Absence of an Effect of Liposuction on Insulin Action and Risk Factors for Coronary Heart Disease
Samuel Klein, M.D., Luigi Fontana, M.D., Ph.D., V. Leroy Young, M.D., Andrew R. Coggan, Ph.D., Charles Kilo, M.D., Bruce W. Patterson, Ph.D., and B. Selma Mohammed, M.D., Ph.D.
Background Liposuction has been proposed as a potential treatmentfor the metabolic complications of obesity. We evaluated theeffect of large-volume abdominal liposuction on metabolic riskfactors for coronary heart disease in women with abdominal obesity.
Methods We evaluated the insulin sensitivity of liver, skeletalmuscle, and adipose tissue (with a euglycemic–hyperinsulinemicclamp procedure and isotope-tracer infusions) as well as levelsof inflammatory mediators and other risk factors for coronaryheart disease in 15 obese women before and 10 to 12 weeks afterabdominal liposuction. Eight of the women had normal glucosetolerance (mean [±SD] body-mass index, 35.1±2.4),and seven had type 2 diabetes (body-mass index, 39.9±5.6).
Results Liposuction decreased the volume of subcutaneous abdominaladipose tissue by 44 percent in the subjects with normal glucosetolerance and 28 percent in those with diabetes; those withnormal oral glucose tolerance lost 9.1±3.7 kg of fat(18±3 percent decrease in total fat, P=0.002), and thosewith type 2 diabetes lost 10.5±3.3 kg of fat (19±2percent decrease in total fat, P<0.001). Liposuction didnot significantly alter the insulin sensitivity of muscle, liver,or adipose tissue (assessed by the stimulation of glucose disposal,the suppression of glucose production, and the suppression oflipolysis, respectively); did not significantly alter plasmaconcentrations of C-reactive protein, interleukin-6, tumor necrosisfactor , and adiponectin; and did not significantly affect otherrisk factors for coronary heart disease (blood pressure andplasma glucose, insulin, and lipid concentrations) in eithergroup.
Conclusions Abdominal liposuction does not significantly improveobesity-associated metabolic abnormalities. Decreasing adiposetissue mass alone will not achieve the metabolic benefits ofweight loss.
Abdominal obesity, manifested by increased waist circumference,increased abdominal subcutaneous fat, and increased visceralfat, is associated with insulin resistance and other metabolicrisk factors for coronary heart disease.1 Although both theabdominal subcutaneous fat mass and the visceral fat mass areassociated with insulin resistance,2 it is not known whetherone or both of these fat depots are actually involved in thepathogenesis of insulin resistance or whether they are simplyassociated with the metabolic complications of obesity.
Diet-induced weight loss improves the metabolic complicationsof abdominal obesity. However, successful long-term weight managementis difficult to achieve, and the majority of obese persons wholose weight by implementing lifestyle changes regain their lostweight over time.3 Frustration with the efficacy of currentobesity therapies has led to increased interest in alternativeapproaches. Recently, it has been suggested that liposuction,which can remove large amounts of body fat, is a potential treatmentfor the metabolic complications of obesity.4,5,6,7
Liposuction, also known as lipoplasty or suction-assisted lipectomy,is the most common aesthetic surgical procedure performed inthe United States; nearly 400,000 procedures are performed annually.8Recent advances in liposuction techniques now make it possibleto remove considerable amounts of subcutaneous adipose tissue.9Therefore, abdominal liposuction provides a unique opportunityto evaluate the importance of subcutaneous abdominal fat inthe pathogenesis of insulin resistance and in the risk of coronaryheart disease in persons with abdominal obesity. However, themetabolic effects of liposuction are unclear because the resultsof studies have varied.5,6,7,10,11 The interpretation of datafrom such studies is confounded by lifestyle and weight changesthat occurred among the subjects after liposuction was performed,by variations in the volume of adipose tissue removed and thesite of its removal, by differences in the methods used to assessinsulin sensitivity, and by differences in the subjects' baselineweight and insulin sensitivity.
