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Original Article |
School of Physical and Health Education (R.R. J.F., I.J.) and Department of Medicine (R.R., R.H.), Division of Endocrinology and Metabolism, Queen’s University, Kingston, Ontario, Canada K7L 3N6; and Nutrition, Exercise Physiology, and Sarcopenia Laboratory (I.J.), Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts 02111
Address all correspondence and requests for reprints to: Robert Ross, Ph.D., School of Physical and Health Education, Queen’s University, Kingston, Ontario, Canada K7L 3N6. E-mail: rossr{at}post.queensu.ca.
Abstract
The independent relationships between visceral and abdominal sc adipose tissue (AT) depots, muscle composition, and insulin sensitivity were examined in 40 abdominally obese, premenopausal women. Measurements included glucose disposal by euglycemic clamp, muscle composition by computed tomography, abdominal and nonabdominal (e.g. leg) AT by magnetic resonance imaging and cardiovascular fitness. Glucose disposal rates were negatively related to visceral AT mass (r = -0.42, P < 0.01). These observations remained significant (P < 0.01) after control for nonabdominal and abdominal sc AT, muscle attenuation, and peak oxygen uptake. Total, abdominal, or leg sc AT or muscle attenuation was not significantly (P > 0.10) related to glucose disposal. Subdivision of abdominal sc AT into anterior and posterior depots did not alter the observed relationships. Further analysis matched two groups of women for abdominal sc AT but with low and high visceral AT. Women with high visceral AT had lower glucose disposal rates compared with those with low visceral AT (P < 0.05). A similar analysis performed on two groups of women matched for visceral AT but high and low abdominal sc AT revealed no statistically different values for insulin sensitivity (P > 0.10). In conclusion, visceral AT alone is a strong correlate of insulin resistance independent of nonabdominal, abdominal sc AT, muscle composition, and cardiovascular fitness. Subdivision of abdominal sc AT did not provide additional insight into the relationship between abdominal obesity and metabolic risk.
EVIDENCE FROM CROSS-SECTIONAL and prospective studies establish that abdominal obesity is a strong predictor of insulin resistance and type II diabetes in both genders independent of total adiposity. At issue is the extent to which the various abdominal adipose tissue (AT) depots contribute to this relationship. Some investigators observe that visceral AT alone is an independent predictor of insulin resistance, whereas others find that abdominal sc AT is responsible for the association between abdominal obesity and insulin resistance. We have recently suggested that the disparate findings may be largely resolved by cohort selection (1). Indeed, in a homogenous group of obese men characterized by marked elevation in visceral obesity, we report that visceral AT is a strong correlate of insulin resistance independent of abdominal sc AT, nonabdominal sc AT (e.g. arm and leg sc AT), and cardiovascular fitness. This observation remained true after statistical control for the AT depots that result from subdivision of abdominal sc AT (posterior and anterior depots) and visceral AT (intra- and extraperitoneal depots). Whether these observations hold true for women is unclear. Toth et al. (2) report that visceral AT does not remain a significant correlate of glucose disposal after control for variation in cardiovascular fitness in a cohort of lean, premenopausal women. That finding contrasts with Brochu et al. (3), who report that visceral AT is a robust marker of insulin resistance in obese postmenopausal women independent of total and abdominal sc AT. These equivocal findings are likely explained by marked differences in visceral AT accumulation between the cohorts studied. The mean value for visceral AT at the L4-L5 level reported by Toth et al. (2) was approximately 60 cm2, a value substantially below the threshold (
120 cm2) thought to be associated with increased metabolic risk (4, 5). By contrast, the postmenopausal women in the Brochu et al. (3) study were characterized by marked elevation in visceral AT (190 cm2). However, in that study the authors did not control for cardiovascular fitness nor was abdominal sc AT subdivided into deep or superficial depots. Because the deep sc AT depot alone is reported to be a strong correlate of insulin resistance in a cohort of men and women combined (6, 7), failure to subdivide abdominal sc AT may mask important observations. To our knowledge, no study has simultaneously examined whether subdivision of abdominal sc AT improves the ability of either depot to predict insulin resistance in a cohort of overweight women.
