Relationship of obesity and body fat distribution with ceruloplasmin serum levels.

OBJECTIVE: To investigate the influence of obesity and body fat distribution on serum levels of ceruloplasmin, a risk factor for myocardial infarction. DESIGN: Fasting concentrations of ceruloplasmin, insulin, glucose, lipid pattern (cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), blood pressure levels, and body fat distribution were determined in a population of non-diabetic subjects. SETTING: University Hospital Outpatient Clinic. SUBJECTS: 87 consecutive individuals (35 men and 52 women), represented by 27 normal weight (BMI: < 25.0), 20 overweight (BMI: > 25.0-30.0) and 40 obese (BMI: > 30.0) subjects. MEASUREMENTS: Serum insulin levels were quantified by radioimmunoassay, plasma glucose and lipid concentrations by enzymatic assays, and serum ceruloplasmin by nephelometry. Intra-abdominal thickness was measured by ultrasound technique. RESULTS: Ceruloplasmin levels were significantly (P < 0.001) higher in obese (36.5 +/- 8.60 mg/dl) than in overweight (30.4 +/- 6.17 mg/dl) and normal weight (29.3 +/- 8.06 mg/dl) subjects. Of several variables associated with ceruloplasmin (BMI, waist circumference, WHR, intra-abdominal thickness, triglycerides, cholesterol, LDL-cholesterol, insulin), only triglycerides (in both men and women) and ultrasound intra-abdominal thickness (in women) maintained a significantly independent relationship with this protein in multiple stepwise analysis. Moreover, both triglycerides and total cholesterol maintained an independent correlation with ceruloplasmin when the data from both men and women were pooled together. CONCLUSION: This study indicates that patients with central obesity have characteristically higher ceruloplasmin serum levels, and that ceruloplasmin concentrations are strongly correlated with serum triglyceride and cholesterol levels (in both sexes) and visceral fat accumulation (in women), independently of the other associated cardiovascular risk factors (insulin and blood pressure levels). Since ceruloplasmin has been shown to increase in response to the atherosclerotic inflammatory process, and to promote coronarosclerosis, the determination of serum ceruloplasmin in subjects with central obesity might be a useful tool to identify patients with the highest risk for myocardial infarction.

The metabolism of ethyl esters of fatty acids in adipose tissue of rats chronically exposed to ethanol.

The concentration of ethyl esters of fatty acids as well as the activity of the enzyme synthesizing these esters (fatty acid ethyl ester synthase) were determined in adipose tissue of rats ingesting ethanol (9-16 g/kg body weight/day) for different periods of time. After 10 and 17 weeks of ethanol exposure about 300 nmol of ethyl esters of oleic, palmitic, stearic, and linoleic acids were found per gram adipose tissue. The ethyl esters disappeared after 1 week of abstinence. Closer analyses, using radioactive ethanol, revealed a half-life of the esters of less than 24 hr. The bulk of the esters was found in a membrane preparation of isolated adipocytes. Hormone-sensitive lipase hydrolyzed emulsified ethyl oleate as efficiently as that of trioleoylglycerol, but in mixed ethyl oleate/trioleoyl glycerol particles the hydrolysis of ethyl oleate was slower, suggesting a decreased accessibility. Synthase activity was found in adipose tissue from rats not exposed to ethanol. It doubled after 10 and 17 weeks of ethanol and decreased with a half-life of at least a week after abstinence. It was concluded that ethyl esters of fatty acids are formed in rat adipose tissue as previously shown in other tissues. They seem to be stored mainly in membranous parts of the adipocytes. Synthase activity is induced by ethanol. The elevated activity has a longer half-life, and may be useful as an indicator of alcohol abuse.

Alcohol consumption and synthesis of ethyl esters of fatty acids in adipose tissue.

Ethyl esters of fatty acids (EEFA) have been found to be formed during ethanol metabolism. Human adipose tissue contains high concentrations of free fatty acids, the substrate for EEFA synthesis, and might therefore be a tissue with great potential for EEFA formation. In order to explore their potential usefulness as markers of alcohol abuse, the EEFA concentration and the activity of EEFA-synthesizing enzyme were therefore determined in adipose tissue from men belonging to the following categories: teetotalers, social drinkers, alcoholics under treatment, or established alcoholics found to have died as a result of alcohol intoxication. In order to estimate the half-life of EEFA and the synthase activity induction, the alcoholics were examined after different time periods of abstinence from alcohol. Comparisons were also made with several established markers of alcohol abuse. EEFA were not found in teetotalers, and were found in low concentrations in some of the social drinkers. EEFA were found in several alcoholics, and the forensic cases had high concentrations. EEFA-synthesizing enzyme activity was found in all subjects, increasing from teetotalers to social drinkers, and being 2-fold higher in alcoholics and 5-fold higher in dead alcoholics. The induction of the enzyme after abstinence appeared to have a half-life of the order of several weeks. Correlations were found between EEFA synthase activity and previously established markers of alcohol abuse known to remain for a long time period after abstinence, such as mean erythrocyte corpuscular volume. This preliminary study suggests the possibility that EEFA synthase induction in adipose tissue might have a longer half-life than previously used markers of alcohol abuse. It is therefore suggested that the induction of EEFA synthase might be a potentially useful new marker for alcohol abuse because of its apparent proportionality to alcohol intake over a prolonged time period, its presumed specificity, and long-term elevation after alcohol abstinence. This potential marker should be analysed further.