Reduced Cardiovascular Risk Following Bariatric Surgeries is Related to a Partial Recovery from...

Reduced Cardiovascular Risk Following Bariatric Surgeries isRelated to a Partial Recovery from “Adiposopathy”

Swathi Appachi, BS1, Karen R Kelly, PhD2, Philip R. Schauer, MD3, John P. Kirwan, PhD2,Stanley Hazen, MD, PhD4, Manjula Gupta, MD3, and Sangeeta R Kashyap, MD3

1 Cleveland Clinic Lerner College of Medicine, Cleveland Clinic OH 441952 Department of Pathobiology, Lerner Research Institute, Cleveland Clinic OH 441953 Endocrinology and Metabolism Institute, Cleveland Clinic OH 441954 Heart and Vascular Institute, Cleveland Clinic OH 44195

AbstractBackground—Altered cytokine secretion from dysfunctional adipose tissue or “adiposopathy” isimplicated in obesity related inflammation and may mediate reduced CVD risk in response toweight loss after bariatric surgery. We hypothesized that bariatric surgery reduces CVD risk byfavorably altering the pro-inflammatory profile of adipose tissue as a result of weight loss.

Methods—In this observational study with repeated measures, 142 patients underwent bariatricsurgery of which 45 returned for follow up at ~6 months. At both time-points, lipid profiles andlevels of plasma adiponectin, leptin, and TNF-α were obtained. Ratios of various adipokineparameters were related to pre- and post- surgical (gastric bypass vs. other restrictive bariatricprocedures) lipid ratios.

Results—Prior to surgery, circulating adiponectin and the adiponectin/TNF-α ratio was stronglyassociated with CVD risk characterized by levels of triglycerides, HDL, and the TC/HDL, LDL/HDL and TG/HDL ratios (all P < 0.05). Following bariatric surgery, BMI was decreased by 22%,adiponectin was increased by 93%, and leptin decreased by 50% as compared to baseline (all P <0.01). TNF-α levels increased by 120% (P < 0.01) following surgery. Post-surgical changes inadiponectin and the leptin/adiponectin ratio were strongly associated with incrementalimprovements in triglycerides, HDL, and TC/HDL, LDL/HDL and TG/HDL ratios (all P < 0.05).Roux-en-y gastric bypass surgery (RYGB) as compared to other bariatric procedures wasassociated with more robust improvements in BMI, HDL, and leptin/adiponectin ratio than othergastric restrictive procedures (P < 0.05).

Conclusions—Thus, bariatric surgery, especially RYGB, ameliorates CVD risk through apartial recovery from “adiposopathy”, distinctively characterized by improved adiponectin and theleptin/adiponectin ratio.

Keywordsobesity; cholesterol; adipokines; adiponectin; tumor necrosis factor; leptin; bariatric surgery;gastric bypass

Correspondence: Sangeeta R. Kashyap, Endocrinology, Diabetes and Metabolism, Cleveland Clinic, 9500 Euclid Ave, Cleveland OH,44195, 216-445-2679, 216-445-1656, [email protected] of Interest Disclosure Statement: SRK and PS receive research funding from Ethicon endo-surgery. Other authors (SA,KRK, JPK, SH, MG) have nothing to disclose.

NIH Public AccessAuthor ManuscriptObes Surg. Author manuscript; available in PMC 2011 December 1.

Published in final edited form as:Obes Surg. 2011 December ; 21(12): 1928–1936. doi:10.1007/s11695-011-0447-5.

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IntroductionObesity is an independent risk factor for cardiovascular disease (CVD) and thus is a majorcontributor to increased mortality in the US 1,2. Dyslipidemia, hypertension, insulinresistance, and glucose intolerance 3 are promoted by obesity and collectively play a criticalrole in the development and progression of CVD 4. However, obesity does not always resultin clinical metabolic syndrome, and it is thought that abnormal adipose tissue function, or“adiposopathy,” is required for the manifestation of the metabolic syndrome 4. Bays coinedthe term “adiposopathy” 5 to describe dysfunctional adipose tissue characterized by impairedadipogenesis, endocrine secretion and fuel metabolism, as well as increasedinflammation 6–10. Identifying specific factors associated with adiposopathy that increasesusceptibility to CVD will help target prevention and treatment strategies in the obesepopulation.