Recent evidence also suggests that the accumulation of triglyceride within skeletal muscle plays an important role in determination of insulin resistance (8). Reports that link muscle triglyceride by percutaneous biopsy and insulin resistance (9, 10, 11) are confirmed in studies that use computed tomography (CT) to determine muscle composition (12, 13, 14). Skeletal muscle composition by CT is based on the measurement of the muscle attenuation characteristics (Hounsfield units), which in turn are a function of tissue density and chemical composition. The lower the mean attenuation value, the greater the infiltration of lipid within the muscle (12, 13, 15). Using this method, Goodpaster et al. (13) report that reduced muscle attenuation remains a significant correlate of insulin resistance after statistical control for visceral, abdominal sc, and total adiposity in a mixed cohort of men and women. Simoneau et al. (14) report similar findings in a group of premenopausal women varying widely in adiposity. However, using the same methodology, others (2, 16) report that muscle attenuation is not a significant correlate of insulin resistance in nonobese premenopausal women or obese postmenopausal women (3). Thus, at present, whether altered muscle composition by CT independently predicts insulin resistance is unresolved.
The primary purpose of this study was, therefore, to determine whether visceral AT predicts insulin resistance independent of abdominal sc AT, muscle composition, and cardiovascular fitness. To test this objective, we studied a cohort of abdominally obese women at increased metabolic risk. We hypothesized that in this homogenous group of women characterized by marked elevation in visceral obesity, visceral AT would be a strong correlate of insulin resistance independent of abdominal sc AT, nonabdominal sc AT, muscle composition, and cardiovascular fitness.
Materials and Methods
Subjects
Forty female volunteers were initially recruited for a weight loss study from the Kingston area through the local media. Inclusion criteria required that all women were premenopausal (regular menses, normal FSH and LH levels), abdominally obese [body mass index (BMI), >25 kg/m2; waist circumference, 
85 cm], weight stable (±2 kg within the last year), sedentary (>1 yr with no structured exercise), and not taking oral contraceptives or any other medications known to affect the study variables. All subjects were nondiabetic according to fasting and oral glucose tolerance test plasma glucose levels (17). All subjects gave their full informed and written consent to participate in the study, which was conducted in accordance with the ethical guidelines of Queen’s University. Financial incentives were not provided to the participants.
Cardiovascular fitness [peak oxygen uptake (peak VO2)]
Peak VO2 was determined using a graded treadmill test that employed a constant walking speed and the use of standard open-circuit spirometry techniques (Teem 100; Aerosport Inc., Ann Arbor, MI). Each subject was required to participate in a practice VO2 treadmill test before initial baseline test. Peak VO2 was attained when at least two of the following three criterion were achieved: 1) no increase in VO2 despite further increases in treadmill grade; 2) a heart rate at or above age-predicted maximum (220-age); and/or 3) a respiratory exchange ratio in excess of 1.0.
Anthropometric measurements
Body mass was measured on a balance scale calibrated to the nearest 0.1 kg with the subjects dressed in standard T-shirts and shorts. Barefoot standing height was measured to the nearest 0.1 cm using a wall-mounted stadiometer. Waist circumference was obtained at the level of the last rib using standard procedures (18).
Magnetic resonance imaging (MRI)
Whole-body MRI data were obtained with a 1.5 Tesla magnet (General Electric, Milwaukee, WI) using an established protocol described in detail elsewhere (19). Briefly, using the intervertebral disk between the fourth and fifth lumbar vertebrae (L4-L5) as the point of origin, approximately 45 equidistant images (1-cm-thick images, 4-cm spaces between two consecutive images) were obtained from the feet to the hands, which were extended above the head. Once acquired, the MRI data were transferred to personal computers for analysis using commercially available software (Slice-O-Matic; Tomovision Inc., Montreal, Canada), the procedures for which are described elsewhere (19, 20). Total AT (sc + visceral + intrapelvic + intrathoracic + intermuscular) and skeletal muscle were determined using all 45 images. Visceral and abdominal sc AT were calculated using the five images extending from 5 cm below L4-L5 to 15 cm above L4-L5. Nonabdominal AT includes all AT other than abdominal sc and visceral AT (92% of nonabdominal AT is sc AT in the arms and legs). Leg sc AT was calculated using the images extending from the femoral head to the foot. Volume units (in liters) were converted to mass units (in kilograms) by multiplying the volumes by the assumed constant densities for adipose tissue (0.92 kg/liter) and adipose tissue-free skeletal muscle (1.04 kg/liter) (21).
