Increased plasma interleukin 6 concentrations and exaggerated adipose tissue interleukin 6 content in severely obese patients after operative trauma

BACKGROUND: The cytokine response to operative trauma may be altered in obesity. Thus, we monitored changes in systemic and adipose tissue content of interleukin 6 (IL-6) and in insulin resistance in nonobese versus severely obese patients before and immediately after abdominal operations. METHODS: At the beginning and the end of operation, blood samples and biopsies consisting of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were collected from 13 nonobese and 33 severely obese patients. Systemic concentrations of glucose, insulin, and IL-6, as well as adipose tissue content of IL-6, were determined. RESULTS: Plasma IL-6 concentration and adipose tissue content of IL-6 increased, compared with baseline in patients after operation (plasma, 13- and 5.7-fold; VAT, 270- and 210-fold; SAT, 79- and 8.2-fold in severely obese vs nonobese patients, respectively). The increase in IL-6 in plasma and in both VAT and SAT was exaggerated in severely obese patients, compared with nonobese patients. Increases after operation in plasma IL-6 concentrations were correlated positively to the corresponding increases in both SAT and VAT IL-6 content (r = 0.57 and 0.66, respectively). Also, we found a positive correlation between the worsening of insulin resistance and increases in both plasma and SAT IL-6 concentrations (r = 0.40 and 0.51, respectively). CONCLUSIONS: Circulating IL-6 concentrations both at baseline and after operation are related strongly to abdominal adipose tissue content of content of IL-6 and are exaggerated in severely obese persons. After operation, worsening of insulin resistance is associated with increasing plasma and adipose tissue content of IL-6.     

Increasing Reoperations and Failures With Increasing BMI in Patients Undergoing 2-Stage Exchange for Infected Total Hip Arthroplasty

BackgroundWhile morbid obesity is associated with increased infection after total hip arthroplasty, little is known on the outcomes after 2-stage reimplantation for prosthetic joint infection (PJI) in this population. The purpose of this study is to evaluate the impact of morbid obesity (body mass index>40 kg/m2) on reinfection, postoperative complications, readmissions, and reoperations.MethodsWe conducted a retrospective review of 107 patients undergoing first time 2-stage reimplantation for PJI from 2013 to 2019. 18 patients (50% women) with body mass index>40 kg/m2 were identified. To minimize confounders, three propensity score matched cohorts were created, yielding 16 nonobese (<30 kg/m2), 16 obese (30-39.9 kg/m2), and 18 morbidly obese (>40 kg/m2) patients. Outcomes were compared using chi-square or Fisher’s exact tests. All patients had minimum 12-month follow-up, with mean follow-up of 36.3, 30.1, and 40.0 months in the nonobese, obese, and morbidly obese cohorts, respectively.ResultsCompared with nonobese patients, morbidly obese patients had a higher rate of reinfection (0% vs 33%, P = .020 and higher likelihood of length of stay>4 days (19% vs 61%, P = .012). In addition, compared with nonobese and obese patients, morbidly obese patients had higher rate of return to the operating room for any reason (13% vs 19% vs 50%, respectively, P = .020). No differences between cohorts were found regarding complications, death, or revision surgery.ConclusionMorbidly obese patients have significantly increased risk of reinfection and reoperation after 2-stage reimplantation for PJI when compared with obese and nonobese patients. These data can be used to counsel morbidly obese patients contemplating total hip arthroplasty and supports the notion of deferring arthroplasty in this population pending optimization.     

Nationwide use and outcomes of ambulatory surgery in morbidly obese patients in the United States

