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Objectives: Comparisons of physical activity measured by accelerometers in overweight/obese adults and their normal-weight counterparts are limited. Compliance with the 2002 Institute of Medicine (IOM) exercise recommendations for 60 minutes of moderate-intensity exercise daily has not been reported. The purpose of this study was to compare physical activity, as measured by accelerometers, in overweight/obese adults vs. normal-weight controls and to assess compliance with recommendations for physical activity by the IOM in 2002 and by the Centers for Disease Control and Prevention and American College of Sports Medicine in 1995 for 30 minutes of moderate-intensity activity, preferably all days of the week., Research Methods and Procedures: Sixty-two overweight/obese subjects, BMI > or = 25, included 31 adults, 12 men and 19 women, 25 to 69 years old, and their normal-weight controls, BMI 18.5 to 24.9, matched for gender, age, and height. Body composition was assessed using DXA. Physical activity was measured with Actigraph accelerometers (MTI, Fort Walton Beach, FL) worn by each participant for 7 consecutive days., Results: Accelerometry data indicated that overweight/obese adults recorded approximately 60 counts per minute less per day and spent 21 minutes less engaged in moderate or greater intensity activity than their normal-weight counterparts. Although 71% to 94% of those studied met 1995 recommendations, only 13% of overweight/obese subjects and 26% of normal-weight participants met 2002 exercise recommendations., Discussion: These results suggest that daily minutes spent in moderate-intensity activity or greater are associated with weight status and that the 2002 IOM recommendations may be difficult to meet even for normal-weight individuals.

Objectives: To assess differences in dietary intake of overweight/obese subjects and sex-, age-, and height-matched controls and to identify dietary components associated with increased deposition of body fat., Design/subjects: A convenience sample of 52 overweight/obese and 52 normal-weight adults matched for sex, age (+/-1 year), and height (+/-1 inch) were recruited from the local area. Dietary intake was assessed with the Block 60-item food frequency questionnaire, physical activity was measured by the Yale Physical Activity Survey, and percent body fat was measured via dual-energy x-ray absorptiometry., Statistical Analyses Performed: Independent t tests compared between-group consumption of dietary components. The ability of dietary components to predict percent body fat before and after controlling for age-, sex-, and physical activity-related energy expenditure and other macronutrients was assessed with multiple regression analyses. Spearman correlation coefficients examined relationships among nutrients, Food Guide Pyramid servings, and percent body fat., Results: Overweight/obese subjects consumed more total fat, saturated fat, and cholesterol and less carbohydrate, complex carbohydrate, and dietary fiber than control subjects. Reported intake of dietary fiber was inversely related to percent body fat without (R(2)=0.052, P=0.02) and with (R(2)=0.045, P=0.013) control for potential confounding factors. Servings of fruit per day were negatively related to percent body fat (r=-0.40, P<0.01)., Conclusions: These findings suggest that the composition of a diet, especially low dietary fiber and fruit intake, plays a role in the etiology of obesity.

Rat adrenal cortical cells have been prepared by collagenase dissociation of trypsin-treated adrenal tissue. The content and compositions of cholesteryl ester, phospholipid, and triglyceride fatty acids compare favorably with those of undissociated rat adrenal tissue. During 2-hour control incubations of adrenal cortical cells, steroidogenesis was not detected, and the levels of sterol ester, phospholipid, and triglyceride fatty acids were not significantly altered. Incubations with adrenocorticotropic hormone (ACTH) resulted in coricosterone production and significant depletions of sterol ester and triglyceride fatty acids, but not of phospholipid fatty acids. Although all fatty acid esters of cholesterol were hydrolyzed under these conditions, the greatest contributions to the net decrease in sterol esters were by oleate, arachidonate, and adrenate. Incubations with dibutyryl cyclic adenosine monophosphate (0.5 mM) resulted in significantly greater levels of corticosterone production than did ACTH (250 muunits), but the effects on cellular lipids were comparable to those seen with the tropic hormone. This study represents the first demonstration of hormone-induced hydrolysis of sterol esters in an in vitro cell suspension system. The results are discussed with respect to hormone-sensitive sterol ester hydrolase of adrenal cortex, and to the role of endogenous cholesteryl esters in the steroidogenic pathway.

