Triglyceride Level in Hypertriglyceridemic Subjects through the Improvement of Very Low-Density Lipoprotein Metabolic Abnormality

To examine the serum triglyceride (TG)-lowering effect of a soluble hesperidin derivative, glucosyl hesperidin (G-hesperidin), and its mechanisms, we carried out a G-hesperidin administration test in hypertriglyceridemic subjects. G-Hesperidin was administered to the subjects at 500 mg/d for 24 wk. In this study, the subjects were classified into high-TG type (TG > 150 mg/dL), borderline-TG type (TG 110-150 mg/dL) and normal-TG type (TG < 110 mg/dL) on the basis of their initial serum TG values. Among these phenotypes, serum TG level significantly decreased in the high-TG type during the G-hesperidin administration period. It was also observed that elevated values of serum remnant-like particle cholesterol (RLP-C), apolipoprotein (apo) B, apo C-II, apo C-III and apo E occurred in the high-TG type and that these serum levels were significantly reduced by G-hesperidin administration. Moreover, polyacrylamide gel electrophoresis analysis of serum lipoproteins revealed that the very low-density lipoprotein (VLDL)/low-density lipoprotein (LDL) ratio and LDL migration index of the high-TG type were remarkably higher than those of the other phenotypes but that their high values were significantly reduced by the administration. These results indicate that G-hesperidin preferentially lowers serum TG in hypertriglyceridemic subjects and that this effect is possibly caused by the improvement of VLDL metabolic abnormality, leading to the reduction of small dense LDL.

Detailed analysis of serum lipids and lipoproteins from Japanese type III hyperlipoproteinemia with apolipoprotein E2/2 phenotype

Background: To clarify a detailed profile of serum lipids, lipoproteins and apolipoproteins (apo) in type III hyperlipoproteinemia (HLP) with apolipoprotein E (apo E) phenotype 2/2. Methods: Nineteen consecutive Japanese type III HLP (9 men, 10 women) were studied. All had hypertriglyceridemia and 74% showed hypercholesterolemia. Results: The degree of hyperlipidemia [total cholesterol (TC) 8.1±3.2 mmol/l, triglycerides (TG) 5.2±2.9 mmol/l] was milder than that in type III HLP in western countries. Lipoprotein fractions analyzed by ultracentrifugation showed that very low density lipoprotein cholesterol (VLDL-C) concentrations were considerably increased and that intermediate density lipoprotein cholesterol (IDL-C) concentrations were also increased, whereas low-density lipoprotein cholesterol (LDL-C) concentrations were low. Serum apo A-I, A-II and B concentrations were not increased, while apo C-II, C-III and E concentrations were considerably increased. However, the increase of apo E concentrations in the study subjects was far more pronounced than that of apo C-III, causing the ratio of apo E/C-III to be considerably higher than hyperlipidemia with other apo E phenotypes. Conclusion: By using this index apo E/C-III, it is possible to segregate type III HLP with apo E2/2 phenotype from other types of hyperlipidemia.

Effects of Greek Orthodox Christian Church fasting on serum lipids and obesity.

BackgroundNo study to date has focused on the impact of Greek Orthodox Christian fasting on serum lipoproteins and obesity yet.Methods120 Greek adults were followed longitudinally for one year. Sixty fasted regularly in all fasting periods (fasters) and 60 did not fast at all (controls). The three major fasting periods under study were: Christmas (40 days), Lent (48 days) and Assumption (August, 15 days). A total of 6 measurements were made during one year including pre- and end-fasting blood collection, serum lipoprotein analyses and anthropometric measurements.ResultsStatistically significant end-fasting total and LDL cholesterol differences were found in fasters. Fasters compared to controls presented 12.5% lower end-total cholesterol (p < 0.001), 15.9% lower end-LDL cholesterol (p < 0.001) and 1.5% lower end-BMI (p < 0.001). The end- LDL/HDL ratio was lower in fasters (6.5%, p < 0.05) while the change in end- HDL cholesterol in fasters (4.6% decline) was not significant. Similar results were found when the pre- and end-fasting values of fasters were compared. No change was found in control subjects.ConclusionsAdherence to Greek Orthodox fasting periods contributes to a reduction in the blood lipid profile including a non-significant reduction in HDL cholesterol and possible impact on obesity.