We divided abdominal sc AT into superficial and deep compartments using the fascia superficialis (Fig. 1
). The rationale for this division presumes that the deep adipocytes are more metabolically active, compared with the superficial adipocytes (22, 23). We also subdivided abdominal sc AT into anterior and posterior compartments by drawing a perpendicular line along the anterior edge of the vertebral bodies (Fig. 1). The rationale for this division is that the fascia superficialis is not always visible on MRI images, as illustrated in the right image in Fig. 1 and the majority of deep sc AT is located in the posterior half of the abdomen (6, 7).
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CT
For each subject a single 10-mm-thick CT image was obtained in the midthigh at the midpoint between the inguinal crease and superior edge of the patella. CT images were obtained on a scanner (General Electric) using 280 mA, a 512 x 512 matrix, and 48-cm field of view. Skeletal muscle attenuation was measured as the mean attenuation value from all pixels within the range of 0–100 Hounsfield units using commercially available software (Slice-O-Matic; Tomovision Inc.), as described previously (12, 13, 15). Low-density muscle was considered all pixels within a range of 0–30 Hounsfield units (12, 13, 15). Lower mean attenuation values and higher low-density muscle area values indicate greater lipid content within the muscle because lipid is characterized by negative attenuation values. A recent validation study has shown that skeletal muscle attenuation of the midthigh is negatively related to muscle fiber lipid content determined by oil red O staining (r = -0.43) and triglyceride extraction (r = -0.58) in percutaneous biopsy specimens from the vastus lateralis (15). The test-retest coefficient of variation for muscle attenuation in two CT scans is less than 1% (15).
Hyperinsulinemic euglycemic clamp (glucose disposal)
On the night before measurement of insulin sensitivity, subjects were admitted to Kingston General Hospital at 2000 h after having consumed a prescribed, standard dinner (50% carbohydrate, 30% fat, 20% protein). Volunteers were asked to refrain from vigorous physical activity for the 3 d before testing. At about 0800 h, following a 12- to 14-h fast, an antecubital vein was catheterized for infusion of insulin and 20% glucose. A retrograde-style iv catheter was inserted into a hand vein, and then the hand was placed in a heating pad for sampling of arterialized blood. Insulin was infused iv at a rate of 40 mU/m2·min for 180 min. Plasma glucose was measured using an automated glucose analyzer (2300 glucose analyzer; YSI, Inc., Yellow Springs, OH) every 5 min in arterialized blood. A variable infusion of 20% glucose was used to maintain euglycemia (target glucose, 5.0 mmol/liter). Glucose disposal rate was calculated using the average exogenous glucose infusion rate during the final 30 min (150–180 min) of euglycemia.
Oral glucose tolerance test (OGTT)
The subjects underwent a 2-h, 75-g OGTT in the morning following a 12-h overnight fast. Blood samples were acquired from the antecubital vein at -15, 0, 30, 60, 90, and 120 min. Glucose was measured using an automated glucose analyzer (2300 glucose analyzer, YSI, Inc.), and insulin was measured by RIA (Intermedico, Toronto, Canada). Areas under the glucose and insulin curves were determined using a trapezoid model (25).
Statistical analysis
Data are presented as group means ± SD. Relationships between body composition and metabolic variables were determined using Pearson product moment correlation coefficients. Independent correlations were determined using multiple regression stepwise analysis. Unpaired t tests were used to determine differences between groups matched for visceral and abdominal sc AT. All statistical procedures were performed using SPSS version 10.0 (SPSS, Inc., Chicago, IL).