Adipose tissue is an active metabolic and endocrine organ that secretes adipokines whichregulate key processes including insulin-mediated glucose metabolism, fatty acid utilization,inflammation, and lipid overloading of ectopic tissues such as the liver 7,6. Adiponectinuniquely reflects the metabolic activity of fat by promoting insulin sensitivity, lipidoxidation in skeletal muscle, and adipocyte differentiation and is markedly reduced inobesity, insulin resistance, and CVD 11. Leptin acts on the hypothalamus operating as asignal of energy sufficiency, thus playing an active role in energy homeostasis 12. Obesity iscommonly associated with high circulating levels of leptin indicating that obesity might be apossible state of leptin resistance 7, and the hypertension associated with adiposopathy iscorrelated with hyperleptinemia 13,14. TNF-α, also secreted by adipose tissue, is elevated inobese patients, and is positively correlated with insulin resistance through reduced insulin-stimulated glucose uptake in insulin-sensitive tissues 7 Therefore, it is possible that a distinctcombination of pro- and anti- inflammatory adipokines may be mediators of disease andtherefore prove valuable as markers for the presence and severity of adiposopathy. It hasalready been reported that other adipose tissue factors such as free fatty acids,mineralocorticoids, and sex hormones all respond favorably to bariatric surgery 15,16. Thus,in order to explore the relationship between adiponectin, leptin, TNF-α, and CVD riskfurther, we observed a cohort of bariatric surgery patients following marked weight loss.

Bariatric surgery effectively reduces morbidity and mortality in severely obese patients- inthe Swedish Obese Subjects study it not only effectively treated severe obesity, but was alsoassociated with favorable rates of recovery for diabetes, hypertriglyceridemia, high lowdensity lipoprotein (LDL) cholesterol, and hypertension17–20. These positive effects ofbariatric surgery were attributed to reduced adipose tissue mass, indicating favorablealterations in the endocrine response of adipose tissue 21,5. Studies have indicated that inrelation to pre-operative measurements, levels of adiponectin increased significantly inrelation to weight loss 22, whereas levels of leptin decreased 23,24. These changes wereshown to correlate with marked improvement in insulin resistance and dyslipidemia 5,25.Thus, changes in the adipokine profile post-bariatric surgery may indicate recovery fromadiposopathy and may be valuable in monitoring CVD risk in response to weight loss.

The purpose of this study was to elucidate the relationship between bariatric surgery,adipokine profiles, and CVD through evaluation of lipid and adipokine profiles fromseverely obese patients before and six months after bariatric surgery at the Cleveland Clinic.We hypothesized that surgical treatment would reduce CVD risk by favorably alteringadipokine secretion following weight loss. We further hypothesized that substantial weightloss would reverse “adiposopathy” reflected by the ratio of pro- and anti-inflammatorymarkers, and that this change will correlate with improvements in CVD risk factors.