The purpose of the present study was to determine the effectof large-volume abdominal liposuction on insulin sensitivityin liver, skeletal muscle, and adipose tissue (evaluated withthe use of a two-stage euglycemic–hyperinsulinemic clampprocedure, in conjunction with stable isotope-tracer infusions)and on risk factors for coronary heart disease (waist circumference,blood pressure, plasma lipid concentrations, and serum markersof inflammation) in women with abdominal obesity. Obese womenwith normal glucose tolerance and those with type 2 diabeteswere studied to assess the potential beneficial effects of liposuctionin persons with moderate or severe insulin resistance.
Methods
Subjects
We studied eight women with abdominal obesity (waist circumference,more than 100 cm) who had normal oral glucose tolerance butmoderate insulin resistance (mean [±SD] age, 42±3years) and seven women with abdominal obesity who had type 2diabetes and more severe insulin resistance (age, 52±3years). The women with type 2 diabetes were being treated witha combination of two or three oral hypoglycemic medications(glipizide, glyburide, glimepiride, rosiglitazone, pioglitazone,or metformin). They were consecutive eligible patients who werescheduled to undergo large-volume liposuction performed by oneof the authors and were enrolled between November 2001 and March2003. No evidence of other serious illnesses or organ dysfunctionwas found after the subjects had completed a comprehensive medicalevaluation, which included a history and physical examination,electrocardiography, standard blood and urine tests, and a two-houroral glucose-tolerance test. All the subjects had had a stableweight (with fluctuations of not more than 2 percent of thebody weight) for at least two months and had been sedentary(exercising for less than one hour per week) for at least sixmonths before entering the study. Each subject provided writteninformed consent before participating, and the study was approvedby the human studies committee of Washington University Schoolof Medicine, St. Louis.
Study Design
Assessments of Body Composition
Each subject's body composition was assessed within nine daysbefore liposuction. Total body fat and fat-free mass were determinedby dual-energy x-ray absorptiometry (Hologic QDR 1000/w). Abdominaland thigh fat masses were quantified by means of magnetic resonanceimaging (Siemens). Eight 10-mm-thick slice images were obtainedboth at the L4–L5 interspace and at the superior borderof the medial condyle of the tibia and were analyzed for subcutaneousand intracompartmental (abdomen or muscle) fat content.
Euglycemic–Hyperinsulinemic Clamp Protocol
The subjects were admitted to the General Clinical ResearchCenter (Washington University School of Medicine) and consumeda standard meal (55 percent carbohydrate, 30 percent fat, and15 percent protein) containing 16 kcal per kilogram of fat-freemass at 7 p.m. At 8 p.m., they consumed a 240-kcal liquid snack(Ensure, Ross Laboratories). The last dose of hypoglycemic medicationwas taken on the day of admission. At 5 a.m. the next morning,after the subjects had fasted overnight, catheters were insertedinto a radial artery for blood sampling and into an antecubitalvein for the infusion of insulin, dextrose, and tracers. At7 a.m., a primed (priming dose, 4.1 mg per kilogram [22.5 µmolper kilogram]), constant infusion of [6,6-2H2]glucose (0.46mg per minute per kilogram [0.25 µmol per minute per kilogram])was started, followed at 9 a.m. by a primed (priming dose, 116µg per kilogram [1.2 µmol per kilogram]), constantinfusion of [1,1,2,3,3-2H5]glycerol (7.8 µg per minuteper kilogram [0.08 µmol per minute per kilogram]) anda constant infusion of [2,2-2H2]palmitate (9.0 µg perminute per kilogram [0.035 µmol per minute per kilogram]).