Study ObjectiveTo compare the overall characteristics and perioperative outcomes in morbidly obese and nonobese patients undergoing ambulatory surgery in the United States.DesignRetrospective, propensity-matched cohort study.SettingAcademic medical center.MeasurementsThe association between duration of surgical procedures, postoperative complications, and unplanned hospital admission was assessed in a propensity-matched cohort of morbidly obese and nonobese patients derived from the 2006 National Survey of Ambulatory Surgery.Main ResultsOnly 0.32% of the ambulatory procedures were performed on morbidly obese patients. The morbidly obese were significantly younger but had a higher burden of comorbidities, were more likely to undergo the procedure in hospital-based outpatient departments (HOPD; 80.1% vs 56.5%; P = 0.004), and had significantly shorter procedures than the nonobese (median [interquartile range], 28 [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38] vs 42 [22–65] min; P < 0.0001). The incidences of postoperative hypertension, hypotension, hypoxia, cancellation of surgery, and unplanned hospital admissions did not differ significantly between groups. Similarly, adjusted rates of delayed discharge were similar in morbidly obese and nonobese patients (odds ratio [OR], 0.46; 95% confidence interval [CI], 0.18 - 1.15; P = 0.09). In contrast, morbid obesity was associated with decreased odds of postoperative nausea and vomiting (OR, 0.27; CI, 0.09 - 0.84; P = 0.01).ConclusionsIn 2006 in the U.S., the prevalence of ambulatory surgery in the morbidly obese was low, with most of the procedures being performed in the HOPD facilities, suggesting a conservative patient selection. The incidence of adverse postoperative outcomes and delayed discharge, as well as unplanned hospital admission after ambulatory surgery in the morbidly obese, was similar to that reported in the nonobese.     

Differential Intra-abdominal Adipose Tissue Profiling in Obese, Insulin-resistant Women

Background

We recently identified differences in abdominal subcutaneous adipose tissue (SAT) from insulin-resistant (IR) as compared to obesity-matched insulin sensitive individuals, including accumulation of small adipose cells, decreased expression of cell differentiation markers, and increased inflammatory activity. This study was initiated to see if these changes in SAT of IR individuals were present in omental visceral adipose tissue (VAT); in this instance, individuals were chosen to be IR but varied in degree of adiposity. We compared cell size distribution and genetic markers in SAT and VAT of IR individuals undergoing bariatric surgery.

Methods

Eleven obese/morbidly obese women were IR by the insulin suppression test. Adipose tissue surgical samples were fixed in osmium tetroxide for cell size analysis via Beckman Coulter Multisizer. Quantitative real-time polymerase chain reaction for genes related to adipocyte differentiation and inflammation was performed.

Results

While proportion of small cells and expression of adipocyte differentiation genes did not differ between depots, inflammatory genes were upregulated in VAT. Diameter of SAT large cells correlated highly with increasing proportion of small cells in both SAT and VAT (r?=?0.85, p?=?0.001; r?=?0.72, p?=?0.01, respectively). No associations were observed between VAT large cells and cell size variables in either depot. The effect of body mass index (BMI) on any variables in both depots was negligible.

Conclusions

The major differential property of VAT of IR women is increased inflammatory activity, independent of BMI. The association of SAT adipocyte hypertrophy with hyperplasia in both depots suggests a primary role SAT may have in regulating regional fat storage.     

Response of adiponectin and its receptors to changes in metabolic state after gastric bypass surgery: dissociation between adipose tissue expression and circulating levels

BackgroundAdiponectin is an adipokine with anti-atherogenic and insulin-sensitizing properties. Specific adiponectin receptors, adiponectin receptors 1 (AdipoR1) and 2 (AdipoR2), are present in adipose tissue, indicating adiponectin might have autocrine/paracrine effects on its production or action. In addition, endoplasmic reticulum oxidoreductase 1-Lα might mediate regulation of its secretion. The study aim was to determine the subcutaneous adipose tissue (SAT) adiponectin gene and protein expression and their correlation to metabolic parameters during metabolically distinct times after gastric bypass surgery.MethodsA total of 12 morbidly obese male patients underwent SAT biopsy during gastric bypass surgery, active weight loss (negative energy state), and at weight stabilization (steady state energy). The SAT mRNA and protein content of adiponectin, AdipoR1 and AdipoR2, and endoplasmic reticulum oxidoreductase 1-Lα protein levels and the serum levels of adiponectin were assessed.ResultsSAT adiponectin, AdipoR1, and AdipoR2 gene expression increased significantly at the negative energy state, with no further change at steady state energy (P <.05, P <.05, and P = .04, respectively), without significant increases in protein at any stage. Changes in SAT adiponectin protein correlated with changes in AdipoR1 and AdipoR2 during steady state energy (P = .003 and P = .002, respectively). Changes in SAT adiponectin expression did not correlate with those in circulating levels. Changes in endoplasmic reticulum oxidoreductase 1-Lα did not correlate with either SAT or circulating levels of adiponectin.ConclusionOur data indicate distinct functions of adiponectin receptors, AdipoR1 and AdipoR2, mediate the autocrine/paracrine actions of adiponectin. The lack of correlation between changes in SAT adiponectin gene and protein expression and its circulating levels suggests that adipose tissue synthesis and release of adiponectin are highly regulated pathways.     