Results
Subject characteristics
Subject characteristics for the 40 premenopausal women are given in Table 1. The women were overweight (BMI, 32.3 ± 3.3 kg/m2) and abdominally obese (waist circumference, 98.3 ± 7.5 cm). The group was characterized by a wide variation in total, visceral, leg, and abdominal sc AT (Table 1). Analysis of the CT data also indicated a wide range of low-density muscle and muscle attenuation scores (Table 1). In addition, there was a wide variation in insulin and glucose values and insulin-mediated glucose disposal values (Table 2).
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Waist circumference was positively correlated with OGTT insulin area (r = 0.37, P < 0.05) and negatively correlated with glucose disposal (r = -0.31, P = 0.05). There were no significant relationships observed between BMI and fasting, OGTT, or insulin-mediated glucose disposal values (P > 0.10). Peak VO2 was not significantly correlated with any of the metabolic variables (P > 0.05).
Relationship between total and abdominal fat distribution, muscle composition, and metabolic risk factors
The univariate correlations between total and regional fat, muscle composition, and metabolic risk factors are given in Table 3. As shown in Fig. 2, visceral AT was negatively correlated with glucose disposal (milligram per kilogram muscle per minute). This relationship remained significant (P < 0.05) after statistical control for nonabdominal and abdominal sc AT, mean muscle attenuation, and cardiovascular fitness (peak VO2). Glucose disposal was not significantly (P > 0.10) correlated with total (r = -0.06), leg (r = 0.12), or abdominal sc (r = 0.01, Fig. 2) AT mass (Table 3). Subdivision of abdominal sc AT into anterior and posterior compartments yielded no significant relationships (P > 0.10). Furthermore, with the exception of fasting insulin, which was significantly related to abdominal sc AT (r = 0.34, P = 0.03), nonsignificant correlations were observed among fasting and OGTT insulin and glucose values with all total and regional AT variables (P > 0.05).
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). However, a significant (P < 0.05) negative relationship was observed between mean muscle attenuation and both fasting (r = -0.34) and OGTT glucose (r = -0.33). These correlations remained significant after control for visceral, abdominal sc, nonabdominal AT, and peak VO2 (P 
0.06).
To further explore the relationships between visceral AT, sc AT, muscle density, and metabolic risk, the data were also analyzed using a matching strategy. First, we used a percentile approach to identify high (>60th percentile) and low (<40th percentile) abdominal sc AT and muscle density values in our cohort. The matching strategy was then performed on the basis of visceral AT after having excluded subjects with intermediate levels (e.g. 40th to 60th percentile) of abdominal sc AT or muscle density. The glucose, insulin, and glucose disposal values were then compared in two subgroups of nine subjects matched for visceral AT but who displayed different levels of abdominal sc AT or muscle density (Table 4). The glucose, insulin, and glucose disposal values were not different in women with high abdominal sc AT by comparison with women with low abdominal sc AT (P > 0.05, Table 4). With the exception of OGTT glucose values, the metabolic variables were not different in women with low muscle density values by comparison with women with high muscle density values (P > 0.05, Table 4).
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). Women with high visceral AT had higher OGTT glucose values and lower glucose disposal values by comparison with women with low visceral AT (P < 0.05, Table 5). The glucose, insulin, and glucose disposal values were not different in women with low muscle density values by comparison with women with high muscle density values (P > 0.05, Table 5).
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The principal finding of this study was that in abdominally obese, premenopausal women characterized by marked elevation in visceral adiposity, visceral AT alone demonstrated a strong, negative association with insulin-mediated glucose disposal. This finding remained true after statistical control for abdominal sc AT, its subdivisions (anterior and posterior depots), skeletal muscle composition, and cardiovascular fitness. These observations reinforce the singular importance of visceral obesity in the modulation of insulin resistance in obese individuals.