After infusion of the tracer for 3.5 hours (the basal period),a two-stage euglycemic–hyperinsulinemic clamp protocolwas initiated and continued for 6 hours. Euglycemia (a glucoselevel of approximately 100 mg per deciliter [5.6 mmol per liter])was maintained by variable-rate infusion of 20 percent dextrosecontaining approximately 2.5 percent [6,6-2H2]glucose. Duringstage 1 of the clamp protocol (from hour 3.5 to hour 6.5 ofthe tracer-infusion study), insulin was infused at a rate of20 mU per square meter of body-surface area per minute afterinitiation by a two-step priming dose of insulin for 10 minutes(80 mU per square meter per minute for 5 minutes, followed by40 mU per square meter per minute for 5 minutes). During stage2 of the clamp protocol (hour 6.5 to hour 9.5 of the tracer-infusionstudy), insulin was infused at a rate of 50 mU per square meterper minute after initiation by a two-step priming dose of insulinfor 10 minutes (200 mU per square meter per minute for 5 minutes,followed by 100 mU per square meter per minute for 5 minutes).
These insulin infusion rates result in plasma insulin concentrationsthat provide an optimal range for evaluating the effect of insulinon glucose production and lipolysis (stage 1) and on glucosedisposal (stage 2). The rates of tracer infusions were decreasedduring each stage of the clamp protocol to account for the expectedchanges in endogenous substrate metabolism. Blood samples wereobtained before the beginning of the tracer infusion to determinebaseline plasma concentrations of C-reactive protein, cytokines,lipids, substrates, and hormones and to determine backgroundsubstrate tracer-to-tracee ratios. Blood was collected every10 minutes during the last 30 minutes of the basal period andduring the last 30 minutes of each stage of the euglycemic–hyperinsulinemicclamp procedure to determine plasma substrate and insulin concentrationsand substrate tracer-to-tracee ratios (i.e., the ratios of labeledto unlabeled substrate in plasma). Plasma was separated by centrifugationwithin 30 minutes after collection and stored at –70°Cuntil final analyses were performed.
Liposuction
Approximately one week after completing the euglycemic–hyperinsulinemicclamp procedure, each subject underwent large-volume tumescentliposuction, defined as the removal of more than 4 liters ofaspirate.12 This procedure involves subcutaneous injection ofa large volume of Ringer's lactate containing dilute epinephrine(1:1,000,000) to induce vasoconstriction and thus to minimizebleeding. All liposuction procedures were performed by one ofthe authors, who primarily removed superficial and deep subcutaneousabdominal fat. In addition, smaller amounts of fat were removedfrom the arms, flanks, hips, or thighs in five subjects withoutdiabetes and in four subjects with diabetes. A total of 16±1liters (12±1 liters from the upper body and 4±2liters from the lower body) of Ringer's lactate plus epinephrine-infiltratedadipose tissue was aspirated from the subjects with normal oralglucose tolerance and a total of 17±2 liters (16±2liters from the upper body and 1±1 liters from the lowerbody) was aspirated from the subjects with type 2 diabetes.
Evaluation after Liposuction
Subjects were instructed to resume their normal lifestyle afterthe initial recovery period and to weigh themselves weekly athome. Each subject was contacted by one of the investigatorsat least once every week by phone to review her medical conditionand to reinforce the importance of maintaining her usual foodintake and physical activity and to maintain a stable body weight.No serious complications occurred in any subject, and all wereable to return to their usual lifestyle within 10 days afterliposuction. For each of the seven subjects with type 2 diabetes,hypoglycemic medications were regulated by the subject's physician.In six of them, the medications were not changed after the clampprocedure; in one, rosiglitazone (4 mg per day) was stopped,and glipizide and metformin were continued.
All the studies performed before liposuction were repeated 10to 12 weeks after liposuction. The 10-to-12-week delay was intendedto eliminate the confounding effects of postsurgical inflammationon our study end points.
