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Obesity: Original Article |
Division of Endocrinology, Diabetes and Metabolism (A.M.X., C.C.C.), Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart Center, and Section of Atherosclerosis, Department of Medicine (P.H.J., R.C.H., M.-Y.L., C.M.B.), and Section of Nutrition, Department of Pediatrics (E.O.S.), Baylor College of Medicine, Houston, Texas 77030; and Methodist Wellness Services (K.W.N.), The Methodist Hospital, Houston, Texas 77030
Address all correspondence and requests for reprints to: Christie M. Ballantyne, M.D., Baylor College of Medicine, 6565 Fannin Street, MS A-601, Houston, Texas 77030. E-mail: cmb{at}bcm.tmc.edu.
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Abstract |
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(3.3 ± 0.2 vs. 2.8 ± 0.3 pg/ml; P = 0.004) levels compared with MS– subjects matched for age and body mass index. Plasma adiponectin and TNF- levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. After 4–6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF- concentrations did not change. Thus, increases in plasma levels of adiponectin or reductions in TNF- are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss. |
Introduction |
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30 kg/m2) men and women (5). Furthermore, caloric restriction and weight reduction are beneficial in enhancing insulin action on peripheral tissues (8, 9) and preventing the development of type 2 diabetes (10).
The relationship between insulin resistance and obesity is complex, and accumulated evidence indicates that adipose tissue is a hormonally active system involved in insulin action as well as glucose and lipid metabolism (11). A variety of adipocyte-derived biologically active molecules termed "adipocytokines" have been identified, including leptin, resistin, TNF-, and IL-6, that may contribute to obesity-linked metabolic abnormalities (12, 13, 14, 15). More recently, adiponectin, which is exclusively expressed in adipose tissue and is abundant in human plasma, has been found to be decreased in individuals with obesity, type 2 diabetes, and coronary heart disease (16, 17, 18, 19, 20). Although the physiological role of adiponectin remains unclear, it appears that it may possess insulin-sensitizing and potentially antiinflammatory and antiatherogenic properties (21, 22, 23, 24, 25, 26). Furthermore, different modalities of weight loss as well as peroxisome proliferator-activated receptor-
(PPAR-) agonist therapy have been shown to increase adiponectin levels longitudinally (17, 27, 28). Although the prevalence of the metabolic syndrome increases markedly with severe obesity, many individuals with severe obesity have no clinical manifestations of the metabolic syndrome. Although the diagnostic criteria for ATP III require that an individual have at least three of the five clinical criteria, risk for cardiovascular events increases with the number of clinical criteria present (29). We have previously shown that moderate acute weight loss of 5–7% in 4–6 wk with a very low-calorie diet (VLCD) in obese subjects with the metabolic syndrome is associated with dramatic improvement in all aspects of the metabolic syndrome, although the individuals remained markedly obese (30). In this study, we examined the association between adiponectin and the number of metabolic abnormalities constituting the metabolic syndrome in obese individuals. In addition, we examined the impact of rapid weight loss on levels of adiponectin and other adipocytokines in conjunction with parameters of the metabolic syndrome and measures of insulin resistance in obese individuals with the metabolic syndrome.
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Subjects and Methods |
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Obese individuals (56 women and 24 men; age, 47.1 ± 0.9 yr; BMI, 38.3 ± 0.7 kg/m2) enrolled in a medically supervised rapid weight loss program were recruited for this study during a 12-month period (September 2001 to September 2002). The study protocol was approved by the Baylor College of Medicine Institutional Review Board, and written informed consent was obtained from each individual. The subjects were classified as metabolic syndrome positive (MS+) if they met three or more of the National Cholesterol Education Program ATP III criteria: waist circumference greater than 40 in. (102 cm) for men or greater than 35 in. (88 cm) for women; triglycerides (TGs) of 150 mg/dl (1.69 mmol/liter) or greater; high-density lipoprotein cholesterol (HDL-C) less than 40 mg/dl (1.03 mmol/liter) for men or less than 50 mg/dl (1.29 mmol/liter) for women; blood pressure of 130/85 mm Hg or greater or treated hypertension; and fasting glucose of 110 mg/dl (6.1 mmol/liter) or greater (3). Sequentially enrolled MS+ subjects (n = 40) were compared with 40 obese subjects matched for age and BMI who did not have the metabolic syndrome (MS–) (Table 1
). Of the MS– subjects, 26 had one criterion for the metabolic syndrome (waist), and 14 had two criteria (five with elevated blood pressure, four with low HDL-C, three with elevated TGs, and two with impaired fasting glucose). The study participants did not receive any medication to lose weight or any other medication known to affect glucose tolerance, insulin secretion, or insulin sensitivity during the active weight loss period.