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MethodsSubjects

One hundred sixty patients were enrolled through the Cleveland Clinic Foundation Bariatricand Metabolic Institute as part of a prospective, observational, pilot study to help elucidatethe effects of adipokines after bariatric surgery on CVD risk. Subjects underwent theinformed consent process and met the current practicing guideline for undergoing bariatricsurgery for weight loss. Of these patients; one hundred forty-two patients underwentlaparoscopic bariatric surgery. As previously described by Kashyap et al 26, the sample was79% female and 21% male (Table 1). The ethnic distribution was 18% African American,81% Caucasian and <1% Hispanic. The mean (± SD) age for the cohort was 49 ± 10 yearsand the mean BMI was 48 ± 7 kg/m2. Over 85% of the cohort had a diagnosis ofhyperlipidemia and was on treatment with one or more cholesterol lowering agents (statins,fibrates). Of this initial patient population, a subset of 45 patients was followed up at sixmonths post surgery. This surgical subset was 73% female and 27% male (Table 1). Theethnic distribution was 22% African American, 75% Caucasian, and 3% Hispanic. The mean(±SD) age for this subset was 49 ±12.4 years and the mean BMI was 38.8 kg/m2.Additionally, 67% of these patients (N=30) underwent a laparoscopic Roux-en-Y procedure,and 33% (N=15) underwent gastric banding or sleeve gastrectomy. Fifty five percent of thesubset (N= 25) were treated with cholesterol reducing agents (primarily statins) prior tosurgery and 10% remained on statins at the follow up visit.

Adipokine AssaysBlood was obtained as part of a research repository preoperatively and postoperatively. Alladipokine assays were performed by a single experienced technician in the EndocrinologyCore Laboratory of Cleveland Clinic. Additionally, a lipid profile was determined onemonth pre-surgery. Leptin, high sensitivity TNF-α and total adiponectin concentrations weremeasured by sandwich enzyme immunoassay (ELISA) techniques (R&D systems,Minneapolis, MN). The interassay coefficient of variations (mean ± SD) was 9.7%(8.3±7.8), 8.0% (231±18.6) and 5.9% (435±26) for leptin; 10.0% (2.3±0.2), 6.4% (10.5±0.7)and 5.2% (18.5±1.0) for TNF-α; and 8.3% (28.8±2.4); 11.0% (87.5±9.6) and 9.9% (163±16)for total adiponectin, respectively.

Lipid Panel AssaysLevels of total cholesterol, LDL, HDL, and triglyceride levels were determined in theclinical pathology labs as previously described 27.

Statistical AnalysisDescriptive statistics were determined for values of BMI, total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL),triglyceride (TG), adiponectin, leptin, and TNF-α, both pre- and 6 months post-surgery, aswell as weight loss post-surgery. Additionally, the ratios TC/HDL, LDL/HDL, TG/HDLwere computed as these are often valuable CVD diagnostic values. The leptin/adiponectinand adiponectin/TNF-α ratios were also computed. Descriptive statistics for all ratios weredetermined. Pearson correlation coefficients were calculated for all quantitative variables toassess the strength of associations between any two variables. Additionally, surgical groupsand genders were compared with respect to categorical variables and genders using chi-square and Fisher’s exact tests, and with respect to quantitative variables using the Wilcoxonrank sum test. The type of surgery (Roux-en-Y versus gastric banding or sleevegastrectomy) was also compared to these quantitative variables. Several group comparisonsand correlation assessments were performed in these analyses. Since overall impression of

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group differences and correlations was of interest, the possibility of some type I errors wasnot of major concern; therefore, no correction for multiple testing to control an overall type Ierror rate was performed, and statistical significance of individual results was defined asp<0.05.

ResultsRelationship Between Pre-surgical Adipokine Concentrations and Lipid Parameters

Lipid parameters were plotted against adipokine levels in order to determine any possiblelinear correlations, and significant relationships were found to exist between severalcholesterol measures and adiponectin, and adiponectin/TNF-α levels (Figure 1). There wereno significant associations between any of the lipid parameters and leptin or TNF-α (data notshown). HDL and adiponectin were directly correlated (R=0.2, P<0.01), and TG andadiponectin were inversely related (R=−0.3, P<0.01) (Figure 1a). Adiponectin was alsoinversely associated with lipid ratios of interest, TC/HDL, LDL/HDL, and TG/HDL (R=−0.2; P=0.01, R=−0.2; P=0.05, R=−0.3; P<0.01, respectively) (Figure 1a). Adiponectin/TNF-α was also significantly associated with HDL and triglycerides (R=0.2; P=0.02, R=−0.3; P<0.01), as well as TC/HDL, LDL/HDL, and TG/HDL (R=−0.3; P<0.01, R=−0.2;P=0.05, R=−0.3, P=0.001, respectively) (Figure 1b). The relationship between adiponectin/TNF-α and HDL was positive, whereas all other associations were inversely related.