Changes in Visceral and Subcutaneous Adipose Tissue and Body Composition in Kidney Transplant Recipients at 1, 3, and 5 Years After Kidney Transplant

BackgroundBody composition changes 1 year after kidney transplant (KT) have been studied extensively. However, the number of reports on midterm body composition changes has been limited.MethodsThe medical records and computed tomography scans of 10 living kidney recipients (6 men, 4 women) before KT and at 1, 3, and 5 years post KT were analyzed. Each patient's body mass index was calculated, and the skeletal muscle mass was evaluated using the skeletal muscle mass index and psoas muscle mass index. Each patient's abdominal adipose tissue mass was also quantified by examining the visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and VAT/SAT ratios. These changes were assessed using repeated-measures analysis of variance.ResultsThe body mass index, skeletal muscle mass index, and psoas muscle mass index values did not differ significantly between the pre-KT and 1-, 3-, and 5-year post KT measurements. Conversely, a significant difference was found in the average VAT, SAT, and VAT/SAT ratio values between the pre-KT and at 1, 3, and 5 years post KT (P < .05). The average VAT measurements before and at 1, 3, and 5 years post KT were 66, 94, 108, and 113 cm², respectively, indicating an increasing trend over time.ConclusionsWe observed an increase in the VAT, SAT, and VAT/SAT ratio in patients at 1, 3, and 5 years post KT.     

Cellularity and Adipogenic Profile of the Abdominal Subcutaneous Adipose Tissue From Obese Adolescents: Association With Insulin Resistance and Hepatic Steatosis

OBJECTIVE

We explored whether the distribution of adipose cell size, the estimated total number of adipose cells, and the expression of adipogenic genes in subcutaneous adipose tissue are linked to the phenotype of high visceral and low subcutaneous fat depots in obese adolescents.

RESEARCH DESIGN AND METHODS

A total of 38 adolescents with similar degrees of obesity agreed to have a subcutaneous periumbilical adipose tissue biopsy, in addition to metabolic (oral glucose tolerance test and hyperinsulinemic euglycemic clamp) and imaging studies (MRI, DEXA, ¹H-NMR). Subcutaneous periumbilical adipose cell-size distribution and the estimated total number of subcutaneous adipose cells were obtained from tissue biopsy samples fixed in osmium tetroxide and analyzed by Beckman Coulter Multisizer. The adipogenic capacity was measured by Affymetrix GeneChip and quantitative RT-PCR.

RESULTS

Subjects were divided into two groups: high versus low ratio of visceral to visceral + subcutaneous fat (VAT/[VAT+SAT]). The cell-size distribution curves were significantly different between the high and low VAT/(VAT+SAT) groups, even after adjusting for age, sex, and ethnicity (MANOVA P = 0.035). Surprisingly, the fraction of large adipocytes was significantly lower (P < 0.01) in the group with high VAT/(VAT+SAT), along with the estimated total number of large adipose cells (P < 0.05), while the mean diameter was increased (P < 0.01). From the microarray analyses emerged a lower expression of lipogenesis/adipogenesis markers (sterol regulatory element binding protein-1, acetyl-CoA carboxylase, fatty acid synthase) in the group with high VAT/(VAT+SAT), which was confirmed by RT-PCR.