The findings here confirm an earlier observation wherein visceral AT was a strong, independent predictor of insulin resistance in a cohort of abdominally obese men (1). In that study, visceral AT remained a significant marker of insulin resistance independent of abdominal sc AT (anterior and posterior depots), nonabdominal AT, and cardiovascular fitness. Together these observations support our contention that disparate findings in the literature regarding the unique contribution of visceral and abdominal sc AT in the development of insulin resistance is explained in large measure by cohort selection. In those studies wherein the cohorts comprise heterogeneous groups of men and women with wide variation in total and abdominal sc AT (6, 13, 26, 27) or homogeneous groups of women with a relatively low accumulation of visceral AT (2), abdominal sc AT is a stronger correlate of insulin resistance than visceral AT. Alternatively, in this and other studies wherein the observations are based on cohorts of abdominal obese men (1, 28) or women (3, 29) characterized by marked elevation in visceral AT (e.g. > 120 cm2 at L4-L5), visceral AT, but not abdominal sc AT, independently predicts insulin resistance. In other words, once visceral AT accumulation exceeds a threshold of approximately 120–130 cm2 (L4-L5 level), the contribution of this depot toward the variation in insulin resistance overwhelms that of total and/or abdominal sc AT.
Previous investigations have used matching strategies to explore the independent relationships between abdominal sc, visceral AT, and metabolic risk factors (3, 29, 30). In those studies it is generally reported that, in cohorts matched for sc AT, those with high visceral AT are at increased metabolic risk, compared with those with low visceral AT. In response to criticism that similar analyses based on cohorts matched for visceral AT, but with high and low sc AT are unavailable (31), we performed a series of analyses using various matching strategies. The principal finding was that, within a cohort of women matched for visceral AT, the metabolic profile of those with high abdominal sc AT was not different from those with low sc AT. On the other hand, for the cohort of women matched for abdominal sc AT, insulin-mediated glucose disposal was 38% lower in women with high visceral AT by comparison with women with low visceral AT. These novel findings for women are comparable with previously reported observations in obese men (1) and once again reinforce the importance of visceral AT as an independent predictor of metabolic risk.
A causal link between visceral AT and insulin resistance in vivo has yet to be elucidated (31). Björntorp (32, 33) hypothesized that the metabolic importance of visceral AT may be due to the excess delivery of free fatty acids into the portal system exerting potent and direct effects on the liver. Indeed, it is now established that plasma free fatty acid concentration is a primary modulator of hepatic insulin resistance (34, 35). With the knowledge that in men and women omental and mesenteric adipocytes are metabolically more active by comparison with abdominal sc adipocytes (36), differences in portal concentration of free fatty acids may at least partially explain the hepatic and peripheral insulin resistance that characterize viscerally obese persons. Although it is not possible to access the portal circulation in vivo, it is reasonable to expect that sustained delivery of free fatty acids to the liver would cause an increase in the infiltration of lipid within the liver-hepatic steatosis or fatty liver. Indeed, preliminary evidence suggests that visceral AT is a positive correlate of liver fat (37, 38, 39). Alternatively, it is equally tenable that cytokines such as IL-6 and TNF explain the metabolic complications associated with visceral obesity (40). Indeed, these adipose tissue-derived cytokines are strongly associated with insulin resistance (40), and the secretion of IL-6 is greater in visceral than abdominal sc adipocytes (41).
It is suggested that discrepancies in the literature regarding the independent relationship between visceral, abdominal sc AT, and insulin resistance may be resolved by a further subdivision of abdominal sc AT according to metabolic characteristics (6, 7). Abdominal sc AT by CT can be subdivided into superficial and deep compartments using the fascia superficialis (42), a rationale for which derives from animal studies indicating that adipocytes within the deep compartment are more metabolically active than superficial adipocytes (22, 23). These earlier findings from animal studies have recently been confirmed by Monzon et al. (43), who report that adipocytes isolated from deep adipose tissue in normal-weight men is higher by comparison with superficial adipocytes. Assuming that the mobilization of nonesterified fatty acids adversely affects insulin action (44, 45), it follows that the deep AT depot would be the stronger predictor of insulin resistance. However, contrary to observations based on isolated adipocytes in vitro, recent evidence obtained by microdialysis in a cohort of normal-weight men suggests that the lipolytic rate of superficial sc AT in the anterior abdominal wall is, in fact, higher than that of deep sc AT located in the posterior abdominal wall (46). Notwithstanding the limitation that microdialysis cannot account for potential variation in blood flow, this latter observation does not support the view that deep abdominal sc AT would be a stronger correlate of insulin resistance.