Post-Surgical Effects on CVD Risk and AdipokinesPre- to six-month post-surgery changes in metabolic and CVD risk factors for the surgicalsubset are displayed in Table 2. Overall, surgery resulted in an average weight loss of 34.1 ±18.3 kg, and a 22% reduction in BMI. Additionally, a significant decrease in TC (−20.1 ±−40.2, P<0.01), LDL (−14.7 ± −33.9, P<0.01), and a 24% decrease in triglycerides werenoted. Following surgery, adiponectin increased by 93% (P=0.001), leptin decreased by 50%(P<0.001), and the leptin/adiponectin ratio, which relates fat mass to its metabolic activity,decreased by 56% (P<0.001). TNF-α increased by 120% (P<0.001) following surgery.

Post-surgical outcomes differed by surgery type shown in Table 2. As expected, RYGBresulted in a greater reduction in BMI (P=0.03) (Table 2). RYGB also resulted in an increasein HDL, whereas restrictive surgery showed a trend towards a decrease in HDL (4.3 ± 9.6vs. −2.1 ± 15.2, P=0.02) (Table 2). RYGB also resulted in greater improvements in the TC/HDL and LDL/HDL ratio ( P=0.03). Additionally, RYGB resulted in a 2.5 fold increase inadiponectin (P=0.06) and a significant 2-fold decrease in leptin (P=0.04), with a significant2-fold decrease in the leptin/adiponectin ratio (P=0.01) (Table 2).

Relationship Between Post-Surgical Weight Loss, CVD Risk and AdipokinesIn the post-surgery cohort, analysis showed significant associations between changes in lipidparameters and circulating adipokines (Figure 2a). The percent change in total cholesterolwas directly related to the percent change in weight (R= 0.4, P < 0.01). Moreover, thepercent change in adiponectin following surgery was significantly and inversely associatedwith the percent difference in triglycerides (R=−0.3, P=0.03) (Figure 2a). This change alsotrended towards an inverse association with the percent difference in the TC/HDL ratio (r=−0.3, P=0.07) and was significantly inversely associated with the percent change in the TG/HDL ratio (r=0.3, P=0.03) (Figure 2a). Thus, as the incremental change in adiponectinincreased, there was a corresponding decrease in triglycerides, TC/HDL, and TG/HDL(Figure 2a).

The most striking associations post-surgery were seen with the change in the leptin/adiponectin ratio (Figure 2b). The percent change in HDL post-surgery was inversely

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associated with the percent difference in the leptin/adiponectin ratio (r=−0.3, P=0.03),whereas the percent change in triglycerides was directly linked to this ratio (r=0.3, P<0.05)(Figure 2b). Other lipid ratios including TC/HDL, LDL/HDL, and TG/HDL were all directlyrelated to the percent difference in the leptin/adiponectin ratio (r=0.4; P=0.02, r=0.3; P=0.04,r=0.4; P=0.01), respectively (Figure 2b). All direct relationships indicate that as the leptin/adiponectin ratio goes down, there is a corresponding decrease in CVD risk estimated bylipid ratios.

Post-surgical Effects Based on GenderOur surgery subset was predominantly female (73.3%) and primarily underwent Roux-en-Ysurgery (75.8%) as opposed to other types of obesity surgery, whereas this difference wasless in the males (41.7%) (Table 3). Comparison between genders, regardless of surgery,revealed that females had a higher baseline total cholesterol and higher HDL than males(193.4 ± 38.9 vs. 153.4 ± 43.8, P=0.02 and 49.2 ± 12.2 vs. 36.4 ± 5.6, P=0.001) (Table 3).Following surgery, females experienced a greater change in BMI (−12.2 ± 8.7 vs. −8.6 ±5.6, P=0.04) (Table 3). Strikingly, post-surgery, females had a significantly greater gain inadiponectin as compared to males, regardless of surgery type (4.0 ± 5.8 vs. −0.7 ± 3.4,P=0.02) (Table 3). Females also experienced a greater decrease in leptin as compared tomales, although this difference was not significant (−32.9 ±29.9 vs. 49.6 ±35.2, P=0.07)(Table 3).

