Safety and efficacy of intravascular ultrasound-guided inferior vena cava filter in super obese bariatric patients.

BACKGROUND: The morbidly obese (body mass index >40 kg/m(2)) are at significant risk of postoperative venous thromboembolism (VTE). Pulmonary embolism is the leading cause of death after Roux-en-Y gastric bypass, approximating .5%. Because of the technical limitations with fluoroscopy and table weight limits, it has been our practice at our university-based bariatric center to offer intravascular ultrasound (IVUS)-guided inferior vena cava filter (IVCF) placement at Roux-en-Y gastric bypass to patients with a history of VTE, hypercoagulable state, or profound immobility. METHODS: The hospital and outpatient records of all 594 patients who underwent Roux-en-Y gastric bypass from January 1, 2004 to October 31, 2006 were reviewed. The patients who had undergone concurrent IVUS-guided IVCF placement were selected. The co-morbidities, outcomes, and complications were recorded. RESULTS: Of the 594 patients, 31 (mean body mass index 71.2 +/- 2.96 kg/m(2)) had undergone concurrent IVUS-guided IVCF placement. The indications included a history of VTE (n = 5), a known hypercoagulable state (n = 2), and profound immobility (n = 25). The technical success rate was 96.8%. One filter was malpositioned in the iliac vein. No catheter site complications occurred. A ventilation/perfusion scan and computed tomography scan each detected pulmonary embolism in 2 surviving patients within 2 months postoperatively. Two patients died, 1 on postoperative day 8 and 1 on postoperative day 15 (6.4%). The mean follow-up time was 262.8 +/- 37.3 days. Autopsy excluded VTE or IVCF-related issues as the cause of death in both patients. CONCLUSION: These results suggest the efficacy of IVUS-guided IVCF placement in preventing mortality from pulmonary embolism in high-risk bariatric patients. IVUS-guided IVCF placement can be safely performed with an excellent success rate in high-risk patients who would not otherwise be candidates for intervention because of the technical limitations of fluoroscopy.

Surgical revision of loop ("mini") gastric bypass procedure: multicenter review of complications and conversions to Roux-en-Y gastric bypass.

BACKGROUND: The claim that the "mini"-gastric bypass (MGB) procedure with its loop gastrojejunostomy is safer and equally effective to the Roux-en-Y gastric bypass (RYGB) procedure has been promoted before validation. Rumors of unreported complications and the accuracy of follow-up are additional concerns. This study was undertaken to identify MGB patients who require or required revisional surgery at 5 hospitals within the region of the United States where the MGB procedure originated to assess the claim that revision to RYGB is rarely needed. METHODS: The databases of 5 medical centers were retrospectively searched to identify patients undergoing surgical revision after a MGB procedure, all of which had been done elsewhere. RESULTS: A total of 32 patients were identified who presented with complications after undergoing an MGB procedure and required or require revisional surgery. The complications included gastrojejunostomy leak in 3, bile reflux in 20, intractable marginal ulcer in 5, malabsorption/malnutrition in 8, and weight gain in 2. Of the 32 patients, 21 required conversion to RYGB and an additional 5 have planned revisions in the future. Also, 2 patients were treated with Braun enteroenterostomies and 4 required 1 or more abdominal explorations. CONCLUSIONS: The results of this preliminary review have confirmed that MGB does require revision in some patients and that conversion to RYGB is a common form of revision. A national registry to record the complications and number of revisions is proposed to gain insight into the need for revision after MGB and other nontraditional bariatric procedures.

Endothelial nitric oxide synthase content in adipose tissue from obese and lean African American and white American women.