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The weight loss program was offered in a tertiary care medical center to individuals who were either self-referred or referred by healthcare professionals. Weight reduction was induced by a protein-sparing VLCD of approximately 600–800 kcal daily, supervised by a team of physicians, registered dietitians, and behaviorists. It consisted of meal replacement products (Nutrimed-Plus; Robard Corp., Mount Laurel, NJ; each serving contained 200 kcal, 6 g of fat, 26 g of protein, and 10 g of carbohydrate) alone or in combination with lean beef, fish, or poultry. Daily protein intake was calculated as 1.5 g per kilogram of predetermined goal weight, and daily fluid intake was at a minimum of 2 liters. Entry criteria for the program included age greater than 18 yr and a BMI of 30 kg/m2 or greater. Exclusion criteria were known eating disorder, cancer, use of lithium or corticosteroids, type 1 diabetes, active inflammatory bowel disease, active gout, liver disease, cardiovascular event within the past 3 months, endocrine causes of obesity, and pregnancy. Diuretic medications were discontinued before entering the program.
Anthropometric and biochemical measurements
All subjects were evaluated with a series of anthropometric measurements and tests for hematology, biochemistry, and hormonal functions after an overnight fast. None of the subjects was on any calorie-restricting diet at the baseline evaluation. Biochemical measurements were performed at baseline for all 80 individuals and prospectively for the 40 MS+ subjects after 4–6 wk of active weight loss. Measurements of insulin resistance were obtained using the homeostasis model assessment [HOMA-IR = fasting glucose (mg/dl) x fasting insulin (µU/ml)/22.5], as described previously (31).
All biochemical measurements were performed on frozen plasma samples obtained by centrifugation of freshly drawn blood (3000 x g for 20 min at 4 C) and subsequent storage at –70 C. Blood lipid profiles, including total cholesterol, HDL-C, calculated low-density lipoprotein cholesterol, TGs, and nonesterified fatty acids (NEFAs), as well as plasma -glutamyltransferase (GGT), concentrations were determined by enzymatic assays using a Hitachi 911 auto-analyzer (Roche Diagnostics, Indianapolis, IN). Plasma levels of adiponectin were measured by RIA according to the manufacturer’s protocol (Linco Research, Inc., St. Charles, MO). High-sensitivity C-reactive protein (hs-CRP) was assessed by the Denka Seiken (Tokyo, Japan) assay, which has been validated against the Dade Behring method. Plasma levels of leptin and insulin were determined on a Luminex-100 multianalyte profiling system using commercially available immunoassay panels (Linco Research, Inc.). Circulating TNF- levels were measured by high-sensitivity ELISA (R&D Systems, Inc., Minneapolis, MN).
Statistical analyses
Unless stated otherwise, data are expressed as the means ± SE. Statistical analysis was made using SPSS version 11.5 (SPSS Inc., Chicago, IL). Because variables were often not normally distributed, group comparison was performed by the Mann-Whitney nonparametric test, and the Kruskal-Wallis test was used for comparison of more than two independent groups. Correlations between different variables were performed by the Spearman rank correlation test. Comparison of variables before and after weight loss intervention in the metabolic syndrome group (MS+) was assessed by the Wilcoxon signed rank test. The independent contribution of each variable was assessed by simultaneously including other variables as covariates by general linear model univariate analysis. Interactions were assessed in the general linear model, and none were detected. The TNF- data were log transformed to satisfy the assumptions of the general linear model. Multiple logistic regression was used to assess adiponectin as an independent predictor of the metabolic syndrome, while adjusting for other variables. P < 0.05 was considered to be statistically significant for all analyses.
