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Adipose tissue was obtained from six women undergoing liposuction twice at 6-mo intervals. Samples obtained bilaterally from abdomen, inner thigh, and outer thigh had fatty acids quantified by gas chromatography. There were no important differences between sides or over time. The saturates 14:0, 16:0, 18:0, and 20:0 were higher in abdominal adipose than in outer thigh (P < 0.002 for all); 16:1 and 18: 1[omega]9 were lower in abdomen vs outer thigh (P < 0.01), whereas 18: 1[omega]7 and 20: 1[omega]9 were unchanged. Polyunsaturates 18:2[omega]6, 20:3[omega]6, and 20:4[omega]6 were higher in outer thigh than in abdomen (P < 0.06), and inner thigh values were intermediate. These changes in fatty acid composition resulted in lower mean triglyceride melting points from abdomen to inner thigh to outer thigh, and suggest that temperature may influence the selection process determining the variation in adipose fatty acid composition with anatomical location. Because the site-specific differences included essential fatty acids, selective uptake as well as potential differences in in situ fatty acid modification are indicated.

To determine whether there is altered liver lipid-fraction fatty acid distribution in a multigenic obese mouse model, we examined livers from eight lean (0.2-4.2% carcass fat), seven intermediate (5.7-13.8%), and five obese (20.2-48.7%) backcross progeny [(C57BL/6J x Mus spretus) x C57BL/6J] aged 2-3 mo. Thirteen males and seven females were fed a nonpurified stock diet. Liver lipid fractions were separated and fatty acids quantitated by thin-layer and gas chromatography. There was a significant effect of obesity on 18:2[omega]6 in liver phospholipids (PL), cholesteryl esters, and triglycerides. PL 18:2[omega]6 was negatively correlated with carcass fat (r = -0.74, P < 0.001); 20:3[omega]6 was elevated in PL with increased obesity (P < 0.0001), and was correlated with carcass fat (r = 0.92, P < 0.0001); and 20:4[omega]6 in PL did not differ with obesity status. PL 20:3[omega]6 and 20:4[omega]6 were lower in males (P < 0.01 and 0.02, respectively) than in females. We conclude that obesity and sex affect distribution of [omega]6 essential fatty acids in mouse liver lipid fractions.

The effect of ethanol feeding on the essential fatty acid content of tissues has been contradictory. To define the effect, we analyzed fatty acid profiles in various tissues from five miniature pigs fed daily 105 kJ basal diet/kg body wt and 146 kJ ethanol/kg body wt, and also five control pigs pairfed the same amount of basal diet but with corn starch substituted for ethanol. After 12 mo, biopsy samples were taken, and tissue fatty acid profiles were analyzed. In the phospholipid fraction from the ethanol group there was a uniform decrease in arachidonic acid (AA) and an increase in oleic acid in liver, serum, and muscle. AA was consistently decreased in the triglyceride fractions of liver, serum and subcutaneous adipose of the ethanol group. Possible explanations for this general reduction in tissue AA with ethanol feeding include decreased activities of [DELTA] 6 and [DELTA] 5 desaturases, and a displacement of AA from lipid fractions by other fatty acids.

Neither diet nor exercise are effective as single modes of intervention in the treatment of obesity. Although it is logical that they be combined in the context of multidisciplinary treatment, restrictions in calorie or protein intakes while dieting may impair short-term or long-term function. The limited evidence available indicates that properly constituted very-low-calorie diets can effectively preserve physical function across major weight loss, but long-term preservation of this weight loss is strongly influenced by postdiet exercise habits. In summary, counseling on and initiation of safe and effective exercise practices during dietary treatment of obesity are appropriate, but the ultimate goal should be to direct the patient towards lifelong exercise behaviors that will contribute to sustained weight maintenance. Am J Clin Nutr 1992;56:190S-4S.

High levels of cholesterol in the blood (hypercholesteremia) increase the risk of developing heart disease. Studies have shown that the risk of developing heart disease can be reduced by reducing the amount of cholesterol in the blood. The therapeutic treatment for people who are overweight and have hypercholesterolemia involves dieting to loose weight. It is expected that weight loss will result in lower blood cholesterol levels. If blood cholesterol levels do not decrease after six months of diet therapy, then the patient is treated with drugs to reduce cholesterol levels. Several studies have been performed to determine if weight loss, using very-low-calorie diets (VLCDs), causes blood cholesterol levels to decrease. In a few studies, weight loss caused cholesterol levels to decrease, while in other studies cholesterol levels actually increased during weight loss. To investigate this further, the effect of VLCDs on weight loss and blood cholesterol were determine in six obese females. Body weight and blood cholesterol were measured before and during the diet period. The women lost an average of 67 pounds in five-to-seven months on the VLCD, and maintained their new body weight for an additional two months. Blood cholesterol levels decreased during the first two months of the diet. However, after the second month of the diet the cholesterol levels increased, even though the women continued to loose weight. After the diet was stopped and the women maintained their new body weight, the cholesterol levels decreased and remained lower than they were at the beginning of the diet period. It is concluded that cholesterol levels increase during weight loss on a VLCD. One explanation for this temporary increase is that the body is breaking down the fat tissue and releasing cholesterol during the diet period. However, when the diet is over and the new body weight is maintained, cholesterol levels decrease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Inadequate protein intake or physiological stress can result in protein malnutrition, either marasmus or kwashiorkor, in the hospitalized patient. Composition analysis to determine somatic protein stores and function assessment to evaluate visceral protein production are critical in charting a course for the nutritional management of a patient. Methods to monitor the response of a patient to nutritional support are presented.

• Cardiac arrhythmias have been implicated in the deaths of 17 morbidly obese individuals subsisting on a collagen hydrolysate preparation ("liquid protein") during a modified fasting regimen for weight loss. Serious cardiac arrhythmias have been noted in three of six subjects studied prospectively within 28 days of starting a similar regimen, which used an inadequate protein source and was nearly devoid of all essential minerals. A comparative study of three 28-day weight loss diets of varying carbohydrate, protein, and energy content (450 to 820 kcal/day) but employing protein of good quality and adequate in micronutrients did not disclose substantial diet-related arrhythmias in five subjects on each of the three diets. The incidence of arrhythmia seen with liquid protein diets is not likely to be related to the absolute energy or carbohydrate content of the modified fasting regimen itself.(Arch Intern Med 1983;143:2258-2261)