Analyses of Blood Samples
Plasma glucose concentrations were determined with use of aglucose analyzer (Yellow Springs Instruments), and plasma fattyacid concentrations were quantified by means of gas chromatography.13Plasma insulin and leptin concentrations were measured by radioimmunoassay(Linco Research). Plasma lipid concentrations were determinedenzymatically (Roche/Hitachi 747 Analyzer, Roche Diagnostics).Enzyme-linked immunosorbent assay kits were used to measureplasma C-reactive protein (American Laboratory Products), adiponectin(B-Bridge International), interleukin-6, and tumor necrosisfactor (Quantakine High Sensitive, R&D Systems). Plasmaglucose, glycerol, and palmitate tracer-to-tracee ratios weredetermined with the use of gas chromatography–mass spectrometry.13,14
Calculations
A physiologic and isotopic steady state was achieved duringthe last 30 minutes of the basal period and the insulin-infusionperiod, so the rates of appearance and disappearance of substratewere calculated as the tracer infusion rate divided by the tracer-to-traceeratio.15 The rate of appearance of total free fatty acid wascalculated by dividing the rate of appearance of palmitate bythe percent contribution of palmitate to total plasma free fattyacids.
Statistical Analysis
The number of subjects to be enrolled was determined as theestimated number needed for the study to detect a statisticallysignificant effect of liposuction on glucose kinetics with apower of at least 0.8, if the subjects had lost a similar amountof body fat by dieting. Data on subjects with diabetes and thosewithout diabetes were analyzed separately. A two-way analysisof variance (time by clamp stage) with repeated measures wasused to compare the effects of liposuction on basal and insulin-mediatedsubstrate metabolism. Changes in body composition and risk factorsfor coronary heart disease were assessed by means of Student'st-test for paired samples. All reported P values are two-sided,and a P value of 0.05 or less was considered to indicate statisticalsignificance.
Results
Body Composition
Liposuction decreased body weight and body-mass index (the weightin kilograms divided by the square of the height in meters)because of a marked decrease in body fat (Table 1). Ten to 12weeks after surgery, the mass of body fat had decreased by 9.1±3.7kg from baseline (18±3 percent of the total fat mass,P=0.002) in the subjects with normal oral glucose toleranceand by 10.5±3.3 kg (19±2 percent of the totalfat mass, P<0.001) in the subjects with type 2 diabetes.The decrease in measured fat mass was consistent with the amountof fat aspirated during liposuction; approximately 60 percentof the liposuction aspirate was composed of fat. The decreasein body fat was greater than the total decrease in body weight,however, because of abdominal-tissue edema, which often persistsfor months after liposuction.16 The measured truncal fat-freemass, which included tissue fluid, increased from 24.5±2.7kg to 27.4±3.0 kg (P<0.001) in the two groups overall.Liposuction decreased the volume of subcutaneous abdominal adiposetissue by 44 percent in the subjects with normal glucose toleranceand 28 percent in those with diabetes, whereas the volumes ofvisceral adipose tissue and thigh adipose tissue did not changesignificantly (Figure 1 and Table 1).
Figure 1. Photographs and Abdominal Magnetic Resonance Images Obtained before and after Liposuction.
The photographs of one study subject and images of another show the large amount of subcutaneous abdominal fat removed by liposuction.
Circulating Inflammatory Mediators and Other Risk Factors for Coronary Heart Disease
Liposuction caused a decrease in waist circumference in bothgroups, but it did not significantly alter other risk factorsfor coronary heart disease (Table 2). Liposuction also decreasedplasma leptin concentrations in both groups, but it did notsignificantly alter the concentrations of other circulatingcytokines or of C-reactive protein (Table 3).
Table 3. Effects of Liposuction on Mediators of Inflammation in Obese Women with Normal Glucose Tolerance or Type 2 Diabetes.