CONCLUSIONS

A reduced lipo-/adipogenic capacity, fraction, and estimated number of large subcutaneous adipocytes may contribute to the abnormal distribution of abdominal fat and hepatic steatosis, as well as to insulin resistance in obese adolescents.White adipose tissue (WAT) plays a critical role in obesity-related metabolic dysfunctions. Danforth (1) and Shulman (2) raised the hypothesis that inadequate subcutaneous fat stores result in lipid overflow into visceral fat and other nonadipose tissues, which was elegantly explored by Ravussin and Smith (3). Sethi and Vidal-Puig proposed that impaired subcutaneous WAT expandability might cause obesity-associated insulin resistance (4). In adults, increased fat cell size, a marker of impaired adipogenesis, was reported to be related to insulin resistance and predicts the development of type 2 diabetes (5). Recent studies by McLaughlin et al. (6) reported in adults that an increase in the proportion of small adipocytes, but not increased fat cell size, and an impaired expression of markers for adipogenesis are related to insulin resistance. Little is known about adipocyte size and adipogenic capacity during adolescence, a time when the expansion of WAT results from combined adipocyte hypertrophy and hyperplasia. In contrast, adult adipocytes exhibit a remarkably constant turnover (7). Recently, we described a group of obese adolescents presenting with a reduced subcutaneous abdominal fat depot, increased visceral fat, hepatic steatosis, and marked insulin resistance (8). Building on these findings, we asked the following question: is the adipogenic capacity of the abdominal subcutaneous fat depot in obese adolescents associated with a decreased proportion of large adipose cells and reduced expression of genes regulating adipocyte differentiation? We hypothesized that, in some obese adolescents, the lack of expandability of the subcutaneous abdominal fat might be linked to adipocyte size, its adipogenic expression, and the fat accumulation in liver and muscle. To test this hypothesis, we used metabolic and imaging techniques, together with direct measurements of adipocyte size and gene expression, in two groups of obese adolescents with marked differences in the proportion of visceral to subcutaneous abdominal fat.     

A Role of the Inflammasome in the Low Storage Capacity of the Abdominal Subcutaneous Adipose Tissue in Obese Adolescents

The innate immune cell sensor leucine-rich–containing family, pyrin domain containing 3 (NLRP3) inflammasome controls the activation of caspase-1, and the release of proinflammatory cytokines interleukin (IL)-1β and IL-18. The NLRP3 inflammasome is implicated in adipose tissue inflammation and the pathogenesis of insulin resistance. Herein, we tested the hypothesis that adipose tissue inflammation and NLRP3 inflammasome are linked to the downregulation of subcutaneous adipose tissue (SAT) adipogenesis/lipogenesis in obese adolescents with altered abdominal fat partitioning. We performed abdominal SAT biopsies on 58 obese adolescents and grouped them by MRI-derived visceral fat to visceral adipose tissue (VAT) plus SAT (VAT/VAT+SAT) ratio (cutoff 0.11). Adolescents with a high VAT/VAT+SAT ratio showed higher SAT macrophage infiltration and higher expression of the NLRP3 inflammasome–related genes (i.e., TLR4, NLRP3, IL1B, and CASP1). The increase in inflammation markers was paralleled by a decrease in genes related to insulin sensitivity (ADIPOQ, GLUT4, PPARG2, and SIRT1) and lipogenesis (SREBP1c, ACC, LPL, and FASN). Furthermore, SAT ceramide concentrations correlated with the expression of CASP1 and IL1B. Infiltration of macrophages and upregulation of the NLRP3 inflammasome together with the associated high ceramide content in the plasma and SAT of obese adolescents with a high VAT/VAT+SAT may contribute to the limited expansion of the subcutaneous abdominal adipose depot and the development of insulin resistance.     

Visceral fat is strongly associated with post‐transplant diabetes mellitus and glucose metabolism 1 year after kidney transplantation

Body composition after kidney transplantation is linked to glucose metabolism, and impaired glucose metabolism is associated with increased risk of cardiovascular events and death. One year after transplantation, we examined 150 patients for post‐transplant diabetes performing oral glucose tolerance tests and body composition measurements including visceral adipose tissue (VAT) content from dual‐energy X‐ray absorptiometry scans. We found that glucose metabolism was generally improved over the first year post‐transplant, and that the levels of VAT and percentage VAT of total body fat mass (VAT_%totBFM) were lowest in those with normal glucose tolerance and highest in those with post‐transplant diabetes mellitus. In a multivariable linear regression analysis, 87.4% of the variability in fasting glucose concentration was explained by insulin resistance (P<.001, HOMA‐IR index), beta cell function (P<.001, HOMA‐beta), VAT_%totBFM (P=.007), and body mass index (BMI; P=.015; total model P<.001), while insulin resistance (P<.001) and beta cell function (P<.001) explained 31.9% of the variability in 2‐hour glucose concentration in a multivariable model (total model P<.001). VAT was associated with glucose metabolism to a larger degree than BMI. In conclusion, VAT is associated with hyperglycemia one year after kidney transplantation, and insulin resistance and beta cell function estimates are the most robust markers of glucose metabolism.     

