Rise In Cholesterol Levels Research Articles

Polyphenol-Rich Aronia melanocarpa Fruit Beneficially Impact Cholesterol, Glucose, and Serum and Gut Metabolites: A Randomized Clinical Trial.

Polyphenol-rich Aronia fruits have great potential as a functional food with anti-inflammatory, hypolipidemic, and hypoglycemic biologic activities. However, clinical intervention trials investigating the impact of Aronia fruit consumption on human health are limited. A randomized, controlled, double-blinded, parallel intervention trial was conducted using 14 human subjects who ingested either 0 mL or 100 mL of Aronia juice daily for 30 days. Anthropometric measurements, fasting, and postprandial measures of glucose and lipid metabolism and inflammation, 16S rRNA fecal microbial composition data, and mass spectrometry-acquired serum and fecal metabolomic data were collected before and after the intervention period. Data were analyzed using general linear models, ANOVA, and t-tests. Daily consumption of Aronia prevented a rise in cholesterol levels (β = -0.50, p = 0.03) and reduced postprandial glucose (β = -3.03, p < 0.01). No difference in microbial community composition by condition was identified at any taxonomic level, but a decrease (β = -18.2, p = 0.04) in microbial richness with Aronia was detected. Serum and fecal metabolomic profiles indicated shifts associated with central carbon and lipid metabolism and decreases in pro-inflammatory metabolites. Our study further informs the development of polyphenol-based dietary strategies to lower metabolic disease risk.

Influence of prenatal stress on metabolic abnormalities induced by postnatal intake of a high-fat diet in BALB/c mice.

Prenatal insults during fetal development result in increased likelihood of developing chronic disease. Obesity, the biggest risk factor for the development of metabolic disease, is affected by several genetic and environmental factors. High-fat diet (HFD) consumption is usually linked with the development of obesity. The main goal of this study was to analyze the impact of the exposure to a HFD in prenatally stressed animals. For this purpose, we subjected pregnant BALB/c mice to restraint stress for 2 h a day between gestational day (GD) 14 and GD 21. Prenatally stressed and control offspring of both sexes were postnatally exposed to a HFD for 24 weeks. We found that prenatal stress (PS) per se produced disturbances in males such as increased total blood cholesterol and triglycerides, with a decrease in mRNA expression of sirtuin-1. When these animals were fed a HFD, we observed a rise in glucose and insulin levels and an increase in visceral adipose tissue gene expression of leptin, resistin, and interleukin-1 beta. Although females proved to be more resilient to PS consequences, when they were fed a HFD, they showed significant metabolic impairment. In addition to the changes observed in males, females also presented an increase in body weight and adiposity and a rise in cholesterol levels.

Can a Mediterranean diet reduce the effects of lipodystrophy syndrome in people living with HIV? A pilot randomised controlled trial

HIV and highly active antiretroviral therapies have been associated with changes in individuals' lipid profiles and fat distribution (lipodystrophy). A pilot study was conducted for a randomised controlled trial to evaluate whether lipodystrophy in HIV patients can be controlled by adopting the low-fat and low-cholesterol diet or the modified Mediterranean diet. Forty-eight HIV patients were randomised into two diet groups. Thirty-six (75%) completed the 1-year pilot study with regular dietetic consultations, during which time lipid levels, weight, body mass index and fat distribution were recorded. Differences between and within groups were determined. Undesirable body fat changes in the low-fat diet group included decreases in tricep skinfold (from 19.9 mm to 15.4 mm (P = 0.03)), hip circumference (from 93.6 cm to 91.7 cm (P = 0.01)) but a significant increase in waist-to-hip ratio (from 0.87 to 0.89 (P = 0.003)). Serum cholesterol increased significantly in the Mediterranean diet group at 9 and 12 months (from 4.6 to 5.06 mmol L(-1) (P = 0.03) and 5.12 mmol L(-1) (P = 0.01)) with no obvious change in the low-fat diet group. Serum triglyceride levels remained the same in the Mediterranean diet group, whereas it increased from 1.9 to 3.22 mmol L(-1) (P = 0.07) in the low-fat diet group. A Mediterranean diet seems to have an advantage over the low-fat diet in maintaining serum triglyceride levels and avoiding lipodystrophy, but this advantage was offset by a rise in cholesterol level. Several procedural and methodological issues were identified which must be rectified before a similar large-scale trial taking place.