Substrate Kinetics and Insulin Sensitivity
In the subjects with normal glucose tolerance, plasma insulinconcentrations after liposuction were similar to those beforeliposuction for both stages 1 and 2 of the clamp procedure (stage1 and 2 values before liposuction, 44±7 and 90±12µU per milliliter [264±42 and 540±72 pmolper liter], respectively; stage 1 and 2 values after liposuction,42±5 and 89±6 µU per milliliter [252±30and 534±48 pmol per liter], respectively); the same wastrue of the subjects with type 2 diabetes (stage 1 and 2 valuesbefore liposuction, 40±2 and 86±7 µU permilliliter [240±12 and 516±42 pmol per liter],respectively; stage 1 and 2 values after liposuction, 41±3and 86±6 µU per milliliter [246±18 and 516±36pmol per liter], respectively). Insulin infusion during stage1 caused the expected decreases in the rates of appearance ofglucose, glycerol, and free fatty acids, and insulin infusionduring stage 2 caused the expected increase in the rate of disappearanceof glucose both in subjects with normal glucose tolerance andin those with type 2 diabetes (Figure 2 and Figure 3). Ratesof appearance of glucose, glycerol, and free fatty acid andthe rate of disappearance of glucose during basal conditionsand during each stage of the clamp procedure were not significantlydifferent before and after liposuction in either group (Figure 2and Figure 3).
Figure 2. Mean Rates of Appearance and Disappearance of Glucose and Rates of Appearance of Glycerol and Free Fatty Acids in the Basal State and during the Euglycemic–Hyperinsulinemic Clamp Procedure in Obese Women with Normal Glucose Tolerance before and after Liposuction.
Stage 1 of the euglycemic–hyperinsulinemic clamp procedure involved the infusion of insulin at a rate of 20 mU per square meter of body-surface area per minute, and stage 2 involved the infusion of insulin at a rate of 50 mU per square meter per minute. The T bars represent the SD.
Figure 3. Mean Rates of Appearance and Disappearance of Glucose and Rates of Appearance of Glycerol and Free Fatty Acids in the Basal State and during the Euglycemic–Hyperinsulinemic Clamp Procedure in Obese Women with Diabetes before and after Liposuction.
Stage 1 of the euglycemic–hyperinsulinemic clamp procedure involved the infusion of insulin at a rate of 20 mU per square meter of body-surface area per minute, and stage 2 involved the infusion of insulin at a rate of 50 mU per square meter per minute. The T bars represent the SD.
Discussion
In the present study, we evaluated the effects of large-volumeliposuction on insulin sensitivity and risk factors for coronaryheart disease in women with abdominal obesity who had eithermoderate insulin resistance and normal glucose tolerance ormore severe insulin resistance and type 2 diabetes. Weight stabilitywas carefully maintained before and after liposuction to eliminatethe confounding effects of changes in energy balance on thestudy end points. Our data show that the aspiration of largeamounts of subcutaneous abdominal adipose tissue resulted ina considerable decrease in body weight, waist circumference,and plasma leptin concentrations but did not have a significanteffect on insulin sensitivity in skeletal muscle (assessed asthe stimulation of glucose uptake), in the liver (assessed asthe suppression of glucose production), or adipose tissue (assessedas the suppression of lipolysis). In addition, liposuction hadno significant effects on other risk factors for coronary heartdisease, including blood pressure; fasting plasma glucose, insulin,and lipid concentrations; and concentrations of plasma markersof inflammation and insulin resistance (C-reactive protein,tumor necrosis factor , interleukin-6, and adiponectin).
The amount of fat removed by liposuction in our subjects isequivalent to the weight loss achieved by optimal behavioraland pharmacologic treatments.3 A total weight loss of approximately12 percent of body weight would be required to achieve the fatloss resulting from liposuction in our study subjects, becauseabout 75 percent of the decrease in body-mass that occurs bydieting is due to loss of body fat.17 This amount of weightloss usually results in marked improvement in the metabolicabnormalities associated with obesity and improves insulin sensitivity,18blood pressure,19 and concentrations of serum lipids20 and circulatingmarkers of inflammation.21 Therefore, it is striking that theamount of fat loss achieved by liposuction in our diabetic andnondiabetic subjects did not improve any of these metabolicvariables.