Hormone changes and diabetes resolution after biliopancreatic diversion and laparoscopic sleeve gastrectomy: a comparative prospective study

BackgroundBiliopancreatic diversion (BPD) is the most effective bariatric procedure in terms of weight loss and remission of diabetes type 2 (T2DM), but it is accompanied by nutrient deficiencies. Sleeve gastrectomy (SG) is a relatively new operation that has shown promising results concerning T2DM resolution and weight loss. The objective of this study was to evaluate and compare prospectively the effects of BPD long limb (BPD) and laparoscopic SG on fasting, and glucose-stimulated insulin, glucagon, ghrelin, peptide YY (PYY), and glucagon-like peptide-1 (GLP-1) secretion and also on remission of T2DM, hypertension, and dyslipidemia in morbidly obese patients with T2DM.MethodsTwelve patients (body mass index [BMI] 57.6±9.9 kg/m²) underwent BPD and 12 (BMI 43.7±2.1 kg/m²) underwent SG. All patients had T2DM and underwent an oral glucose tolerance test (OGTT) before and 1, 3, and 12 months after surgery.ResultsBMI decreased more after BPD, but percent excess weight loss (%EWL) was similar in both groups (P = .8) and T2DM resolved in all patients at 12 months. Insulin sensitivity improved more after BPD than after SG (P = .003). Blood pressure, total and LDL cholesterol decreased only after BPD (P<.001). Triglycerides decreased after either operation, but HDL increased only after SG (P<.001). Fasting ghrelin did not change after BPD (P = .2), but decreased markedly after SG (P<.001). GLP-1 and PYY responses during OGTT were dramatically enhanced after either procedure (P = .001).ConclusionsSG was comparable to BPD in T2DM resolution but inferior in improving dyslipidemia and blood pressure. SG and BPD enhanced markedly PYY and GLP-1 responses but only SG suppressed ghrelin levels.     

Mucosa-associated microbiota in the jejunum of patients with morbid obesity: alterations in states of insulin resistance and metformin treatment

BackgroundStool samples have been widely used to evaluate gut microbiota; however, little is known about the composition of human small intestinal microbiota and the alterations provoked by insulin resistance.ObjectiveTo describe the composition of jejunal microbiota in morbidly obese patients, as well as its link with insulin resistance and metformin treatment.SettingVirgen de la Victoria University Hospital and Regional University Hospital, Málaga, Spain.MethodsJejunal biopsies from 46 morbidly obese patients were analyzed by next-generation sequencing method. Patients were classified in the following 3 groups: low homeostasis model assessment of insulin resistance index (HOMA-IR) value, high HOMA-IR value, and metformin-treated type 2 diabetes patients (T2D-metf).ResultsRichness (q = .011) together with Proteobacteria (W = 2), Fusobacteria (W = 2), and Bacteroidetes (W = 1) phyla were significantly higher in high HOMA-IR compared with low HOMA-IR group. At family level, several differences were found between low HOMA-IR and T2D-metf group, being the most important the higher abundance of Halomonadacea in T2D-metf group (W = 22). PICRUSt analysis showed that predicted genes involved in trimethylamine-N-oxide biosynthesis pathway could be increased in jejunal microbiota of T2D-metf group compared with the low HOMA-IR group, while indole biosynthesis pathway could be increased in the low HOMA-IR group compared with the high HOMA-IR group.ConclusionAn increase in richness and an enrichment in Proteobacteria, Fusobacteria, and Bacteroidetes was observed in jejunal from morbidly obese patients with high insulin resistance. Halomonadaceae family was significantly increased in metformin-treated patients. Functional analysis of predicted metagenome suggests that trimethylamine-N-oxide biosynthesis pathway could be increased in the jejunal microbiota of T2D-meft group, while indole biosynthesis pathway could be increased in low HOMA-IR group. These results contribute to the increase in the scarce knowledge about the mucosal microbiota of the hardly accessible small intestine.     

