Secondary prevention of ischemic heart disease: closing the gap.
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Biomedical subjects
Publications and source records attributed to Menahem Fainaru.
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The role of leptin in anorexia associated with liver cirrhosis remains controversial. The aim of this study was to quantify the serum leptin level in patients with hepatocellular or cholestatic liver disease and to assess its relationship with serum insulin, body mass index, and serum lipoproteins. The study population included 30 women, 15 with chronic hepatocellular liver disease and 15 with primary biliary cirrhosis; severity of disease was determined by Child-Pugh and histological criteria, respectively. Ten healthy, age-matched women served as controls. Levels of serum leptin and insulin were determined by radioimmunoassay. Mean serum leptin level was significantly lower in the primary biliary cirrhosis group compared to both the control (P < or = 0.05) and the hepatocellular groups (P < or = 0.05). Serum leptin level strongly correlated with body mass index in the hepatocellular group (P < 0.0001) and the controls (P < 0.001), but not in the primary biliary cirrhosis group; it showed no correlation with severity of liver disease. A positive correlation was found between serum leptin and serum cholesterol (P = 0.02), low density lipoprotein (P = 0.01), and triglycerides (P = 0.04) in the hepatocellular group and in the controls between serum leptin and serum high density lipoproteins (P = 0.01). Serum leptin is low in patients with primary biliary cirrhosis. The combined findings of normal insulin response less insulin resistance, and lower serum leptin level in primary biliary cirrhosis compared to hepatocellular liver disease may indicate that serum leptin is merely a passive marker and not a cause of anorexia in liver disease.
Kinetic studies of copper-induced LDL peroxidation commonly assume that the availability of molecular oxygen in the reaction media is not a limiting factor. The present study reveals that this assumption is valid only at low LDL concentrations. At high LDL concentrations, accumulation of oxidation products, as monitored spectroscopically under conditions of various oxygen concentrations in the medium, comes to a halt when the oxygen concentration in the solution, as measured by an oxygen electrode, decreases to near zero levels. Bubbling of the oxygen into the solution results in resumption of peroxidation. These results are important with respect to the ex vivo assaying of lipoprotein peroxidation because many previous studies have been conducted with LDL concentrations that corresponded to polyunsaturated fatty acid concentrations in access of the concentration of molecular oxygen. The possible pathophysiological significance of the results of this study has yet to be evaluated.