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Cholesterol normal

Part of the cholesterol newly synthesized in the liver is excreted into bile in a free non-esterified state (in constant, amount). Cholesteiol in bile is normally complexed with bile salts to form soluble cholic acids, Free cholesterol is not readily soluble and with bile stasis or decreased bile salt concentration may precipitate as gallstones. Most common gallstones are built of alternating layers of cholesterol and calcium bilirubin and consist mainly (80-90%) of cholesterol. Normally. 80% of hepatic cholesterol arising from blood or lymph is metabolized to cholic acids and is eventually excreted into the bile in the form of bile salts. [Pg.198]

Figure 2. Volatile irradiation products of cholesterol --------- Normal alkanes... Figure 2. Volatile irradiation products of cholesterol --------- Normal alkanes...
There have been numerous attempts to discover diagnostic procedures that would accurately predict cardiovascular disease risks in the general population. "Phenotyping" (i.e., electrophoresis) of lipoproteins has been used, as have determinations of total cholesterol, HDL cholesterol, triglyceride, and LDL cholesterol. "Normal" although not optimal values for these parameters are 140-310, 30-70, 60-300, and 90-200 mg/dl, respectively. These values are both age and sex related. LDL cholesterol cannot be determined directly but can be calculated from Equation (19.3) ... [Pg.506]

Subsequently, serum lipid and lipoprotein profiles were obtained 70 mg/dL total cholesterol (normal is 130-200 mg/dL), 1 mg/dL HDL cholesterol (optimal is > 60 mg/dL), 180 mg/dL triglycerides (normal is 100-150 mg/dL), and less than 5 mg/dL apolipoprotein A-I (apoA-I normal is 140 mg/dL). Cholesterol efflux from patient skin fibroblasts to apoA-I, the main protein component of HDL, was reduced to 30% of normal. These results indicated Tangier disease, the definitive diagnosis of which was made when the sequencing of the ATP-binding cassette transporter A1 (ABCA /) gene revealed a nonsense mutation within exon 12. [Pg.160]

Increase in cholesterol deposition (see above) Retention of cholesterol normally excreted in the bile Xanthomas... [Pg.45]

In oitr own studies, we modified membrane microviscosity by incubating nomoal platelets overnight as 22 with cholesterol-rich, cholesterol-normal and cholesterol or liposomes. Under these conditions, and considering only high affinity sites since moderate and low affinity sites were combined in this analysis, the number of receptors was proportional to membrane microviscosity while the affinity at those receptors was inversely proportional to membrane microviscosity (Table 2). [Pg.24]

The hypolipidemic effects of niacin may be due to its ability to inhibit lipolysis (i.e.. prevent the release of FFAs and glycerol from fatty tissues). As a consequence, there is a reduced reserve of FFA in the liver and diminution nf lipoprotein binsynthesis. which reduces the production nf VLDL. The decreased formation nf lipoproteins leads to a pool nf unused cholesterol normally incorporated in VLDL. This excess cholesterol is then excreted through the biliary tract. [Pg.661]

The interruption of enterohepatic recirculation of bile acids by the resins effectively lowers plasma cholesterol levels since cholesterol must now be diverted to de novo synthesis of bile acids. In addition, intestinal absorption of dietary cholesterol, normally facilitated by bile acids, is also reduced due to their excretion. Two significant compensatory mechanisms are called into action increased activity of hydroxymethylglutaryl coenzyme A reductase (HMG CoA reductase), which is the rate-controlling enzyme in the hepatic synthesis of cholesterol (see Fig. 11-4 and discussion to follow), and an increase in the number of LDL receptors. The latter mechanism offered the first meaningful treatment of heterozygous FH. Homozygous FH patients lacking LDL receptors, of course, do not respond. [Pg.524]

Study Design and Population Thirty-two patients were selected from the Hennepin County Medical Center s Hyperlipidemia Clinic on the basis of their willingness to cooperate and make frequent clinic visits. One patient, a four-year-old child, withdrew from the study before the food products were fed because of fear of blood drawing. The FHC patients were defined by published criteria which include elevation of total cholesterol and LDL cholesterol, normal levels of VLDL cholesterol and triglycerides, one parent and one child, and at least one first-degree relative, with FHC. The families also often had individuals by family history with premature cardiovascular disease. Twenty-one adults (aged 22-53) and 10 children (aged 10-18) completed... [Pg.72]

As discussed in section 4.3.2.1, the bile salts required for the absorption of dietary fat are synthesized in the liver from cholesterol. Normally about 90—95% of the 30 g of bile salts secreted daily is reabsorbed and reutilized. Non-starch polysaccharides adsorb bile salts, so that they are excreted in the faeces. This means that there has to be increased synthesis de novo from cholesterol to replace the lost bile salts, so reducing the total body content of cholesterol. [Pg.209]

These conflicting observations indicate that fat related influence on fecal bile acid levels may be dependent upon the availability and composition of the dietary fat. Furthermore, varying the Intake of cholesterol, normally comprising only a small proportion of the total fat intake, may exert a disproportionate effect on bile acid loss. [Pg.120]