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Results |
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Plasma adiponectin level was significantly lower in MS+ subjects compared with age- and BMI-matched MS– individuals (7.6 ± 0.6 vs. 10.4 ± 0.6 µg/ml; P = 0.003) (Table 1
; Fig. 1A). When the MS+ and MS– groups were compared with respect to adiponectin and other variables, the difference remained significant after adjustment for age (P = 0.001), gender (P = 0.003), BMI (P = 0.002), insulin (P = 0.01), HOMA-IR (P = 0.01), leptin (P = 0.002), and all these together (P = 0.01). Although plasma adiponectin concentration was higher in women compared with men in the overall group, consistent with observations by others, this difference did not reach statistical significance (9.4 ± 0.6 vs. 8.0 ± 0.8 µg/ml; P = 0.1). There was a stepwise decrease in plasma adiponectin levels in parallel to the number of metabolic syndrome components present, and subjects with four or five components of the metabolic syndrome had the lowest adiponectin concentration, 6.5 ± 0.9 µg/ml (Table 2; Fig. 1B). This stepwise decrement in adiponectin levels remained significant even after adjustment for insulin (P = 0.01) and HOMA (P = 0.01). Using multiple logistic regression, we calculated that the odds ratio (OR) of the metabolic syndrome as predicted by adiponectin was 0.83 [95% confidence interval (CI), 0.73–0.94; P = 0.004], indicating that there was a 17% decrease in the odds of having the metabolic syndrome for each 1-µg/ml increment in adiponectin levels. The OR did not change appreciably after adjustment for weight and BMI (OR, 0.85; 95% CI, 0.75–0.97; P = 0.02). Furthermore, the ORs were not substantially different when adjusted for waist (OR, 0.81; 95% CI, 0.70–0.94; P = 0.005), blood pressure (OR, 0.77; 95% CI, 0.65–0.90; P = 0.002), glucose (OR, 0.84; 95% CI, 0.74–0.95; P = 0.009), and TG (OR, 0.81; 95% CI, 0.67–0.98; P = 0.03) but became nonsignificant after adjusting for HDL-C (P = 0.3).
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levels were significantly higher in the MS+ group compared with the MS– group (3.3 ± 0.2 vs. 2.8 ± 0.3 pg/ml; P = 0.004) (Fig. 2A). This difference remained significant after adjustment for age (P = 0.02), BMI (P = 0.04), insulin (P = 0.05), and leptin (P = 0.02) but not when adjusted for gender (P = 0.1). Levels of hs-CRP were not significantly different between the two study groups. There was a stepwise increase in plasma TNF- levels in parallel to the number of metabolic syndrome components present (Fig. 2B).
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In univariate analysis of baseline variables in all subjects (MS+ and MS–), plasma adiponectin was inversely correlated with surrogate measures of total and visceral adiposity (weight and waist circumference) and was reciprocally associated with insulin, HOMA-IR, and all traits of the metabolic syndrome, except blood pressure (Table 3). Furthermore, plasma adiponectin was inversely correlated with hs-CRP but not with TNF-, NEFA, or leptin. Plasma adiponectin had the strongest correlation to HDL-C levels of all variables examined (Fig. 3).
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was positively correlated with measures of adiposity (weight and waist circumference) and inversely correlated with insulin and HOMA-IR. There were also significant associations between TNF-, TG, and HDL-C (Table 3). Effects of rapid weight loss on anthropometric and metabolic parameters in subjects with the metabolic syndrome
At 4–6 wk of intervention (mean follow-up of 36 d), the subjects lost, on average, 7% of their initial weight (17.6 ± 1.2 lbs). Values at baseline and 4–6 wk after active weight reduction for all measured variables are displayed in Table 4. All components of the metabolic syndrome, except HDL-C, improved significantly. HDL-C decreased significantly, as seen in other studies with acute weight loss through caloric restriction (32, 33). Plasma levels of insulin, HOMA-IR, leptin, and hs-CRP decreased significantly, and changes in HOMA-IR and hs-CRP correlated significantly with weight loss. In contrast, adiponectin, NEFA, and TNF- levels did not change significantly after 4–6 wk of rapid weight loss.