It has been demonstrated that the enzyme endothelial nitric oxide synthase (eNOS) is present in adipose tissue, resulting in nitric oxide production and subsequent inhibition of lipolysis. A higher eNOS content has also been reported in the subcutaneous abdominal adipose tissue of obese than in that of lean white men. Furthermore, a lower lipolytic rate in obese than in lean women and a lower lipolytic rate in African American (AA) than in white American (WA) women have been demonstrated. The purpose of this study was to determine if eNOS protein content is higher in the subcutaneous and omental adipose tissues of obese than in those of lean women and if eNOS protein content is higher in the subcutaneous and omental adipose tissues of AA than in those of WA women. Whole tissue homogenates were prepared from frozen omental and subcutaneous adipose tissue samples obtained from lean and obese and AA and WA elective abdominal surgery patients and were analyzed for eNOS protein content using enzyme-linked immunosorbent assay. The adipose tissue eNOS protein content was approximately 40% higher in obese than in lean individuals (omental, 326.9 +/- 40.5 pg/mL lean and 445.3 +/- 38.0 pg/mL obese; subcutaneous, 246.8 +/- 20.8 pg/mL lean and 343.1 +/- 19.0 pg/mL obese; P < .05). There was no difference between the races for eNOS protein content in omental adipose tissue. In subcutaneous adipose tissue, there was a higher eNOS content in obese (417.1 +/- 78.9 pg/mg total protein) than in lean (216.7 +/- 29.9 pg/mg total protein) (P < .05) WA women, but there was no difference in subcutaneous adipose eNOS content between obese and lean AA women (250.7 +/- 47.4 and 294.1 +/- 42.2 pg/mg total protein, respectively). The higher eNOS content in the adipose tissue of obese than in that of lean WA women in the fasted state may contribute to the reduced lipolytic activity in WA women; however, eNOS protein content probably does not contribute to differences in lipolytic rates between AA and WA women.

Analysis of insulin-stimulated insulin receptor activation and glucose transport in cultured skeletal muscle cells from obese subjects.

Obesity is associated with impaired insulin-stimulated glucose disposal in the skeletal muscle, but whether this is an intrinsic or acquired factor is unknown. In many patients with type 2 diabetes mellitus (T2D) and their nondiabetic relatives, who have a genetic predisposition for diabetes, insulin resistance is maintained in cultured muscle cells. To study the association of obesity with defects in insulin action, we investigated insulin stimulation of both insulin receptor (IR) autophosphorylation and subsequent glucose transport in primary skeletal muscle cell cultures obtained from both nonobese and obese nondiabetic subjects. In these 2 groups, there was no difference in the ability of insulin to induce autophosphorylation of the IR, phosphorylation of the downstream serine kinase Akt/PKB, or stimulation of glucose transport. Moreover, there were no major differences in cultured muscle cell content of either the IR, the IR antagonist PC-1, or GLUT 1 and GLUT 4. These data therefore indicate that the insulin resistance associated with obesity is not maintained in cultured muscle cells and suggest that this insulin resistance is an acquired feature of obesity.

Suppression of hepatic cholesteryl ester transfer protein expression in obese humans with the development of type 2 diabetes mellitus.

Cholesteryl ester transfer protein (CETP) is a plasma enzyme that can modulate the profile of lipoproteins and is thus considered: 1) a mediator of vascular disease; and 2) a therapeutic target for vascular disease. In the present study, we pursued a better understanding of the effect of type 2 diabetes on the expression of CETP in obese patients. Obesity was accompanied by a 20% elevation in plasma CETP that was eliminated with the development of diabetes. These differences were observed for both men and women and were due to variations in the amount of CETP protein in the plasma. The mRNA and protein of both the full-length (CETPFL) and alternatively spliced (CETPDelta9) forms of CETP were lower in the liver, but not in either sc or omental adipose tissue depots, of diabetic obese subjects. Sterol response element binding proteins 1 and 2 were also lower in liver homogenates, suggesting that these transcription factors may mediate the effects of type 2 diabetes on hepatic CETP expression. Thus, the suppressive effects of type 2 diabetes in obese subjects are observed in both men and women and may be due, at least in part, to a suppression of hepatic CETP expression.

Ethnic differences in adiponectin levels.

Adiponectin levels were measured in African American and Caucasian women of varying body mass index (BMI). Plasma adiponectin levels were compared and the relationship between adiponectin and insulin sensitivity was assessed. Adiponectin levels were similar in the Caucasian obese (7.0 +/- 0.8 microg/mL), African American obese (7.3 +/- 3.5 microg/mL), and African American non-obese women (7.1 +/- 1.2 microg/mL), but were significantly higher in Caucasian non-obese women (12.2 +/- 1.4 microg/mL). Correlational analyses demonstrated that BMI, insulin, and homeostasis model assessment (HOMA) correlated significantly with adiponectin levels in only the Caucasian women. These results provide support for the notion that what applies to other ethnic populations might not apply to the African American population, and that the association between adiponectin and insulin sensitivity needs to be clarified in the African American population.

Fatty acid oxidation by skeletal muscle homogenates from morbidly obese black and white American women.

