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From The Clinical Research Centers |
Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington (J.Q.P., S.E.K., D.N.N., J.D.B.); Department of Gerontology and Geriatric Medicine, University of Washington (R.S.S.); and Northwest Lipid Research Laboratories, University of Washington (J.J.A.), Seattle, Washington 98195
Address all correspondence and requests for reprints to: Jonathan Q. Purnell, M.D., Division of Metabolism, Endocrinology, and Nutrition, University of Washington, Box 359757, Seattle, Washington 98104. E-mail: purnell{at}u.washington.edu
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Abstract |
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 Top Abstract IntroductionExperimental SubjectsMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionExperimental SubjectsMaterials and MethodsResultsDiscussionReferences |
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This study sought to determine whether a loss of IAF in a group of healthy obese older men would be associated with improvements in lipid metabolism that are seen after undergoing diet-induced weight loss.
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Experimental Subjects |
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TopAbstractIntroductionExperimental SubjectsMaterials and MethodsResultsDiscussionReferences |
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Materials and Methods |
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TopAbstractIntroductionExperimental SubjectsMaterials and MethodsResultsDiscussionReferences |
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All subjects maintained weight stability as out-patients for 14 days before and at the end of the weight loss protocol. Weight stability was achieved by having subjects weighed on weekday mornings at the General Clinical Research Center. Total caloric intake was adjusted during the first week to reduce weight fluctuation during the last 7 days when their weights did not change. The weight stabilization diet was composed of foods available in the marketplace (50% carbohydrate, 30% fat, and 20% protein) that were prepared, packaged, and distributed by the research kitchen of the University of Washington General Clinical Research Center. Any required supplement was added as a liquid with the same nutrient content as the overall diet. Body composition and computed tomography (CT) scans were completed on days 1 and 6 of the weight stabilization period, respectively. The insulin sensitivity studies were carried out on the morning of day 14 of the weight stabilization period. Fasting blood samples for lipids, lipoproteins, and postheparin lipase activity were also drawn on this morning.
Weight loss protocol
Subjects met with a research dietitian and were given instructions in a low fat, 1200 Cal/day diet that was similar to the weight-stable diet in overall macronutrient content. All subjects received a daily multiple vitamin and mineral supplement. During the 3-month weight loss period, subjects were weighed on a metabolic scale 3 days each week and met with the research dietary staff at least weekly to discuss progress and/or problems.
Lipids and lipoproteins
Blood was collected in 0.1% ethylenediamine tetraacetate after a 12- to 16-h overnight fast for measurements of lipids and post-heparin lipase, and CETP activities. A heparin bolus of 60 U/kg was given, and blood was collected after 10 min in lithium-heparin tubes for the measurement of lipase activity. Blood was immediately centrifuged at 4 C at 3000 rpm for 15 min. Lipid measurements were made in fresh plasma within 2 days. Lipase activities were determined in plasma that had been immediately frozen and stored at -70 C. Plasma total cholesterol, tri-glycerides, HDL-C, HDL2-C HDL3-C, apolipoprotein B (apo B), and apolipoprotein AI were measured at the Northwest Lipid Research Laboratory as previously described (13, 14).
LDL size
LDL size was determined by nondenaturing PAGE (15). Whole plasma
and LDL standards of known diameter were electrophoresed for 24 h
at 125 V (3000 V-h), stained, and subjected to densitometry, and the
diameter (Å) of the major peak of LDL was determined using a quadratic
calibration curve of migration distance and particle diameters of the
standards. LDL subclass phenotypes were defined as previously described
(16). Phenotype A is characterized by a predominance of large LDL
particles (generally >255 Å) exhibiting rightward skewing of their
LDL particle size distribution, phenotype B is characterized by a
predominance of small LDL particles (usually 
255 Å) exhibiting a
leftward skewing of their LDL particle size distribution, and the
intermediate phenotype I is when the peak LDL particle is close to 255
Å but there is no skewing of the curve or two distinct LDL peaks are
seen.