It is important to note that we did not subdivide abdominal sc AT into deep and superficial depots because, in our hands, the sc fascia (faschia superficialis) was not entirely visible on numerous MRI images; thus, the coefficient of variation (interobserver) for repeat measures was poor. So we used a method similar to that described by Misra et al. (47) wherein a perpendicular line is drawn through the MRI image dividing the sc AT into anterior and posterior depots (Fig. 1). Using this method, it is assumed that the anterior and posterior depots act as surrogates for the superficial and deep AT depots, respectively. To the extent that this is true, in this study subdivision of sc AT did not alter the relationships observed between sc AT per se and insulin resistance. This disagrees with Misra et al. (47), who report that the posterior depot displayed a stronger relationship with insulin-mediated glucose disposal than the anterior AT depot in men. Because we used a similar MRI protocol, it is unlikely that the discrepant findings are explained by methodological differences. It is also unlikely that gender explains the discordant results because we report similar findings in obese men (1).
In this study, cardiovascular fitness (peak VO2) was not a significant correlate of insulin resistance or glucose tolerance. Further, the strength of the relationship between visceral AT and insulin sensitivity was not diminished after statistical control for variation in fitness. These findings are consistent with previous reports wherein visceral AT was more closely related to insulin sensitivity than cardiovascular fitness (3, 13). However, they conflict with those of Toth et al. (2), who report that cardiovascular fitness is a stronger correlate of insulin sensitivity than visceral AT and visceral AT is not a significant predictor of insulin sensitivity after statistically controlling for peak VO2. These discrepant findings may be due to differences in subject selection. Toth et al. (2) recruited both inactive and active individuals, whereas only sedentary subjects were included in our study and those finding an independent relationship between visceral fat and insulin resistance (3, 13). The exclusion of active individuals may have reduced the correlation between peak VO2 and insulin sensitivity by limiting the range of the dependent variable.
The relationship between CT-measured skeletal muscle composition and insulin resistance is unclear. That muscle attenuation is a positive correlate of insulin resistance is reported by some investigators (12, 13, 14) but not others (2, 3, 16). Our findings suggest that skeletal muscle attenuation is not related to insulin resistance in abdominally obese women. Although a rationale that clearly explains the equivocal findings is unknown, it is important to note that muscle attenuation values by CT are not analogous to intramyocellular lipid values obtained by percutaneous biopsy or proton magnetic resonance spectroscopy (48). This is relevant because intramyocellular lipid, but not extramyocellular lipid, is related to insulin resistance (49). Because muscle attenuation values cannot distinguish between the concentration of intra- and extramyocellular lipid, it is not possible to determine whether a potential relationship between intramyocellular lipid and insulin resistance is masked by variation in extramyocellular lipid. This is not a trivial concern and raises questions as to the use of CT to determine the relationship between skeletal muscle lipid and insulin resistance.
In conclusion, the findings of this study confirm that visceral AT is a strong predictor of insulin resistance in a group of abdominally obese, premenopausal women at increased health risk independent of abdominal sc AT (posterior or anterior depots), skeletal muscle composition, and cardiovascular fitness. These observations reinforce the importance of treatment strategies designed to reduce visceral AT. Accordingly, it is important to note that both abdominal sc and visceral AT are substantially reduced in response to modest weight loss independent of gender (19, 28, 50).
Acknowledgments
We thank Jody Dawson, Diana Hall, Cindy Little, SoJung Lee, and Suzy Wong for assistance with this study.
Footnotes
This work was supported by grants from the Canadian Institutes of Health Research and Mars Corporation (to R.R.) and a Heart and Stroke Foundation of Canada Research Trainee Award and Canadian Institutes of Health Research Postdoctoral Fellowship (to I.J.). Any opinions or recommendations in this publication are those of the authors and do not necessarily reflect the view of the U.S. Department of Agriculture.
Abbreviations: AT, Adipose tissue; BMI, body mass index; CT, computed tomography; MRI, magnetic resonance imaging; OGTT, oral glucose tolerance test; VO2, oxygen uptake.
Received April 10, 2002.
Accepted August 5, 2002.
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