Plasma lipids changes

Prevention of the expected loss of lumbar spine bone density and plasma lipid changes consistent with a reduction in the risk for atherosclerosis have also been reported in tamoxifen-treated patients following spontaneous or surgical menopause. However, this agonist activity also affects the uterus and may increase the risk of endometrial cancer. 

Xenobiotic-induced pancreatitis may be accompanied by gross plasma lipid changes that may result from marked changes of carbohydrate metabolism (see Chapter 9). The observation of the presence of gross macroscopic fecal fat content (steatorrhea) can indicate effects on pancreatic function, biliary dysfunction, or intestinal malabsorption. In longer-term studies, malabsorption of fat-soluble vitamins may be reflected by the clinical condition of vitamin-deficient animals. 

Hypomagnesaemia, hypoalbuminaemia and plasma lipid changes in rats following the oral administration of ciclosporin. Comparative Biochemistry and Physiology 89C 375-376. 

There is a 2.5-fold increased incidence of gallbladder disease in postmenopausal women receiving estrogens. This occurrence may be related to changes in plasma lipid metabolism. 

Anon. Clinical trials on AIDS start. Reprowatch 1999 1—28 6—11. Garcia-Fuentes, E., A. Gil-Villarino, M. F. Zafra, and E. Garcia-Peregrin. Changes in plasma lipid composition induced by coconut oil. Effects of dipyridamole. J Physiol Biochem 2002 58(1) 33-41. 

It is interesting that the use of -adrenoceptor antagonists such as prazosin has been found to be associated with either no changes in plasma lipids or increased concentrations of high-density lipoproteins (HDL), which could be a favorable alteration. The mechanism for this effect is not known. 

Prazosin and other quinazolines are associated with small but significant changes in plasma lipid profiles. Generally these are potentially beneficial changes, with reductions in LDL cholesterol, total cholesterol, and triglycerides, and increases in HDL cholesterol. 

Data on the proportions of different fatty acids in plasma lipid esters (cholesteryl esters, phospholipids, free fatty acids, or triacylglycerol), erythrocyte membranes, or adipose tissue may provide a more objective and accurate path to evaluating dietary fatty acid composition (Arab, 2003 Baylin and Campos, 2006). The fatty acid composition in blood and body tissues reflects the fatty acid composition of the diet at different time points after ingestion. Short and medium-term changes in the composition of dietary fatty acid intake are reflected in plasma lipids and erythrocyte membranes, weeks and months after intake, respectively. The incorporation of fatty acids in adipose tissue reflects long-term changes in the diet (years) (Baylin and Campos, 2006 Katan et al., 1997 Ma et al., 1995 Zock et al, 1997). 

The exact mechanism of these drugs is unclear, but they probably work by binding to a specific nuclear receptor known as the peroxisome proliferator activated receptor.52,141 This receptor, found primarily in the liver and adipose tissues, affects the transcription of genes that affect lipid metabolism.89 Fibrates activate this receptor, thereby mediating several changes at the nuclear level that ultimately cause a decrease in triglycerides and other beneficial changes in plasma lipid metabolism.30,52 In a manner similar to the statins, fibrates may also exert anti-inflammatory, antioxidant, and other beneficial effects in addition to their positive effects on plasma lipids.42,49... 

In addition to the studies of clinical biological changes in lipid profile levels in patients with major depression, the mechanism of lipid metabolism should be noted and discussed [133], In past studies, the main plasma lipid transport forms have been free fatty acids, triglycerides, and cholesteryl esters. 

Although hyperlipidemia may be partly reversed by the increase of plasma oncotic pressure with dextran infusion, decreased albumin and plasma oncotic pressure cannot fully explain nephrotic hyperlipidemia. In analbuminemic rats, lipid changes are different from those in nephrotic subjects (D4). There may be a direct causal link between proteinuria and lipid abnormalities because a 1 -acid glycoprotein isolated from urine of nephrotic patients may correct the impaired lipolysis of nephrotic rats (SI 6, K12). Thus, impaired lipoprotein metabolism may be caused by the loss of some regulatory substance into urine due to increased glomerular permeability. 

HDL-cholesterol levels are increased by 4—8% (Maron et al., 2000). These changes in plasma lipids are claimed to reduce the risk of major coronary events by around 30%. However, this value is misleading because it refers to the relative risk of CHD the absolute risk reduction is only about 2%. 

Table II. Overall Changes in Plasma Lipids and Lipoproteins Following an Exercise Program...

Plasma Lipid/ Lipoprotein Factor Change in Llpid/Llpoprotein... 

Mechanisms of Exercise-Induced Changes in Plasma Lipids Lipoprotein Lipase, Hepatic Triglyceride Lipase and Lecithin Cholesterol Acyl Transferase... 

In response to exercise there are significant increases in postheparin and adipose tissue LPL activity concomitant with changes in plasma lipids. These synchronous changes in LPL activity and plasma lipids and lipoproteins are suggestive of a possible relationship between both. 

At present, the mechanism (5) of the exercise-induced changes in plasma lipids and lipoproteins is/are undefined. While significant attention in this section has been directed toward understanding the roles of various enzymes in lipoprotein production, catabolism and metabolism with exercise, no definite information is available to support the hypotheses raised. An alternative, yet highly viable possibility includes simply the availability of substrate which may well exist in considerable excess or substrate activity of relevant lipoprotein particles... 

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