The purpose of this study was to determine if there were differences in the capacity of skeletal muscle from morbidly obese Black and White American women to oxidize fatty acids. The oxidation rates of (14)C-palmitate, (14)C-palmitoyl-CoA, and (14)C-palmitoyl-carnitine were measured in whole homogenates of rectus abdominus from Black and White women who were similar in age and body mass index (BMI). The activities of muscle citrate synthase (CS), beta-hydroxy acyl-CoA dehydrogenase (beta-HAD), and mitochondrial and microsomal acyl-CoA synthetase (ACS) were measured in the 2 groups. The results showed that the rate of (14)C-palmitate oxidation by muscle of Black women was 25% that of Whites (8.7 +/- 1.5 v 34.4 +/- 6.8 nmol (14)CO(2) produced/gram tissue wet weight/ hour; P <.05), but the rates of (14)C-palmitoyl-CoA and (14)C-palmitoyl-carnitine oxidation were not different in the 2 groups. No differences were found in the activities of CS or beta-HAD. However, the activities of both mitochondrial and microsomal ACS were lower in the Black women than the Whites (mitochondrial ACS 25.1 +/- 3.9 v 36.4 +/- 5.0 nmol/mg protein/min; P <.05; microsomal ACS 6.2 +/- 0.5 v 8.5 +/- 0.5; nmol/mg protein/min; P <.005). The lower rate of palmitate oxidation, and the lack of differences in the rates of palmitoyl-CoA and palmitoyl-carnitine oxidation indicate that there is a defect in the activation of the fatty acid in the muscle of the Black women. This was confirmed by the decrease in mitochondrial ACS activity in the Black women. The decreased fatty acid oxidation by skeletal muscle of obese Black women could result in shunting these fuels from muscle to adipose tissue for storage, which may contribute to the maintenance of obesity in the Black women.

Skeletal muscle lipid metabolism with obesity.

The objectives of this study were to 1). examine skeletal muscle fatty acid oxidation in individuals with varying degrees of adiposity and 2). determine the relationship between skeletal muscle fatty acid oxidation and the accumulation of long-chain fatty acyl-CoAs. Muscle was obtained from normal-weight [n = 8; body mass index (BMI) 23.8 +/- 0.58 kg/m(2)], overweight/obese (n = 8; BMI 30.2 +/- 0.81 kg/m(2)), and extremely obese (n = 8; BMI 53.8 +/- 3.5 kg/m(2)) females undergoing abdominal surgery. Skeletal muscle fatty acid oxidation was assessed in intact muscle strips. Long-chain fatty acyl-CoA concentrations were measured in a separate portion of the same muscle tissue in which fatty acid oxidation was determined. Palmitate oxidation was 58 and 83% lower in skeletal muscle from extremely obese (44.9 +/- 5.2 nmol x g(-1) x h(-1)) patients compared with normal-weight (71.0 +/- 5.0 nmol x g(-1) x h(-1)) and overweight/obese (82.2 +/- 8.7 nmol x g(-1) x h(-1)) patients, respectively. Palmitate oxidation was negatively (R = -0.44, P = 0.003) associated with BMI. Long-chain fatty acyl-CoA content was higher in both the overweight/obese and extremely obese patients compared with normal-weight patients, despite significantly lower fatty acid oxidation only in the extremely obese. No associations were observed between long-chain fatty acyl-CoA content and palmitate oxidation. These data suggest that there is a defect in skeletal muscle fatty acid oxidation with extreme obesity but not overweight/obesity and that the accumulation of intramyocellular long-chain fatty acyl-CoAs is not solely a result of reduced fatty acid oxidation.

Effect of weight loss on muscle lipid content in morbidly obese subjects.

The purpose of this study was to test the hypothesis that weight loss results in a reduction in intramuscular lipid (IMCL) content that is concomitant with enhanced insulin action. Muscle biopsies were obtained from morbidly obese individuals [body mass index (BMI) 52.2 +/- 2.5 kg/m(2); n = 6] before and after gastric bypass surgery, an intervention that improves insulin action. With intervention, there was a 47% reduction (P < 0.01) in BMI and a 93% decrease in homeostasis model assessment, or HOMA (7.0 +/- 1.9 vs. 0.5 +/- 0.1). Histochemically determined IMCL content decreased (P < 0.05) by approximately 30%. In relation to fiber type, IMCL was significantly higher in type I vs. type II fibers. In both fiber types, there were reductions in IMCL and trends for muscle atrophy. Despite these two negating factors, the IMCL-to-fiber area ratio still decreased by approximately 44% with weight loss. In conclusion, despite differing initial levels and possible atrophy, weight loss appears to decrease IMCL deposition to a similar relative extent in type I and II muscle fibers. This reduction in intramuscular triglyceride may contribute to enhanced insulin action seen with weight loss.