DiscussionWe have shown bariatric surgery, particularly RYGB, resulted in marked weight loss,improvements in all lipid parameters, and the adipokines adiponectin and leptin. Womenwho underwent RYGB had greater weight loss and a three-fold increase in adiponectin ascompared to men. Additionally, post-surgical changes in adiponectin and the leptin toadiponectin ratio significantly correlated with the change in triglycerides, TC/HDL, LDL/HDL, and TG/HDL. Thus bariatric surgery, especially RYGB, ameliorates CVD riskthrough improved adiponectin and the leptin/adiponectin ratio potentially representingpartial recovery from “adiposopathy”5; that is an index that relates fat mass to its metabolicactivity (ie. leptin/adiponectin ratio) appears to be strongly associated with reduced CVDrisk in a severely obese, predominantly female population

As expected, bariatric surgery overall resulted in substantial weight loss and improvementsin lipid profile (Table 2). As previously shown, RYGB had a more profound effect on BMIand CVD risk parameters, compared to all other obesity surgeries, including gastricbanding 28,29. Specifically, previous reports have shown that weight loss related to RYGB isassociated with significant reductions in the triglyceride and cholesterol composition oflipoproteins, and also has been seen to have a favorable effect on hypercholesterolemia ascompared to gastric banding and gastroplasty 20,30. Our study further adds to the body ofevidence that RYGB is associated with improvements in CVD risk related to weight loss.However, in spite of the weight loss, it is interesting to note that obesity still persisted – theaverage BMI was ~39 kg/m2 following surgery.

Our data also show significant changes in the adipokine profile following bariatric surgery,and suggest that these patients have recovered from some of the endocrine changesassociated with adiposopathy (Table 2). In particular, as seen in other studies 31, there was agreater decrease in leptin following RYGB, since leptin is correlated to total fat mass andBMI 7,32. Modulation of leptin, could result in a favorable effect on CVD because decreasedlevels are associated with a reduction in intimal hyperplasia, and high levels are related toincreased intima-media thickness, atheroma formation, and myocardial infarction 33. Wealso observed a significant increase in adiponectin levels following surgery, which has been

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noted by many other studies 5. Moreover, the post-surgery leptin/adiponectin ratio correlatedwell with several parameters used to estimate CVD risk. Adiponectin may improve CVDrisk because of its anti-inflammatory, anti-atherogenic properties related in part to reducedfoam cell formation, and suppression of endothelial cell apoptosis 34,32. Drugs that are usedto lower CVD risk in patients such as beta-blockers also increase adiponectin levels,suggesting that adiponectin is inversely correlated with CVD risk 35. Therefore, our findingthat the change in the leptin/adiponectin was correlated with favorable changes in CVD riskfactors is further supported by these studies and indicates a favorable change in themetabolic state or activity of the fat cell following surgery.

Unexpectedly, our results showed an increase in TNF-α levels following surgery. Thechange in TNF-α following bariatric surgery is a controversial topic in the literature, withsome studies showing this cytokine decreases post-surgery 36,37, and others indicating thereis no change 38,39. We expected this marker to decrease since it is secreted in an autocrinefashion by adipose mass (Reviewer 2, Comment 4) 40, which is reduced following surgery;however we uncovered a significant increase. Thus, it may be possible that inflammationpersists following surgery, especially following more invasive surgeries such as RYGB.Another recent study also found elevation of TNF-α 6 months post RYGB 23, but a study inwhich weight loss was achieved using caloric restriction did not show any changes in TNF-α 41. Additionally, while we did not measure vitamin D in these patients, it is possible thatlower levels of vitamin D as commonly noted following RYGB may contribute to increasedTNF-α levels six months post-surgery. Many studies have documented vitamin D and otherfat-soluble vitamin deficiencies in patients following bariatric surgery 42,43, and it has beenshown that TNF-α is activated by low levels of vitamin D 44. This is further corroborated bythe fact that low levels of vitamin D are seen in states of inflammation 45. Further studies arewarranted to explore the relationship between these parameters after bariatric surgery.