The first application of the Gaussian distribution is in medical decision making or diagnosis. We wish to determine whether a patient is at risk because of the high cholesterol content of his blood. We need several pieces of input information an expected or normal blood cholesterol, the standard deviation associated with the normal blood cholesterol count, and the blood cholesterol count of the patient. When we apply our analysis, we shall anive at a diagnosis, either yes or no, the patient is at risk or is not at risk. [Pg.17]

The Problem. Suppose that the total serum cholesterol level in normal adults has been established as 200mg/100mL (mg%) with a standard deviation of 25 mg%, that is, p = 200 and ct = 25. (Please distinguish between mg% and % probability.) A patient s serum is analyzed for cholesterol and found to contain 265 mg% total cholesterol. [Pg.17]

A 0-9% salt solution is considered to be isotonic with blood. Other electrolytes present include bicarbonate ions (HCOj ) and small amounts of potassium, calcium, magnesium, phosphate, sulphate and organic acid ions. Included among the complex compounds and present in smaller amounts are phospholipids, cholesterols, natural fats, proteins, glucose and amino acids. Under normal conditions the extracellular body fluid is slightly alkaline with a pH of 7-4. ... [Pg.472]

The organism would probably grow quite well. The structure shown is simply analogous to the acetyl ester of cholesterol except that the side chain has been removed. The organism would, presumeably, degrade the sterol nucleus by its normal route. [Pg.373]

Lipid regulators are ordinarily applied drugs in clinical practice, and they are used to lower the level of cholesterol and regulate the metabolism of lipids. Clara et al. [13] detected a lipid regulator bezafibrate at concentrations up to 7.6 pg L although normally they are found at lower nanograms per liter range [8,18,21,22]. [Pg.202]

Figure 38, Patterns obtained from the extract of 10 fd of serum for lipid fraction by thin-layer chromatography. In sequence, starting from the bottom, phospholipids, pee cholesterol, cholesterol aniline as an internal standard, triglycerides, and cholesterol esters. The free fatty acids occur between cholesterol and the internal standard and are only barely visible in the print, on the extreme right. They are readily visible, normally, to the eye. Figure 38, Patterns obtained from the extract of 10 fd of serum for lipid fraction by thin-layer chromatography. In sequence, starting from the bottom, phospholipids, pee cholesterol, cholesterol aniline as an internal standard, triglycerides, and cholesterol esters. The free fatty acids occur between cholesterol and the internal standard and are only barely visible in the print, on the extreme right. They are readily visible, normally, to the eye.
Figure 39, A lipid pattern from normal serum which has been scanned for density of the thin-layer chromatograph, showing the various peaks, P, phospholipids C, cholesterol F, free fatty acids S, internal standard, T, triglycerides CE, cholesterol esters. Figure 39, A lipid pattern from normal serum which has been scanned for density of the thin-layer chromatograph, showing the various peaks, P, phospholipids C, cholesterol F, free fatty acids S, internal standard, T, triglycerides CE, cholesterol esters.
Phosphorylation of cholesterol followed by the normal hydrolytic work-up gives the phosphate monoester, not the symmetrical pyrophosphate diester as previously claimed. Cholesteryl phosphorodichloridate and some related steroidal phosphorodichloridates have been prepared from the action of pyrophosphoryl chloride on the appropriate alcohol ... [Pg.97]

Rice bran is the richest natural source of B-complex vitamins. Considerable amounts of thiamin (Bl), riboflavin (B2), niacin (B3), pantothenic acid (B5) and pyridoxin (B6) are available in rice bran (Table 17.1). Thiamin (Bl) is central to carbohydrate metabolism and kreb s cycle function. Niacin (B3) also plays a key role in carbohydrate metabolism for the synthesis of GTF (Glucose Tolerance Factor). As a pre-cursor to NAD (nicotinamide adenine dinucleotide-oxidized form), it is an important metabolite concerned with intracellular energy production. It prevents the depletion of NAD in the pancreatic beta cells. It also promotes healthy cholesterol levels not only by decreasing LDL-C but also by improving HDL-C. It is the safest nutritional approach to normalizing cholesterol levels. Pyridoxine (B6) helps to regulate blood glucose levels, prevents peripheral neuropathy in diabetics and improves the immune function. [Pg.357]

The plasma concentration of LP(a) has been measured in patients with RA and significantly increased levels have been reported (Rantapaa-Dahlqvist et al., 1991). Whilst the plasma concentration of cholesterol is lower in patients with RA than in normal controls the concentration of LP(a) is increased, whether or not the concentration is corrected for total lipids. Rantapaa-Dahlqvist et al. (1991) surest that LP(a) may be an important cause of coronary heart disease in patients with RA. [Pg.105]

Blake, 1989 Winyard et al., 1989). We suggest that within the inflamed rheumatoid joint (or the artery wall in atherogenesis), the production of ROM and proteases by endothelial cells and/or macrophages may cause the release of copper ions from Cp (see Section 2.2.3.2). It has been reported that Cp is cleaved faster in serum from patients with inflammatory diseases when compared to normal serum (Laurell, 1985). The oxidative modification of LDL by Cp-derived copper ions may explain the observation that increased serum cholesterol values are associated with accelerated atherosclerotic progression in men with high serum copper concentrations (Salonen et al., 1991). [Pg.107]


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