CT测量腹部脂肪相关参数诊断冠心病

目的 探讨CT测量腹部脂肪相关参数对诊断冠心病的价值。方法 对211例疑诊冠心病患者于30天内行冠状动脉造影及腹部CT平扫，分析冠心病发生危险因素，采用ROC曲线观察各危险因素单独及联合诊断冠心病的效能。结果 211例中，经冠状动脉造影明确诊断冠心病112例，非冠心病99例。单因素分析结果显示，冠心病与非冠心病患者间年龄、性别、吸烟、糖尿病、高血压、高密度脂蛋白胆固醇（HDL-C）、内脏脂肪（VAT）面积、皮下脂肪（SAT）面积及VAT面积/SAT面积（VAT/SAT）差异均有统计学意义（P均<0.05），体质量指数（BMI）、腹围（WC）及腹部总脂肪（TAT）面积差异均无统计学意义（P均>0.05）。多元Logistic回归分析结果显示，年龄、吸烟、糖尿病及VAT/SAT为冠心病独立危险因素（P均<0.01）。ROC曲线显示年龄、吸烟、糖尿病及VAT/SAT诊断冠心病的AUC分别为0.67、0.61、0.62及0.73，4者联合的AUC为0.80，高于各参数单独检测（P均<0.05）。结论 CT测量的腹部脂肪相关参数可用于诊断冠心病。     

Necdin–E2F4 interaction provides insulin-sensitizing effect after weight loss induced by gastric bypass surgery

BackgroundThe insulin-like growth factor-1 (IGF-1) signaling pathway promotes adipocyte differentiation and, therefore, insulin sensitivity by suppression of necdin expression, which represses peroxisome proliferator-activated receptor-gamma promoter activity by interaction with E2F4 in mouse adipocytes. The aim of the present study was to test the hypothesis that this pathway represents one of the mechanisms by which Roux-en-Y gastric bypass surgery (RYGB) induces resolution of insulin resistance.MethodsClinical samples were collected and the key biomarkers measured to test the hypothesis that the IGF-1 pathway represents 1 of the mechanisms by which RYGB induces resolution of insulin resistance in obese individuals.ResultsFree IGF-1 levels were significantly greater in the post-RYGB patients than in the pre-RYGB obese patients (2.55 ± 1.54 versus 1.32 ± .65 μg/L, P = .03) and similar to that in normal weight controls (2.54 ± 1.27 μg/L). Necdin and E2F4 gene expression in the adipose tissue was significantly downregulated after RYGB compared with obese and were similar to the levels observed in the controls. In mature human adipocytes cultured in vitro, treatment with des-IGF-1 induced downregulation of necdin and E2F4 gene expression in a dose-dependent manner (P = .01).ConclusionAfter RYGB, the insulin/IGF-1 signaling pathway is activated and could account for the observed decrease in the expression of necdin, which represses peroxisome proliferator-activated receptor-gamma promoter activity by interaction with E2F4. This could represent one of the mechanisms that induce resolution of insulin resistance after RYGB.     

The Association of Metabolic Syndrome on Complications and Implant Survivorship in Primary Total Knee Arthroplasty in Morbidly Obese Patients

BackgroundMetabolic syndrome (MetS) includes interrelated conditions such as insulin resistance, abdominal obesity, hypertension, and dyslipidemia. This study sought to determine the association of MetS in morbidly obese patients (body mass index >40) on complications and clinical outcomes after primary total knee arthroplasty (TKA).MethodsA retrospective review was performed to include all morbidly obese patients who underwent primary elective TKA for osteoarthritis at a single academic institution. Patients who did and did not have MetS were propensity-matched 1:1 based on baseline characteristics. A total of 391 patients who did and 935 who did not have MetS were included having a mean body mass index of 44.2 (range, 40.0 to 68.9).ResultsThe MetS patients had longer lengths of stay (LOS) (3.5 ± 2.4 versus 3.0 ± 1.5 days, P = .001) and were more likely to be discharged to skilled nursing facilities (23.8 versus 15.3%, P = .007). At 90 days postoperatively, major (P = .756) and minor (P = .652) complication rates and readmissions (P = .359) were similar. Revision rates as well as improvements in KOOS-JR, and VR-12 mental and physical component scores from preoperative to 1 year (P = .856, P = .524, and P = .727, respectively) postoperatively did not significantly differ between groups. MetS and non-MetS patients had similar 5-year freedom from all-cause revision (90.2 versus 94.2%, P = .791).ConclusionMorbidly obese patients who have MetS had longer LOS and higher discharges to skilled nursing facilities. The 90-day complications, readmissions, revision rates, and patient-reported outcomes were similar, suggesting that resource allocation should be focused on perioperative protocols that can help optimize LOS and discharge dispositions in morbidly obese MetS patients undergoing TKA.Level of evidenceIII.     