There are limitations to our study. Our post-surgery sample size and follow-up time wasrelatively small, as this was a pilot observational study. But even with the small cohort, wewere able to determine significant post-surgical associations between adipokine changes andweight loss. Additionally, the majority of our cohort was treated with cholesterol-loweringmedications, such as statins, a fact that is reflected in Table 1, as the average totalcholesterol, LDL, and HDL levels were all within high-normal limits pre-surgery. Thus, ourcohort of patients represents a real-life clinical scenario, and controlling for statin use wasout of the scope of this pilot study. Therefore, we did not see the full consequence ofbariatric surgery on CVD parameters, and may indeed be underestimating the effect ofobesity surgery. Thus, a larger, controlled trial is needed to validate these observations.

In summary, a pro-inflammatory profile represented by decreased adiponectin, increasedleptin, and increased TNF-α is associated with CVD risk in severely obese patients. Bariatricsurgery, especially Roux-en-Y surgery, significantly decreases CVD risk in obese patientsby reducing some adipogenic signals associated with increased adiponecitn and reducedleptin/adiponectin ratio. Further studies are warranted to further examine surgical effects onTNF-α and gender differences.

AcknowledgmentsWe are grateful to the skilled technical assistance of Rose Lounsbury for performing adipokine measurements andSteve Maximuk in the Preventive Cardiology Core Laboratory for processing serum samples. This work wassupported by National Institutes of Health, RO1 DK089547-01 NIDDK/NIH (JPK, SRK, PRS).

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Abbreviations

TC total cholesterol

HDL high density lipoprotein

LDL low density lipoprotein

TG triglyceride

RYGB roux-en-y gastric bypass

TNFα tumor necrosis factor alpha

BMI body mass index

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Figure 1.Cholesterol parameters represented by HDL, Triglycerides, and the ratio of TC/HDL, LDL/HDL and Triglyceride/HDL shown as the y-axis are displayed as box plot and dot plotfigures in relation to adiponectin tertile levels (x-axis) in figure 1a, and adiponectin/tnfαlevels in figure 1b. Linear relationship between the respective lipid parameter andadiponectin levels and adipoenctin/tnfα levels respectively are shown in the upper rightcorner of each graph. All relationships are highly statistically significant.

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Figure 2.Post-surgical percent difference in cholesterol parameters in relation to percent difference inadiponectin concentration (2a) and leptin/adiponectin ratio (2b) is displayed in the post-surgery cohort ( N = 45).

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Table 1Baseline Characteristics of Cohort and Surgical Subgroup

All continuous variables are reported as mean ± SD.

Variable Cohort Subgroup

N 142 45

Male (%) 34 (21) 12 (26.7)

Ethnicity

Caucasian (%) 130 (81) 36 (80.0)

African American (%) 29 (18) 7 (15.6)

Hispanic (%) 1 (1) 1 (2.2)

Unknown (%) 0 (0) 1 (2.2)

Age (yrs) 49 ± 10 49.2 ± 12.4

BMI (kg/m2) 48 ± 7 50.1 ± 7.8

Total Cholesterol (mg/dL) 191.1 ± 37.2 182.7 ± 43.6

LDL (mg/dL) 110.0 ± 33.1 105.9 ± 38.4

HDL (mg/dL) 50.2 ± 12.1 45.8 ± 12.2

Triglycerides (mg/dL) 167.6 ± 129.6 155.9 ± 89.3

Adiponectin (μg/mL) 6.4 ± 4.1 2.8 ± 5.7

Leptin (μg/mL) 60.3 ± 31.2 52.3 ± 31.7

TNF-α (pg/mL) 2.0 ± 0.7 1.8 ± 0.8


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Table 2Post-Surgical Effects on Metabolic and CVD Risk Profile

Changes for surgery overall are shown in the second column. P-values<0.05 indicate a significant change inthis parameter from pre- to post-surgery. P-values <0.05 in the last column indicate a significant differencebetween types of surgery.