Adiponectin is not altered with exercise training despite enhanced insulin action.

Adiponectin is an adipocytokine that is hypothesized to be involved in the regulation of insulin action. The purpose of the present investigation was to determine whether plasma adiponectin is altered in conjunction with enhanced insulin action with exercise training. An insulin sensitivity index (S(I)) and fasting levels of glucose, insulin, and adiponectin were assessed before and after 6 mo of exercise training (4 days/wk for approximately 45 min at 65-80% peak O(2) consumption) with no loss of body mass (PRE, 91.9 +/- 3.8 kg vs. POST, 91.6 +/- 3.9 kg) or fat mass (PRE, 26.5 +/- 1.8 kg vs. POST, 26.7 +/- 2.2 kg). Insulin action significantly (P < 0.05) improved with exercise training (S(I) +98%); however, plasma adiponectin concentration did not change (PRE, 6.3 +/- 1.5 microg/ml vs. POST, 6.6 +/- 1.8 microg/ml). In contrast, in a separate group of subjects examined before and after weight loss, there was a substantial increase in adiponectin (+281%), which was accompanied by enhanced insulin action (S(I), +432%). These data suggest that adiponectin is not a contributory factor to the exercise-related improvements in insulin sensitivity.

Effect of weight loss on insulin sensitivity and intramuscular long-chain fatty acyl-CoAs in morbidly obese subjects.

Increases in intramyocellular long-chain fatty acyl-CoAs (LCACoA) have been implicated in the pathogenesis of insulin resistance in skeletal muscle. To test this hypothesis, we measured muscle (vastus lateralis) LCACoA content and insulin action in morbidly obese patients (n = 11) before and after weight loss (gastric bypass surgery). The intervention produced significant weight loss (142.3 +/- 6.8 vs. 79.6 +/- 4.1 kg for before versus after surgery, respectively). Fasting insulin decreased by approximately 84% (23.3 +/- 3.8 vs. 3.8 +/- 0.5 mU/ml), and insulin sensitivity, as determined by minimal model, increased by approximately 360% (1.2 +/- 0.3 vs. 4.1 +/- 0.5 min(-1). [ micro U/kg(-1)]) indicating enhanced insulin action. Muscle palmityl CoA (16:0; 0.54 +/- 0.08 vs. 0.35 +/- 0.04 nmol/g wet wt) concentration decreased by approximately 35% (P < 0.05) with weight loss, whereas stearate CoA (18:0; -17%; 0.65 +/- 0.05 vs. 0.54 +/- 0.03 nmol/g wet wt) and linoleate CoA (18:2; -30%; 2.47 +/- 0.27 vs. 1.66 +/- 0.19 nmol/g wet wt) were also reduced (P < 0.05). There were no statistically significant declines in muscle palmitoleate CoA (16:1), oleate CoA (18:1), or total LCACoA content. These data suggest that a reduction in intramuscular LCACoA content may be responsible, at least in part, for the enhanced insulin action observed with weight loss in obese individuals.

Muscle fiber type is associated with obesity and weight loss.

The purpose of this study was to test the hypothesis that muscle fiber type is related to obesity. Fiber type was compared 1) in lean and obese women, 2) in Caucasian (C) and African-American (AA) women, and 3) in obese individuals who lost weight after gastric bypass surgery. When lean (body mass index 24.0 +/- 0.9 kg/m(2), n = 28) and obese (34.8 +/- 0.9 kg/m(2), n = 25) women were compared, there were significant (P < 0.05) differences in muscle fiber type. The obese women possessed fewer type I (41.5 +/- 1.8 vs. 54.6 +/- 1.8%) and more type IIb (25.1 +/- 1.5 vs. 14.4 +/- 1.5%) fibers than the lean women. When ethnicity was accounted for, the percentage of type IIb fibers in obese AA was significantly higher than in obese C (31.0 +/- 2.4% vs. 19.2 +/- 1.9%); fewer type I fibers were also found in obese AA (34.5 +/- 2.8% vs. 48.6 +/- 2.2%). These data are consistent with the higher incidence of obesity and greater weight gain reported in AA women. With weight loss intervention, there was a positive relationship (r = 0.72, P < 0.005) between the percentage of excess weight loss and the percentage of type I fibers in morbidly obese patients. These findings indicate that there is a relationship between muscle fiber type and obesity.