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Discussion |
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, and IL-6 (11, 14, 15, 34). Of these proteins, adiponectin has recently been proposed as an important mediator of insulin action and glucose metabolism (13). Adiponectin has been reported to be decreased in obesity and type 2 diabetes and to be inversely correlated with insulin and TG levels and positively correlated with HDL-C levels (16, 17). The present study confirms and extends these associations by demonstrating that plasma adiponectin levels are significantly lower in obese individuals with the metabolic syndrome when compared with obese individuals, matched for age and BMI, who do not have the metabolic syndrome. Furthermore, stepwise decreases in adiponectin were observed with increasing numbers of metabolic syndrome components. The predictive ability of adiponectin to distinguish the MS+ from the MS– obese subjects remained significant after adjusting for both weight and BMI, suggesting that adiponectin may contribute to the expression of the metabolic syndrome phenotype independent of total adiposity. When each component of the metabolic syndrome was introduced separately as a covariate, the predictive ability of adiponectin to distinguish the MS+ from the MS– obese subjects did not change substantially after adjusting for each variable but became nonsignificant after adjusting for HDL-C, suggesting an important role of adiponectin in modulating HDL metabolism.
Surprisingly, no change in adiponectin levels was observed after 4–6 wk of weight loss. Despite the persistence of obesity, there was a marked improvement in some aspects of the metabolic syndrome, such as blood pressure, glucose, and TG, but no significant change in TNF- and only a modest (statistically but not clinically significant) drop in hs-CRP. As reported previously with acute weight loss associated with ongoing caloric restriction, HDL-C decreased.
There are several reports suggesting that adiponectin directly modulates glucose tolerance and peripheral tissue insulin sensitivity, possibly through AMP kinase activation (35, 36). Weight loss studies in humans have been used to support the hypothesis that increases in adiponectin may mediate improvement in insulin action and carbohydrate metabolism observed with weight loss (17, 28, 37). Three studies have demonstrated that a 10–22% weight reduction in obese individuals with VLCD or bariatric surgery was associated with a 36–51% increase in adiponectin levels (17, 28, 37). One study of 22 patients showed a substantial increase in adiponectin levels after 2 months of VLCD with an average weight loss of more than 10% (28), whereas the other studies with bariatric surgery observed improved adiponectin levels with even greater weight loss (17, 37). In contrast, in our study of acute VLCD-induced weight loss, which specifically assessed adipocytokines in an obese population with the metabolic syndrome, we observed marked improvements in glucose, insulin levels, and HOMA-IR within 4–6 wk that were not associated with any significant change in adiponectin levels. In general, expression of adiponectin in plasma correlates well with expression in adipose tissue. Therefore, it is unlikely that the improvements in glucose, insulin, and HOMA-IR, which are all reflective of improved whole-body insulin sensitivity, were related to changes in adiponectin. Our data are consistent with the data from a 6-month weight loss study that achieved a 6% reduction in BMI with diet and exercise and had no significant change in adiponectin levels but did have modest significant reductions in insulin (15%) and glucose (6%) (38). This 6-month study differs from our study in numerous aspects: TG was not reported, patients were not selected on the basis of the metabolic syndrome, average BMI was lower (32 vs. 37), and only postmenopausal women were included.
The data from our study are consistent with a proposed model in which reductions in adiponectin levels reflect adipocyte dysregulation or malfunction rather than being causative of insulin resistance. Although unlikely, we cannot exclude the possibility that specific metabolic consequences induced by the VLCD resulted in the lack of change in adiponectin. In the same context, one potential limitation of our study is the lack of an isocaloric steady state at the follow-up evaluation, because subjects were in persistent caloric deficit at that time point. In agreement with our observations, Abbasi et al. (39) have recently shown that there is a significant overlap in adiponectin values between insulin-sensitive and insulin-resistant individuals (assessed by steady state plasma glucose concentration at the end of a 180-min infusion of octreotide, insulin, and glucose) and that a low adiponectin concentration is not uncommon in insulin-sensitive subjects. Furthermore, intervention modalities known to increase peripheral glucose disposal and insulin sensitivity, such as exercise or metformin therapy, do not alter adiponectin levels (40, 41). Thiazolidinediones or PPAR- agonists have been shown to increase adiponectin levels in vitro and in vivo, although the exact mechanism for this action has not been elucidated (27, 42, 43). It has been suggested that the up-regulation of PPAR- transcriptional activity and the resulting effect on adipocyte differentiation positively influences adiponectin secretion independent of the insulin-sensitizing properties of these compounds (41). An emerging paradigm proposed to explain the link between excess adiposity and insulin resistance involves the metabolic diversion and ectopic storage of energy substrates (predominantly TG) from adipose to nonadipose tissues, particularly muscle and liver (44, 45). Our results are consistent with this hypothesis, because early mobilization of intracellular lipid from muscle (46) and liver (47) in response to rapid weight loss would be expected to enhance insulin action and decrease plasma levels of insulin, glucose, TG, and GGT acutely, by augmenting substrate transport and utilization (9, 48), despite the fact that our patients remained markedly obese. It is possible that a substantially greater and sustained weight reduction is necessary to correct altered adipocyte function, which could be determined by increased levels of adiponectin and reduced levels of TNF- and NEFA (49).