Variable Overall (N=45) RYGB (N=30) Other (N=15) P-value

Weight Loss (kg) 34.1 ± 18.4 34.4 ± 16.1 33.5 ± 22.8 0.6

Post-surgical change in BMI (kg/m2) −11.2 ± 8.1P<0.001

−12.4 ± 8.4 −8.8 ± 7.1 0.03

Post-surgical change in TC (mg/dL) −20.1 ± 40.2P < 0.01

−23.2 ±38.5 −13.9 ± 44.2 0.4

Post-surgical change in LDL (mg/dL) −14.7 ± 33.9P < 0.01

−18.4 ± 35.2 −7.4 ± 30.9 0.3

Post-surgical change in HDL (mg/dL) 2.1 ± 12.0P=0.06

4.3 ± 9.6 −2.1 ± 15.2 0.02

Post-surgical change in TG (mg/dL) −38.0 ± 84.2P=0.001

−46.5 ± 89.9 −20.9 ± 71.4 0.4

Post-surgical change in Adiponectin (μg/mL) 2.8 ± 5.7P=0.001

3.5 ± 4.8 1.3 ± 7.1 0.06

Post-surgical change in Leptin (μg/mL) −30.0 ± 29.4P<0.001

−36.3 ± 25.8 −17.5 ± 32.9 0.04

Post-surgical change in TNF-α (pg/mL) 2.2 ± 2.2P<0.001

2.0 ± 1.8 2.4 ± 3.0 0.9

Post-surgical change in Leptin/Adiponectin −7.8 ± 6.2P<0.001

−9.4 ± 5.6 −4.6 ± 6.4 0.01


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Table 3Post-Surgical Effects on Metabolic and CVD Risk Profile by Gender

P-values <0.05 indicate a difference between genders.

Variable Female (N=33) Male (N=12) P-value

Baseline TC 193.4 ± 38.9 153.4 ±43.8 0.02

Baseline LDL 112.4 ± 35.5 88.2 ± 42.1 0.1

Baseline HDL 49.2 ± 12.2 36.4 ± 5.6 0.001

Baseline TG 161.7 ± 96.6 139.8 ± 65.9 0.6

RYGB (%) 25 (75.8) 5 (41.7) 0.07

Weight Lost (kg) 35.3 ± 19.2 30.8 ± 16.0 0.5

Post-surgical change in BMI (kg/m2) −12.2 ± 8.7 −8.9 ± 5.6 0.04

Post-surgical change in TC (mg/dL) −25.0 ± 40.9 −6.6 ± 36.8 0.1

Post-surgical change in LDL (mg/dL) −16.7 ± 34.5 −9.2 ± 32.7 0.3

Post-surgical change in HDL (mg/dL) 1.0 ± 12.8 −5.2 ± 9.2 0.5

Post-surgical change in TG (mg/dL) −48.7 ± 90.9 −8.3 ± 55.1 0.1

Post-surgical change in Adiponectin (μg/mL) 4.0 ± 5.8 −0.7 ± 3.4 0.02

Post-surgical change in Leptin (μg/mL) −32.9 ± 29.9 −22.2 ± 27.8 0.07

Post-surgical change in TNF-α (pg/mL) 2.4 ± 1.7 1.4 ± 3.2 0.09

Post-surgical change in Leptin/Adiponectin −8.6 ± 5.8 −5.5 ± 7.1 0.09


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