Some physiological studies on the effect of onion and garlic juices on the fish, Clarias lazera

Fish, Clarias Lazera were orally administered onion (Allium cepa) or garlic (Allium sativum) juices. Contents of glucose, free amino acids, total lipids, triglycerides, cholesterol, albumin, total protein, urea, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum as well as glycogen, free amino acids, total lipids, triglycerides and cholesterol contents in liver, white and red muscle were determined 5 h and 24 h after a single dose or after repeated doses (1 dose every 24 h for 5 days). Both onion and garlic treatments caused a temporary hypoglycemia as well as liver glycogen muscle depletion accompanied with a significant elevation in white muscle glycogen suggesting that dietary onion or garlic may enhance the process of glycogenesis in white muscle. Onion feeding caused hypolipidemia accompanied with significant decreases in liver content of total lipids in response to the repeated doses for 5 days and a severe rise in the lipid content of red muscle at all periods. Such results suggest that dietary onion may enhance the process of lipogenesis in red muscle of Clarias lazera. Probably, the main precursor of such lipogenesis in the red muscle was the serum fatty acids. Moreover, dietary onion led to hypocholesterolemia accompanied with a significant rise in cholesterol level of both liver and red muscle. On the other hand, dietary garlic significantly decreased serum free amino acids after 5 h and 5 days. Furthermore, significant elevations of liver free amino acids were dedected in the onion-treated fish group (24 h and 5 days) and in the garlic-treated fish group (5 h), probably due to oxidation of thiol components (sulfur attached to the proteins). This result was accompanied with either a marked increase in white muscle free amino acids at all periods of garlic fish group, or a noticeable drop in the onion group (repeated doses). Also, dietary onion and garlic treatment led to an elevation in hepatic ureagenesis in spite of the unchanged serum urea level. Significant decreases of both serum AST and ALT in garlic groups (all periods) and in onion groups (repeated doses) were observed. In liver, AST and ALT showed temporary rises after onion or garlic supplementation. In general, it could be concluded that both dietary onion and garlic have a transitory hypoglycemic action as well as a promoting effect on the process of glycogenesis in white muscle whereas dietary onion promotes lipogenesis in red muscle of fish. Also, dietary garlic may enhance the white muscle uptake of free amino acids which, in turn, may promote protein synthesis.

Apolipoprotein A-1 of Japanese quail: cDNA sequence and modulation of tissue expression by cholesterol feeding.

Apolipoprotein (apo) A-1 cDNA was amplified by the reverse-transcriptase-polymerase chain reaction (RT-PCR). Primers were synthesized according to the nucleotide sequence of chicken apo A-1, and the identity of apo A-1 cDNA was confirmed by comparing with the N-terminal amino acid sequence. The open reading frame of apo A-1 cDNA consists of 795 nucleotides, and it is capable of coding a polypeptide of 264 amino acids. A comparison between quail and chicken apo A-1 revealed 94.5% homology in the nucleotide sequence and 91.7% homology in the amino acid sequence. There was a similar 11- or 22-amino acid repeat in quail apo A-1 as was the case for chicken apo A-1. Apo A-1 mRNA was evaluated to be 1.4 k in length and was expressed in various tissues of Japanese quail: the liver, small intestine, lung, kidney, heart, and muscle. A quantitative evaluation, however, revealed that the liver and small intestine were the major organs for apo A-1 synthesis, accounting for more than 90% of the total expression of apo A-1 mRNA. Besides apo A-1 mRNA (1.4 k in length), a transcript of 4.1 k was detected in all the tissues examined, with a magnitude ranging from 5 to 10% of the apo A-1 mRNA level. The effect of cholesterol level on the expression of apo A-1 mRNA was studied to address the physiological significance of apo A-1 in the liver, small intestine, and muscle. The level of cholesterol in the liver and breast muscle was increased by feeding with cholesterol and reached a saturation level at day 7. There was also a temporal rise of cholesterol level at day 7 in the small intestine. Dietary cholesterol increased the expression of apo A-1 mRNA two fold in both the liver and small intestine. This was not the case for breast muscle, in which the expression of apo A-1 mRNA was not modulated by the cholesterol level.

Effects of administration of different intravenous lipid emulsions on plasma LP-X concentrations in the rat.

Prolonged parenteral nutrition with lipid emulsions is essential to provide sufficient energy supply and to avoid essential fatty acid deficiency in preterm infants. However, chronic administration of lipid emulsions may lead to the development of pathological plasma lipid and LP-X concentrations. The aim of this study was to evaluate the relative importance of the phospholipid-triglyceride (PL-TG) ratio and the source of phospholipid in lipid emulsions, with respect to plasma lipid and LP-X levels. Rats were infused for 9 days with IV lipid emulsion containing 10% (IL-10) or 20% (IL-20) egg lecithin or Lipofundin containing 20% soya lecithin (LF), with PL-TG ratios of .12, .06, and 0.75, respectively. LF significantly increased plasma triglyceride concentration (p < .01), whereas the rise in cholesterol levels observed with all emulsions was primarily caused by the increase in low-density lipoprotein cholesterol concentrations. The plasma phospholipid concentration was increased most by IL-10 (p < .005). There was a strong correlation between the PL-TG ratio of emulsions and the developing plasma phospholipid and LP-X concentrations (r2 = .91 and .96, respectively), despite the different origin of phospholipids in the emulsions, suggesting that it is the PL-TG ratio, rather than the source of phospholipids in lipid emulsions that primarily influences developing plasma lipid and LP-X concentrations. These results indicate that the administration of lipid emulsions with lower PL-TG ratios should be considered, to avoid the development of pathological plasma lipoprotein concentrations.