Postheparin lipase activities and CETP
The total lipolytic activity was measured in plasma after administration of a heparin bolus as previously described (17). Glycerol tri- [1-14C]oleate (Amersham Pharmacia Biotech, Arlington Heights, IL) and lecithin were incubated with postheparin plasma for 60 min at 37 C, and the liberated 14C-labeled free fatty acids were then extracted and counted. LpL activity was calculated as the lipolytic activity removed from the plasma by the incubation with a specific monoclonal antibody against LPL, and HL activity was determined as the activity remaining after incubation with the LPL antibody. Enzyme activity is expressed as nanomoles of free fatty acid released per min/mL plasma at 37 C. For each assay, a bovine milk LPL standard was used to correct for interassay variation, and a human postheparin plasma standard was included to monitor interassay variation. The intraassay coefficient of variation for HL is 6%; the between-assay coefficient of variation is 14%.
Plasma CETP activity was measured as previously described (18). Briefly, 20 µL [14C]HDL3 donor and 40 µL LDL acceptor were incubated with 5 µL plasma in a final volume of 500 µL at 37 C for 18 h. The donor and acceptor lipoproteins were separated (19). Activity was expressed as the percentage of transfer of labeled CE per 5 µL/18 h.
Insulin sensitivity (Si)
The tolbutamide-modified, frequently sampled, iv glucose tolerance test was performed as previously described (20). Three basal samples were drawn for insulin and glucose at 5-min intervals; glucose was injected (11.4 g/m2) at time zero as a bolus over 60 s, and tolbutamide was injected over 30 s (125 mg/m2) at 20 min after the glucose injection; blood samples for glucose and insulin measurements were drawn at 32 time points over 4 h. Plasma glucose concentrations were measured in triplicate using the glucose oxidase method. Plasma insulin was measured in duplicate using a modification of a double antibody RIA (21). Si was quantified using Bergman’s minimal model of glucose kinetics (22).
Body composition and distribution
The percent body fat was determined by underwater weighing after a 12-h overnight fast (23). With a minimum of six trials, the highest three weights that differed by less than 100 g were used. Residual lung volume was measured using the helium dilution technique. The average of three trials that differed by less than 150 mL was used. Using this technique, a day to day coefficient of variation for body composition is 2.6%. Fat mass (kilograms) was calculated by multiplying the percent body fat by total weight (kilograms). Nonfat mass was calculated by subtracting fat mass from total body weight. Intraabdominal fat (IAF) and sc abdominal fat (SQF) depots were manually separated and quantified by a blinded reader using single abdominal CT images obtained on inspiration at the level of the umbilicus. The CT image was analyzed for cross-sectional area of fat using a density contour program available in the standard GE computer software (General Electric, Milwaukee, WI) as described previously (24). A single blinded observer made all of the CT measurements of IAF and SQF. The coefficient of variation of reading the same scan is less than 2%. To minimize exposure of each patient to radiation, measurements were made from a single CT image at the level of the umbilicus. The amounts of IAF and SQF measured at this level have been shown to correlate with total visceral and sc fat determined from multiple abdominal images, with r values between 0.93–0.99 (25, 26).
Statistical methods
For baseline and follow-up comparisons, the paired t test was used unless the data were nonnormally distributed, in which case the Wilcoxon signed rank test was used. Correlation relationships were tested using linear regression. Independence of linear relationships was tested using multiple linear regression. All statistical analysis was performed using SigmaStat (Windows 95, version 2.0; SPSS, Chicago, IL).
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Results |
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TopAbstractIntroductionExperimental SubjectsMaterials and MethodsResultsDiscussionReferences |
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). Subjects who were pattern
B at baseline had significantly lower BMI than subjects with pattern A
(mean ± SD BMI, 32 ± 2.8 vs. 29
± 2.0 kg/m2; P = 0.04, pattern B
vs. pattern A, respectively), but had greater IAF (186 ± 53
vs. 231 ± 34 cm2;
P = 0.056) and lower HDL (38 ± 7.6 vs.
31 ± 2.8 mg/dL; P = 0.025). All other variables
were not significantly different between the groups (data not shown).
On the average, the group that was pattern B at baseline had greater
reductions in absolute IAF and HL activity and greater improvement in
Si with weight loss than the pattern A group, although these findings
did not quite reach statistical significance (data not shown).