The absence of an apparent therapeutic effect of liposuctionprovides insight into the mechanism by which conventional therapyfor obesity — namely, diet, pharmacotherapy, and bariatricsurgery — improves insulin sensitivity. Our results suggestthat induction of a negative energy balance, not simply a decreasein the mass of adipose tissue, is critical for achieving themetabolic benefits of weight loss. Even small amounts of weightloss induced by a negative energy balance affects many variablespertaining to body-fat composition and lipid metabolism —variables that probably contribute to the metabolic abnormalitiesassociated with obesity.22,23,24,25 Weight loss decreases visceralfat mass,26 intramyocellular fat,27 intrahepatic fat,28 fat-cellsize,29 and the rate of release of fatty acids from adiposetissue.30 In contrast, liposuction removes subcutaneous abdominalfat and reduces the total number of body fat cells, withoutaltering visceral fat mass,31 the size of the remaining fatcells,10 intramyocellular fat, or intrahepatic fat.
The results of the present study also show that removing a largeamount of abdominal subcutaneous fat by liposuction does notsignificantly affect the levels of circulating mediators ofinflammation that are probably involved in the development ofinsulin resistance and coronary heart disease.32 Adipose tissueis now recognized as an important endocrine organ that producesseveral bioactive proteins, including interleukin-6, tumor necrosisfactor , and adiponectin. Interleukin-6 and tumor necrosis factor can cause insulin resistance and atherosclerosis by impairinginsulin signaling, stimulating lipolysis and fatty acid release,increasing hepatic synthesis of C-reactive protein, and increasingsystemic inflammation,32,33,34 whereas the production of adiponectinby adipose tissue can improve insulin sensitivity and inhibitvascular inflammation.35,36 Fat loss achieved by conventionalobesity treatments decreases the plasma concentrations of C-reactiveprotein, interleukin-6, and tumor necrosis factor 37,38 andincreases the concentration of adiponectin39; in contrast, liposuctionin our subjects did not significantly change the plasma concentrationsof any of these markers. However, fat removal by liposuctiondid decrease the plasma leptin concentration, which is a markerof adipose-tissue mass.40 These results suggest that a negativeenergy balance influences adipocyte and monocyte activationand the gene expression of selected cytokines, but that long-termleptin production is influenced primarily by total fat mass.
The results of the present study suggest that abdominal liposuctionshould not, by itself, be considered a clinical therapy forobesity. Aspiration of large amounts of subcutaneous abdominalfat in women with abdominal obesity may have cosmetic benefits,but the procedure does not significantly improve insulin sensitivityin the liver, skeletal muscle, or adipose tissue; serum concentrationsof markers of inflammation; or other risk factors for coronaryheart disease. These findings offer important insights intothe mechanisms responsible for the metabolic benefits observedwith moderate diet-induced weight loss, which decreases hepaticand muscle fat content, fat-cell size, visceral fat mass, andcirculating concentrations of proinflammatory cytokines. Theeffects of a negative energy balance on specific endogenoustriglyceride depots and inflammation, which are not alteredby liposuction, may be necessary to achieve many of the clinicalbenefits of therapy for obesity.
Supported by grants (HD 01459, DK 37948, RR-00954 [to the BiomedicalMass Spectrometry Resource], RR-00036 [to the General ClinicalResearch Center], and DK 56341 [to the Clinical Nutrition ResearchUnit]) from the National Institutes of Health.
We are indebted to the nursing staff of the General ClinicalResearch Center for their help in performing the studies, toFreida Custodio and Junyoung Kwon for their technical assistance,and to the subjects for their participation in the study.
Source Information
From the Center for Human Nutrition, Washington University School of Medicine, St. Louis (S.K., L.F., V.L.Y., A.R.C., C.K., B.W.P., B.S.M.); and the Division of Food Science, Human Nutrition and Health, Istituto Superiore di Sanità Rome, Rome (L.F.).
Address reprint requests to Dr. Klein at Washington University School of Medicine, 660 South Euclid Ave., Campus Box 8031, St. Louis, MO 63110.
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, and adiponectin; and did not significantly affect other risk factors for coronary heart disease (blood pressure and plasma glucose, insulin, and lipid concentrations) in either group. 
B signaling through a cAMP-dependent pathway. Circulation 2000;102:1296-1301. 
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