Plasma cholesterol responsiveness to saturated fatty acids

The variability in responsiveness to saturated fatty acids has not been studied systematically. For this reason data from three dietary studies carried out in our laboratory were pooled and used to evaluate how individuals vary in their responses in plasma concentrations of total cholesterol and low-density-lipoprotein cholesterol to the substitution of saturated fatty acids for unsaturated fatty acids. The data showed a marked variability in response. Some patients demonstrated a striking rise in cholesterol levels whereas others had more modest increases. This finding points to the need for further investigation on this issue.

Cardiovascular Drugs and Atherosclerosis

Primary cell culture derived from atherosclerotic plaque of human aorta was used to assess direct effects of calcium antagonists, beta-blockers, and nitrates on vessel wall cells. Within 24 h, calcium antagonists (verapamil, nifedipine, darodipine, isradipine, diltiazem, etc.) reduced the cholesterol level in cultured cells. Furthermore, these agents decreased the incorporation of [3H]thymidine. Thus, the calcium antagonists manifested direct antiatherosclerotic action in culture by normalizing major manifestations of atherosclerosis at the cellular level. On the other hand, beta-blockers (propranolol, alprenolol, metoprolol, atenolol, pindolol, and timolol) caused a 1.5- to twofold rise in cholesterol level of cultured cells and stimulated their proliferation. Nitrates (nitroglycerin, isosorbide dinitrate, and nitroprusside) had no effect on atherosclerotic characteristics. Within 2-4 h after a single dose of oral administration of beta-blocker (propranolol), patients' blood plasma turned atherogenic, i.e., its addition to culture-induced cholesterol accumulation and stimulated proliferation. At the same time, blood plasma of patients who received calcium antagonists (verapamil and nifedipine) acquired antiatherosclerotic properties manifested in its ability to lower the intracellular cholesterol level and inhibit proliferative activity of cultured cells. These findings allow the assumption that not only in vitro, but in vivo as well, calcium antagonists and beta-blockers are antiatherosclerotic and atherogenic drugs, respectively.

Specific Inhibition of Cholesterol Absorption in Sulfaguanidine-fed Rats

The influence of sulfaguanidine on the absorption of cholesterol was studied in the rat. In rats fed a diet without added cholesterol, feeding of 1% sulfaguanidine for 2 weeks did not significantly affect the cholesterol con centrations in the serum and the liver. Conversely, sulfaguanidine inhibited the rise of cholesterol levels in serum and liver of rats fed a 1% cholesterol diet. In rats with a thoracic duct fistula, feeding of 1% sulfaguanidine had no influence on lymphatic output of endogenous cholesterol but markedly inhibited the uptake of exogenous cholesterol. These experiments demonstrated that sulfaguanidine primarily inhibited the absorption of cholesterol from the intestine. The inhib itory effect on cholesterol absorption did not seem to be mediated via an effect on bile salts since sulfaguanidine did not promote fecal bile salt excretion, did not disturb micelle formation and did not displace cholesterol from preformed mixed micelles. Esterification of cholesterol by pancreatic esterase in vitro was not inhibited by concentrations of up to 10 mg of sulfaguanidine per milliliter. The effect of sulfaguanidine on cholesterol was highly specific, and minor modi fications of the molecule resulted in almost complete loss of the inhibitory effect on cholesterol absorption. J. Nutr. 101: 1515-1524, 1971.

Anticholesterolic Effects of Unsaponifiable Fractions of Vegetable Oils in Chicks: 1. Short-Term Effects of Soy Sterols

PLANT sterols constitute a naturally occurring group of compounds with a remarkable activity in counteracting the rise in cholesterol levels in blood and/or livers which follows the ingestion of cholesterol-rich diets by experimental animals. This is usually referred to as “hypocholesterolemic” effect, though the term “antihypercholesterolemic,” used by Boorman and Fisher (1966), constitutes a more suitable description. Strictly speaking, however, these terms refer to blood changes only and cannot be applied to tissue cholesterol without violating accepted nomenclature. We shall use the expression “anticholesterolic” in connection with the above-defined effects of phytosterols, so as to avoid any restriction in meaning to blood cholesterol only.Since Peterson’s (1951) first description of anticholesterolic action of soy sterols in chicks, numerous reports involving chicks (Peterson et al., 1952Peterson et al., 1953; Diller et al., 1960; Reiner et al., 1962; Fisher et al., 1963; Pick et al., 1965; Konlande and Fisher, 1969; Bartov et al., 1969)…