Bariatric surgery reduces cancer risk in morbidly obese patients

BackgroundTo assess the effect of bariatric surgery on the cancer risk of patients with morbid obesity because evidence is mounting of an association between obesity and cancer.MethodsWe performed an observational 2-cohort study. The treatment cohort (n = 1035) included patients who had undergone bariatric surgery from 1986 to 2002. The control group (n = 5746) included age- and gender-matched morbidly obese patients who had not undergone weight-reduction surgery and who were identified from a single-payor administrative database. The subjects with physician or hospital visits for a cancer-related diagnosis or treatment within the 6 months previous to the beginning of the study were excluded. The cohorts were followed up for a maximum of 5 years from study inception.ResultsBariatric surgery resulted in a significant reduction in the mean percentage of excess weight loss (67.1%, P <.001). The surgery patients had significantly fewer physician/hospital visits for all cancer diagnoses (n = 21, 2.0%) compared with the controls (n = 487, 8.45%; relative risk .22, 95% confidence interval .143–.347; P = .001). The physician/hospital visits for common cancers such as breast cancer were significantly reduced in the surgery group (P = .001). For all other cancers, the physician/hospital visits showed a trend toward being lower in the surgery group. Because of the low frequencies, statistical significance could not be demonstrated for individual cancer diagnoses.ConclusionThe data suggest that bariatric surgery improves the cancer outcomes in some morbidly obese patients.     

Fibronectin Gene Expression in Human Adipose Tissue and Its Associations with Obesity-Related Genes and Metabolic Parameters

Background

Limited data are available on the in vivo expression of fibronectin, one of the main extracellular matrix components. We investigated the expression of fibronectin in abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) and the associations of leptin, adiponectin, and vaspin gene expression with metabolic parameters in obese women.

Methods

We recruited female subjects undergoing bariatric surgery for obesity (n?=?24) and patients undergoing benign gynecological surgery as the control group (n?=?23). We measured anthropometric variables, abdominal fat distribution, metabolic parameters, serum concentrations of leptin, adiponectin, and vaspin, and depot-specific mRNA expression of fibronectin, leptin, adiponectin, and vaspin.

Results

Fibronectin expression in both VAT and SAT was significantly lower in the obese group than in the control group. Fibronectin expression in both VAT and SAT were negatively correlated with body mass index or waist circumference, with higher prominence in VAT. In multiple regression analysis, fibronectin expression in both VAT and SAT was negatively correlated with serum leptin concentration. Fibronectin expression in VAT was negatively correlated with leptin expression in VAT. Additionally, fibronectin expression in SAT was negatively correlated with leptin expression in SAT and positively correlated with adiponectin expression in VAT and SAT.

Conclusions

We found significant negative associations between depot-specific fibronectin expression in human adipose tissue and obesity indices and obesity-related biomarkers. Our results suggest that fibronectin expression may contribute to obesity and metabolic dysregulation in humans.     

Patterns of surgical weight loss and resolution of metabolic abnormalities in superobese bariatric adolescents

PurposeThe aim of the study was to compare the baseline and the 18-month follow-up for weight and metabolic characteristics of superobese (SO) (body mass index [BMI] ≥50 kg/m²) and morbidly obese (MO) (BMI <50 kg/m²) adolescents who participated in a prospective longitudinal study of gastric banding delivered in an adolescent multidisciplinary treatment program.MethodsClinical information was extracted from an institutional review board–approved database of bariatric adolescents. Fasting cytokine and acute phase protein serum levels were analyzed by enzyme-linked immunosorbent assay. Liver histopathologies were assessed using the Kleiner's classification score.ResultsOther than BMI, MO (n = 11) and SO (n = 7) patients have similar degree of insulin resistance, dyslipidemia, and nonalcoholic fatty liver disease. Serum C-reactive protein (10.2 ± 5.6 SO vs 4 ± 3.9 μg/mL MO [P < .02]) and leptin (71 ± 31 SO vs 45 ± 28 MO ng/mL [P = .04]) were more elevated in SO patients. Although weight loss is similar (30 ± 19 kg MO vs 28 ± 12 kg SO, P = .8 at 18 months; mean percent change in BMI, 22.8% ± 11.6% vs 20.5% ± 10.3% SO, P = .2), SO patients has less resolution of insulin resistance and dyslipidemia but experienced significantly improved health-related quality of life.ConclusionsThe SO adolescents demonstrate equivalent short-term weight loss and improved quality of life but delayed metabolic response to a gastric banding–based weight loss treatment program compared with MO patients, illustrating the importance of early referral for timely intervention of MO patients.