Our study confirmed the association between adiponectin and dyslipidemia in nondiabetic obese subjects, demonstrating a reciprocal association with TG and a strong positive correlation with HDL-C. Although the precise mechanism for this association is unknown, it has been postulated that insulin resistance and/or hyperinsulinemia might offer an explanation in the case of insulin-resistant states, such as obesity, type 2 diabetes, and the metabolic syndrome. Interestingly, in our study the strong positive correlation between adiponectin and HDL-C remained significant even after adjusting for all components of the metabolic syndrome, insulin resistance, and adiposity measures both at baseline and after weight reduction. The adiponectin receptors AdipoR1 and AdipoR2 are associated with PPAR- activity and fatty acid oxidation (50), and thus the strong positive correlation between adiponectin and HDL-C levels may be secondary to modulation of HDL metabolism by adiponectin (51).
Adiponectin may also play a role in regulating inflammatory responses. We confirmed the reciprocal association between adiponectin and hs-CRP. Although we did not find a clear association of adiponectin and TNF-, which differs from in vitro data (52, 53), the relationship between TNF- and adiponectin in vivo may be complex because it has been suggested that TNF- may regulate adiponectin expression through autocrine and paracrine pathways (37). TNF-, in addition to adiponectin, has been postulated to play a causal role in the development of obesity-induced insulin resistance. To our knowledge, this is the first study demonstrating the stepwise increase in TNF- levels in parallel to the number of metabolic syndrome components present. In vitro studies have shown that adiponectin can decrease endothelial-leukocyte adhesion through inhibition of endothelial nuclear factor-
B signaling (18, 23). Mice deficient in adiponectin have increased neointimal proliferation after injury and increased atherosclerosis (24).
In summary, we have shown that adiponectin is inversely associated with the expression of the metabolic syndrome and its individual traits in obese individuals, with a stepwise decrease in adiponectin levels with greater numbers of metabolic syndrome-defining criteria. Rapid weight loss through ongoing caloric restriction (7%, on average, over 4–6 wk) by a protein-sparing VLCD in obese individuals with the metabolic syndrome led to impressive reductions in insulin, glucose, TG, and blood pressure without the expected concomitant change in adiponectin or TNF- and only a modest reduction in hs-CRP. These data are supportive of a proposed model that relates rapid weight loss to early mobilization of ectopic fat from liver and skeletal muscle, thereby reducing GGT, TG, glucose, insulin, and HOMA-IR, although subjects remained markedly obese after weight loss. We postulate that the lack of change in adiponectin and TNF- and the very modest decrease in hs-CRP reflect persistent adipocyte dysregulation despite initiation of a rapid weight loss intervention and that a critical amount of total adiposity must be lost before the adipocyte resumes a more balanced function. The association of adiponectin with HDL and inflammation merits additional studies in humans to examine whether pharmacological manipulation of adiponectin levels would favorably influence these parameters.
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Footnotes |
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Abbreviations: ATP III, Adult Treatment Panel III; BMI, body mass index; CI, confidence interval; GGT, -glutamyltransferase; HDL-C, high-density lipoprotein cholesterol; HOMA-IR, insulin resistance of the homeostasis model assessment; hs-CRP, high-sensitivity C-reactive protein; MS+, metabolic syndrome positive; MS–, metabolic syndrome negative; NEFA, nonesterified fatty acid; OR, odds ratio; PPAR-, peroxisome proliferator-activated receptor-; TG, triglyceride; VLCD, very low-calorie diet.
Received October 20, 2003.
Accepted February 24, 2004.
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