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). HDL-C increased with weight loss as a result of a
greater amount of cholesterol in HDL2 and no
change in HDL3 cholesterol. Accompanying these
changes in lipids and lipoproteins, LDL particle size also increased,
although this did not reach statistical significance in the whole group
(264 Å before weight loss vs. 268 Å after weight loss;
P = 0.06; Table 1). If the change in LDL particle size
was analyzed according to LDL pattern A or B assignment at baseline,
those with pattern B LDL showed the greatest change with weight loss,
with an increase from an average size of 253 to 262 Å
(P = 0.047), whereas the LDL size of those with pattern
A did not change (270 Å before weight loss vs. 271 Å after
weight loss; P = 0.45). In fact, of those who were
pattern B at baseline (n = 7), only one remained pattern B at
follow-up, two became an intermediate phenotype, and four became
pattern A (Table 2). Of those subjects
who were pattern A at baseline, one decreased in LDL size from 271 to
252 Å and became pattern B.
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). Neither mean postheparin LpL activity
nor CETP activity changed significantly after weight loss (Table 3).
However, postheparin HL activity was significantly reduced by 21%.
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and Table 4). The only parameter of body
composition change that significantly correlated with the change in HL
activity was loss of IAF (Fig. 1). The one subject mentioned above
whose LDL particle diameter decreased despite weight loss (converting
from pattern A to B) is represented in Fig. 1 by an open
box. In this individual, despite an overall weight loss, IAF
paradoxically increased and was accompanied by an increase in HL
activity. A second subject also experienced an increase in IAF despite
overall weight loss (see also Fig. 1). HL activity increased in this
individual as well.
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). Because of the
known correlation between IAF and Si, the relationship between the
change (
) in IAF and HL activity was tested with multiple linear
regression analysis by adding Si as an independent variable and was
found to no longer be significant (r2 for
combined effect of IAF and Si on HL activity = 0.357;
standard coefficient for IAF = 0.331, P
= 0.131; standard coefficient for Si = -0.392,
P = 0.08). Of the two subjects who experienced an
increase in IAF and HL activities in this study, the first had no
change in Si (0.52 vs. 0.73 x
10-4 µU/min, pre- and postweight loss,
respectively), and the second experienced an improvement (0.66
vs. 1.5 x 10-4 µU/min, pre-
and postweight loss, respectively). |
Discussion |
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TopAbstractIntroductionExperimental SubjectsMaterials and MethodsResultsDiscussionReferences |
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Although numerous studies have demonstrated improvements in insulin sensitivity and total lipid levels with weight loss (8, 9, 10, 11, 36, 37), only a handful have studied the effect of weight loss on postheparin hepatic and LpL activities and cholesterol content of atherogenic lipoprotein subfractions. Sörbris et al. measured lipids and postheparin lipase activities in 14 obese subjects before and after an average weight loss of 10% of their initial body weight (9). After 1 week of weight stabilization following weight loss, only HDL-C changed (increased), and neither LpL nor HL activities were different compared with baseline values. Katzel et al. reported a decrease in HL, but not LpL, in obese men 1 month after weight stabilization following an 11% reduction in initial body weight (36). Accompanying these changes were reductions in waist to hip ratio, triglyceride levels, and LDL-C and an increase in HDL-C. Because HL is thought to be an important mediator in the processing of larger HDL2 particles during conversion to the smaller HDL3 particles (38, 39), it is possible that the reduction in the activity of this enzyme that accompanied weight loss was in part responsible for the increase in HDL cholesterol that was found. Finally, CETP activity has been shown to decrease in 4 women after 2 months of caloric restriction (6), although no information was given as to whether these subjects were studied during a hypocaloric period or when weight stable.
In the older men who underwent moderate weight loss by caloric restriction in the present study, following weight stabilization significant reductions were demonstrated in overall fat mass, IAF, and SQF. Accompanying these changes in fat mass, subjects experienced an improvement in insulin sensitivity (increased Si) and a reduction in HL, but not LpL or CETP, activity. These changes in Si and HL activity (and the lack of change in LpL activity) that accompanied weight loss in the present study are consistent with findings reported by others (8, 36, 40). The finding that CETP activity did not change with weight loss in the present study compared with the reduction in CETP activity reported by Arai et al. (6), however, may have been the result of several factors. The greater number of subjects in the present study would reduce random selection bias from any individuals or small groups of subjects. In addition, subjects in the present study were sampled during periods of weight stability both before and after weight loss to avoid metabolic effects resulting from caloric restriction. Whether subjects were studied during weight stability was not commented on by Arai et al., but, if not, the lower CETP activity in their study could have been the result of caloric restriction rather than weight loss.