ASSOCIATION BETWEEN CIRCULATING HÆMOGLOBIN LEVEL, SERUM-CHOLESTEROL, AND BLOOD-PRESSURE

A large community-based study of the association in women between circulating hæmoglobin and serum-cholesterol, and the effect of correction of anæmia, is reported. In a population sample of 4070 women a statistically significant association (p<0·001) was detected between serum-cholesterol and hæmoglobin level, and this represents a mean difference between women with hæmoglobin levels above and below 10·5 g. per 100 ml. blood of about 30 mg. cholesterol per 100 ml. blood. A difference of this size is probably similar to what can be achieved with dietary control in free-living population samples, and is likely to explain the supposed lower mortality from cardiovascular disease in anæmic subjects. Correction of the anæmia appeared to lead to a rise in cholesterol level; but this rise was not statistically significant, and did not remove the difference which had existed between the anæmic and the normal women. There was no evidence of an association between hæmoglobin level and blood-pressure, and treatment of anæmia had no effect on blood-pressure.

17&amp;beta;-Hydroxy-17&amp;alpha;-methyl-5&amp;alpha;-androstano[2,3-c]furazan (Furazabol)のウサギ実験的動脈硬化症に対する治療効果

Furazabol, a new anabolic steroid, inhibited a rise in cholesterol levels in the serum and liver induced by cholesterol feeding, although its effects on phospholipids, triglycerides, and free fatty acids were not marked. Fatty acid compositions of serum esterified cholesterol and triglycerides were not so much affected by the furazabol treatment. Furazabol has been expected to possess the therapeutic effect on atherosclerosis, that is, the progression of atheromatous changes was significantly inhibited by the treatment with this compound. In addition, furazabol clearly lightened fatty degeneration of the liver.

The Effect of Riboflavin on Hypertension induced by High Salt Diet in the Rat

The effect of riboflavin on development of hypertension in rats given a high salt diet was studied. Large doses of riboflavin prevented both elevation of blood pressure and rise of cholesterol levels in the serum. The increase in liver monoamine oxidase activity of the rats fed riboflavin was confirmed.

The Effect of Riboflavin on Hypertension induced by High Salt Diet in the Rat

The effect of riboflavin on development of hypertension in rats given a high salt diet was studied. Large doses of riboflavin prevented both elevation of blood pressure and rise of cholesterol levels in the serum. The increase in liver monoamine oxidase activity of the rats fed riboflavin was confirmed.

Further studies on cholesterol levels in the Johns Hopkins medical students: The effect of stress at examinations

1. 1. Serum cholesterol determinations on 52 male medical students were carried out at admission to medical school (Test I), at final anatomy examination (Test II), and during a period of regular academic work (Test III). 2. 2. The mean cholesterol levels at Tests I and II were significantly higher than at Test III. 3. 3. The cholesterol levels of two additional subjects showed a similar pattern when the values at final biochemistry examination (Text IV) were compared with Test III. 4. 4. For certain students, Test III fell close to the final biochemistry examination; the fall from Test II to Test III was less marked in these subjects. 5. 5. The total eosinophil count was significantly lower at Test II than Test III. 6. 6. There was no significant difference in body weight between Tests I, II, and III. 7. 7. The findings are consistent with the hypothesis that stress such as accompanies the first few weeks of medical school or important final examinations is accompanied by a significant mean rise in cholesterol level.

Effect of antioxidants on muscle and plasma lipids of vitamin E-deficient guinea pigs.

SummaryIn guinea pigs with muscular dystrophy induced by feeding of Vit. E-deficient ration, there is a rise in cholesterol levels of plasma and skeletal muscle; these rises precede onset of dystrophy. Supplementation of Vit. E-deficient ration with antioxidants DPPD. BHT. DBH and Santoquin, although delaying onset of dystrophy symptoms, does not prevent the rise in plasma and muscle cholesterol and muscle total lipid in Vit. E-deficiency.

Cholesterol and phospholipid concentration in hepatic lymph and bile during phosphatide induced hypercholesteremia.

SummaryRate of disappearance of intravenously injected phosphatide from plasma was markedly retarded in the liverless rat. When hypercholesteremia was provoked in normal rats by constant infusion of phosphatide, the elevated blood cholesterol concentration was not reflected in any rise of cholesterol level in hepatic or intestinal lymph, or in bile. The elevated phospholipid level was not reflected in bile or intestinal lymph, but did cause a moderate rise in the phospholipid level of hepatic lymph.