Adrenocortical cells were prepared from rats maintained on essential fatty acid-deficient diets and control litter mates. Cells from control rats had high concentrations of essential fatty acids in the cholesteryl ester fraction of which approximately 22% was arachidonate. In contrast, cells from EFA-deficient rats had only 2.5% arachidonate in the cholesteryl esters, even though the total esterified cholesterol level was comparable to that of controls. In place of the essential fatty acids, the cholesteryl esters of these cells were rich in 20:3(n--9) and 22:3(n--9). When cells from EFA-deficient rats were incubated with ACTH or dibutyryl cyclic AMP, the output of corticosterone was the same as in controls. Also sterol esters were hydrolyzed to the same extent as in controls despite the unusual composition of the fatty acid esters. The phospholipids in both control and EFA-deficient cells contained high levels of arachidonate but were not hydrolyzed in either type of cell during incubation with ACTH or dibutyryl cyclic AMP. The results indicate that high levels of the prostaglandin precursors, namely linoleate and arachidonate, are not a sine qua non for the steroidogenic action of ACTH or cyclic AMP.

Rat adrenocortical cells were incubated with labeled arachidonate, and the radioactivity in unesterified fatty acids was reduced by washing with 2% albumin solutions. These cells were then incubated for two hours in the absence and presence of 7.1 x 10(-10)M ACTH. During subsequent incubation of prelabeled cells with ACTH, both the mass and radioactivity of arachidonate in adrenocortical cholesteryl esters was depleted to the same extent (30--32%). The released arachidonate was in part incorporated into phospholipids, and there was also a significant increase in unesterified arachidonic acid. During this period, there was also increased incorporation of arachidonate into labeled prostaglandins. Of this increase, 92% by isotope analysis, and 88% by radioimmunoassay techniques was attributable to prostaglandins of the E pathway. These data demonstrate that prostaglandin E synthesis is specifically increased during ACTH stimulation of rat adrenocortical cells and suggest that a major source of the arachidonate substrate for this synthesis is derived from hormone-dependent hydrolysis of cortical cholesteryl esters.

The biosynthesis of prostaglandins by isolated rat adrenocortical cells has been studied by determinations of products formed during incubations with labeled arachidonic acid and by radioimmunoassays. Analysis by thin-layer chromatographic separation of silicic acid column fractions indicated that PGE2, PGA2, (B2) and PGF2 alpha were the predominant prostaglandins formed by rat adrenocortical cells. Approximately 75% of the incorporated isotope was associated with the prostaglandins of the PGE pathway [PGE2 + PGA2 (B2)]. This was a consistent finding whether cells were incubated directly with arachidonic acid or with cells prelabeled with the substrate prior to study. ACTH did not affect the uptake or oxidation of [1-14C]-arachidonate, but did significantly increase incorporation of labeled substrate into [14C]prostaglandins. Of the ACTH-induced increase, 92% was accounted for by an increase in prostaglandins of the E pathway. Studies with prelabeled cells indicated that 77% of the prostaglandins synthesized in both control and ACTH-stimulated adrenocortical cells was released into the incubation medium during the 2-hr study. These had the same composition [88% PGE2 + PGA2 (B2)] as did the intracellular prostaglandins. Analysis by radioimmunoassays gave comparable data on the distribution of E- and F-type prostaglandins in control cells and cells incubated with ACTH or dibutyryl cyclic AMP. Thus, with these techniques, 88-92% of the increased prostaglandin synthesis due to ACTH or cyclic AMP was produced by the PGE2 rather than the PGF2 alpha pathway.