Loss of IAF, but not other measures of body adiposity or fat distribution, correlated with the reduction in HL activity in the present study. A decrease in insulin resistance also significantly correlated with a reduction of HL activity, but in multiple linear regression this association was not independent of the effect of reduction of IAF on HL activity. Therefore, whether the reduction in HL was the result of the improvement in IAF, the effect of weight loss to improve insulin sensitivity, or both could not be clearly determined from this study. It should be pointed out that two subjects experienced a paradoxical increase in IAF despite loss of total body fat. These are the only two subjects who also experienced an increase in HL activity with weight loss. Other than being slightly older (70 and 71 yr old) and having greater fat mass (40 and 45 kg), lower HL activities (138 and 161 nmol FFA/min·mL), and lower insulin sensitivity (Si, 0.52 and 0.66 x 10-4 µU/min) at baseline, these subjects did not differ from the group as a whole. HL activity increased in these subjects despite either no change or an improvement in their insulin sensitivity, which would have been expected to result in no change or a reduction in HL activity based on the relationship between Si and HL activity. The finding that their HL activities increased at the same time as IAF increased, therefore, strengthens the physiological relationship between these variables.
The reduction in IAF and improvement in insulin resistance combined to explain 36% of the reduction in HL activity with weight loss. It is known that the level of HL activity is also influence by a polymorphism of the HL gene (41, 42), but this polymorphism is unlikely to have had a major effect on the change in HL activity in this study because each subject acted as his own control. It is possible that changes in the levels of other endogenous hormones may have occurred with weight loss and affected HL activity (43), but measurement of these variables were not performed as part of this study.
Given the association of visceral adiposity with increased triglyceride, VLDL-C, and apo B levels and decreased HDL-C, improvements in these lipid parameters with loss of body weight and IAF was expected. A possible mechanism by which weight loss resulted in decreased apo B-containing particles could have occurred through a reduction in the VLDL production rate, which has been previously described in obese subjects after weight loss (8, 44, 45). The increases in LDL particle size, particularly in those subjects with pattern B LDL at baseline, and HDL2 cholesterol were probably a result of the reduction in HL activity. Evidence to support this mechanism comes from studies demonstrating that increased HL activity is an important mediator of conversion of HDL2 to HDL3 particles (38, 39), and decreased activity has been associated with larger, more buoyant LDL particles (5, 46). In the present study the changes in LDL particle size and HDL subfractions did not appear to be mediated by CETP, as the activity of this enzyme did not change with weight loss.
It is of interest to note that subjects with pattern B LDL particles at baseline experienced the greatest benefit with regard to an increase in LDL particle size with weight loss. Indeed, six of the seven subjects converted to either pattern A or an intermediate pattern, whereas only one remained pattern B at follow-up. Therefore, this study extends the existing literature reporting improvements in cardiovascular risk factors with weight loss to include both an increase in LDL particle size and a decrease in HL activity. The importance of an increase in LDL particle size and a decrease in HL activity with weight loss is illustrated by prospective studies demonstrating that a smaller LDL size predicts future risk of cardiac events (47, 48, 49) and that reduction of LDL density (or change to larger, more buoyant particles) and HL activity with lipid-lowering therapy was a better predictor of coronary stenosis regression than reduction of total lipid levels in men (50).
In summary, weight loss in older men through caloric restriction is associated with improvements in visceral adiposity, insulin sensitivity, HL activity, and the dyslipidemia of the visceral adiposity syndrome, including an increase in LDL particle size. The reduction in HL activity with weight loss may be an important contributor to the increase in LDL size and HDL2 cholesterol, especially in those subjects who have pattern B LDL particles before weight loss. CETP and LpL activity did not change, however, as a result of weight loss. These data suggest that HL activity is influenced by changes in IAF and may mediate in part the beneficial changes in cholesterol content of lipoprotein subfractions as a result of weight loss.
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Footnotes |
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Received June 8, 1999.
Revised September 29, 1999.
Accepted November 9, 1999.
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References |
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