Modulation of cholesterol induced hypercholesterolemia through dietary factors in Indian desert gerbils ( Meriones hurrianae)

Modulation of cholesterol-induced hypercholesterolemia through dietary factors in Indian desert gerbils fed a formulated diet based on cereals and pulses incorporated with spices and either coconut oil (CNO) or crude palm oil (CPO) or soybean oil (SBO) with or without cholesterol showed no significant difference either in growth rate or feed consumption. Analysis of serum lipids and lipoproteins showed no significant increase in total cholesterol levels in various experimental groups. The LDL-c + VLDL-c/HDL-c ratio was highest in the cholesterol supplemented CNO group followed by CPO and SBO groups. While significantly high levels of cholesterol were observed in liver in the experimental groups, no increase was observed in heart. Excess excretion of cholesterol in bile was observed. The 16:0/20:4 ratio, an indicator of atherogenic potential while significantly high in all the experimental groups in both serum and liver was almost comparable in heart. Moderate to heavy generalized fatty infiltration was observed in liver tissue in all the experimental dietary groups. In conclusion, the study indicated that SBO was effective in lowering cholesterol levels followed by CPO.

Cardiac Mass and Function, Carotid Artery Intima-Media Thickness, and Lipoprotein Levels in Growth Hormone-Deficient Adolescents

The objective of our study was to evaluate whether cardiac mass and function, carotid artery intima-media thickness, and serum lipid and lipoprotein(a) levels are abnormal in adolescents with GH deficiency. Young adults with childhood-onset and adulthood-onset GH deficiency have been found to have a higher cardiovascular risk, as manifested among other factors by reduced left ventricular mass, impaired systolic function, significant increase in arterial intima-media thickness, and dyslipidemia. Twelve adolescents (seven males and five females) with GH deficiency (10 idiopathic and 2 organic), with an age of 14.2 ± 2.8 yr and a height of 140.6 ± 17.9 cm (height sd score,− 2.6 ± 0.3), were studied. Six children had received GH in the past but were off therapy for several years, whereas six patients had never been treated with GH. Fasting blood samples were obtained for serum lipids and lipoprotein(a) analysis. Patients underwent transthoracic M-mode and two-dimensional echocardiographic evaluation for measurement of interventricular septal thickness, left ventricular posterior wall thickness, and left ventricular mass, as well as left ventricular ejection fraction at rest and pulmonary venous flow velocities; carotid artery intima-media thickness was measured using high-resolution mode B ultrasound. Seven GH-deficient (GHD) adolescents on GH at the time of the study and 19 healthy adolescents, all comparable for age, pubertal status, height, weight, blood pressure, and pulse, participated in this study as controls. Interventricular septal thickness (6.5 ± 1.3 vs. 7.0 ± 1.5 mm), left ventricular posterior wall thickness (7.0 ± 1.8 vs. 7.5 ± 2.0 mm), and left ventricular mass after correction for body surface area (71.2 ± 21.8 vs. 70.7 ± 18.0 g/m2) were similar in untreated GHD patients and healthy controls. Similarly, the left ventricular ejection fraction at rest was similar in untreated GHD subjects and controls (70.0 ± 0.7 vs. 70.0 ± 0.6%), as were the pulmonary venous flow velocities (0.54 ± 0.16 vs. 0.55 ± 0.10 m/s for diastolic peak velocity; 0.51 ± 0.16 vs. 0.50 ± 0.09 m/s for systolic peak velocity; and 0.19 ± 0.06 vs. 0.19 ± 0.05 m/s for atrial reversal filling). Carotid artery intima-media thickness (0.60 ± 0.02 mm and 0.59 ± 0.02 mm for the right and left carotid arteries, respectively) was also normal in our untreated GHD patients when compared with healthy controls. In addition, all echocardiographic measurements were similar in GHD subjects on or off GH at the time of the study. Low-density lipoprotein cholesterol levels were increased in untreated GHD patients when compared with healthy controls (3.17 ± 0.70 vs. 2.33 ± 0.36 mmol/L; P < 0.01), whereas total cholesterol, high-density lipoprotein cholesterol, and triglyceride concentrations were similar to that of controls. Total cholesterol levels were increased in our untreated GHD adolescents when compared with GHD subjects receiving GH therapy at the time of the study, while low-density lipoprotein cholesterol and triglyceride levels were also elevated, although not significantly. Lipoprotein(a) levels were elevated in untreated GHD adolescents when compared with healthy controls, and untreated GHD subjects had higher lipoprotein(a) concentrations than GH-treated patients. GHD adolescents, regardless of whether or not they received GH therapy, do not seem to show alterations in cardiac mass and function or early atherosclerotic changes. They must, however, be followed carefully because they already present cardiovascular risk factors such as dyslipidemia, which may increase their cardiovascular morbidity over time.