Hypertriglyceridemia diseases caused

High-dose glucocorticoid therapy can cause marked hypertriglyceridemia, with milky plasma (SEDA-15, 421 SEDA-16, 450). It has been suggested that this is caused by abnormal accumulation of dietary fat, reduced postheparin lipolytic activity, and glucose intolerance (126). An association between glucocorticoid exposure and hypercholesterolemia has been found in several studies (127) and can contribute to an increased risk of atherosclerotic vascular disease. 

Overall, results from all these studies suggest that the long-term reduction in fat consumption improved both in vivo and ex vivo measures of immune functions. Increased response in these immune functions will generally indicate increased protection that may be of clinical significance. Only one study has compared the effects of lipid infusion on ex vivo measures of immune functions and the in vivo markers for diseases (van der Poll et al., 1995). In this study, intralipid infusion caused up to a 70% reduction in the in vitro secretion of IL-lp, IL-6, and TNF-ot however, it did not influence inflammatory responses to endotoxin (fever, leukocytosis, release of TNF and its receptor) and even potentiated plasma endotoxin responses (release of IL-6 and IL-8 and neutrophil degranulation). The authors concluded that hypertriglyceridemia does not inhibit the in vivo responses to endotoxin. 

Heart disease is the leading cause of mortality in uremic patients, accounting for half of all deaths. Hypertension and diabetes mellitus, both common causes of chronic renal failure, clearly play an important role in the prevalence of cardiovascular disease. Furthermore, coronary atherosclerosis is common in Caucasian uremic patients, many of whom have hypertriglyceridemia and low serum levels of high-density lipoprotein (HDL) cholesterol. 

The hypertriglyceridemia of renal failure resembles the endogenous familial variety, and may likewise coexist with insulin resistance, glucose intolerance, and hyperuricemia. In dialysis patients it is associated with a high rate of coronary artery disease in women and white men under 60 years (C26). The low HDL cholesterol levels, found mainly in white men on hemodialysis, are attributed to decreased activity of the enzyme lecithin cholesterol acyltransferase (L-CAT). Decreased enzyme activator apo-apo A1 and inhibitory uremic toxins have been proposed as causes for the decreased enzyme activity. Low HDL cholesterol levels are associated with an increased risk of atherosclerotic heart disease (C26). 

Diseases that enhance LDL oxidation include diabetes and hypertriglyceridemia (115). Hyperglycemia increases LDL oxidation, in part, through an increase in glycation products, which subsequently enhances free radical production in stimulated inflammatory cells (115). Insulin and IGF-I cause an upregulation of LDL receptor and down regulation of HDL receptor (281). Insulin increases uptake and esterification of... 

In addition to obesity and hypertriglyceridemia, hypercholesterolemia is another health concern linked to various lifestyle-related diseases. Clinical investigations have revealed that the administration of phytosterols to human subjects reduces plasma total cholesterol and LDL cholesterol levels (see also Chapter 7). Meguro et al. (2(X)1) recently investigated the relative effects on semm cholesterol and TAG levels in humans caused by phytosterols dissolved in DAG compared with phytosterols dissolved in TAG. 

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