title: Obesity modifies the association between plasma phospholipid polyunsaturated fatty acids and markers of inflammation: the Multi-Ethnic Study of Atherosclerosis Plasma adiponectin concentration is associated with skeletal muscle insulin receptor tyrosine phosphorylation, and low plasma concentration precedes a decrease in whole-body insulin sensitivity in humans. Effect of Different Obesity Phenotypes on Incidence of Chronic Kidney Disease in Tehranian Adults Impact of Bariatric Surgery on Ghrelin and Obestatin Levels in Obesity or Type 2 Diabetes Mellitus Rat Model Markers of chronic inflammation and obesity: a prospective study on the reversibility of this association in middle-aged women undergoing weight loss by surgical intervention Short-term very low-calorie diet in obese females improves the haemostatic balance through the reduction of leptin levels, PAI-1 concentrations and a diminished release of platelet and leukocyte-derived microparticles Reduction of Inflammatory Cytokine Concentrations and Improvement of Endothelial Functions in Obese Women After Weight Loss Over One Year A Prospective Study on Inflammatory Parameters in Obese Patients After Sleeve Gastrectomy Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Gut Hormones as Mediators of Appetite and Weight Loss After Roux-en-Y Gastric Bypass
abstract: Background and objective : Systemic inflammation is a well-known risk factor for diseases such as atherosclerosis and is augmented by the presence of obesity . In addition , it has been shown that inflammation may be negatively influenced by certain macronutrients , specifically the omega-3 and omega-6 fatty acids . The primary aim of this study is to determine whether obesity modifies the association between plasma phospholipid polyunsaturated fatty acids ( PUFAs ) and markers of inflammation and endothelial activation in Multi-Ethnic Study of Atherosclerosis ( MESA ) participants .Subjects : A sample of 2848 adults ( 25 % African American , Chinese , Hispanic , and White ) r and omly selected from the MESA cohort . Measurements : Relative plasma PUFA concentrations were determined using gas chromatography-flame ionization detection . Levels of three inflammatory markers ( high-sensitivity C-reactive protein , interleukin (IL)-6 and tumor necrosis factor-receptor 1 ) and two endothelial activation markers ( soluble intercellular adhesion molecule-1 ( sICAM-1 ) and E-selectin ) were determined with enzyme immunoassays . Linear regression analysis was used to evaluate the relationship between these markers and plasma PUFAs . Results : Obesity modified the associations of linoleic acid ( Pint=0.01 ) , dihomo-γ-linolenic ( Pint=0.07 ) and eicosapentaenoic acid ( EPA ) ( Pint=0.04 ) with sICAM-1 concentrations ; in addition , obesity modified the association of IL-6 with dihomo-γ-linolenic ( Pint=0.01 ) . In obese individuals  , sICAM-1 was inversely related to EPA levels ( P=0.02 ) , but directly related to linoleic acid levels ( P<0.001 ) . Conversely , sICAM-1 was inversely related to linoleic acid levels in normal weight individuals ( P=0.04 ) . IL-6 concentrations were significantly and directly related to dihomo-γ-linolenic acid ( DGLA ) in normal weight ( P=0.01 ) and obese participants ( P<0.001 ) , but the scale of increase across tertiles was greater in obese adults . Main effects of fatty acid and inflammatory marker associations are also reported . Conclusion : The modifying effect of obesity on the association of plasma PUFAs with IL-6 and sICAM-1 suggests differences in fatty acid metabolism and may also have implication s in dietary fatty acid intake for obese individuals , particularly for linoleic and EPAs . Further study is warranted to confirm and explain the strong associations of DGLA with inflammatory and endothelial activation markers Adiponectin , the most abundant adipose-specific protein , has been found to be negatively associated with degree of adiposity and positively associated with insulin sensitivity in Pima Indians and other population s. Moreover , adiponectin administration to rodents has been shown to increase insulin-induced tyrosine phosphorylation of the insulin receptor ( IR ) and also increase whole-body insulin sensitivity . To further characterize the relationship between plasma adiponectin concentration and insulin sensitivity in humans , we examined 1 ) the cross-sectional association between plasma adiponectin concentration and skeletal muscle IR tyrosine phosphorylation and 2 ) the prospect i ve effect of plasma adiponectin concentration at baseline on change in insulin sensitivity . Fasting plasma adiponectin concentration , body composition ( hydrodensitometry or dual energy X-ray absorptiometry ) , insulin sensitivity ( insulin-stimulated glucose disposal , hyperinsulinemic clamp ) , and glucose tolerance ( 75-g oral glucose tolerance test ) were measured in 55 Pima Indians ( 47 men and 8 women , aged 31 + /- 8 years , body fat 29 + /- 8 % [ mean + /- SD ] ; 50 with normal glucose tolerance , 3 with impaired glucose tolerance , and 2 with diabetes ) . Group 1 ( 19 subjects ) underwent skeletal muscle biopsies for the measurement of basal and insulin-stimulated tyrosine phosphorylation of the IR ( stimulated by 100 nmol/l insulin ) . The fold increase after insulin stimulation was calculated as the ratio between maximal and basal phosphorylation . Group 2 ( 38 subjects ) had follow-up measurements of insulin-stimulated glucose disposal .  Cross-sectionally , plasma adiponectin concentration was positively associated with insulin-stimulated glucose disposal ( r = 0.58 , P < 0.0001 ) and negatively associated with percent body fat ( r = -0.62 , P < 0.0001 ) in the whole group . In group 1 plasma adiponectin was negatively associated with the basal ( r = -0.65 , P = 0.003 ) and positively associated with the fold increase in IR tyrosine phosphorylation ( r = 0.69 , P = 0.001 ) before and after the adjustment for percent body fat ( r = -0.58 , P = 0.01 and r = 0.54 , P = 0.02 , respectively ) . Longitudinally , after adjustment for age , sex , and percent body fat , low plasma adiponectin concentration at baseline was associated with a decrease in insulin sensitivity ( P = 0.04 ) . In conclusion , our cross-sectional data suggest a role of physiological concentration of fasting plasma adiponectin in the regulation of skeletal muscle IR tyrosine phosphorylation . Prospect ively , low plasma adiponectin concentration at baseline precedes a decrease in insulin sensitivity . Our data indicate that adiponectin plays an important role in regulation of insulin sensitivity in humans Background : The aim of this community-based study is to ascertain the effect of different obesity phenotypes on the incidence of chronic kidney disease in Iranian adults . Study Design : A prospect i ve cohort study , the Tehran Lipid Glucose Study ( TLGS ) . Setting and Participants : Adults aged ≥ 20 years with a mean age of 40.38 years ( 54.8 % female ) who were free from chronic kidney disease ( CKD ) at baseline ( phase 1 ) and were followed up at 3 time stages ( phases 2 , 3 , and 4 ) for a mean duration of 9.4 years to assess the risk for CKD . Predictor : Obesity phenotypes . Outcome : Incidence of chronic kidney disease . Measurements : Glomerular filtration rate ( GFR ) was estimated from the simplified equation developed using data from the Modification of Diet in Renal Disease ( MDRD ) Study . Results : CKD events occurred in 1162 participants . The prevalence of the 2 known obesity phenotypes ( metabolically obese normal weight [ MONW ] and metabolically healthy but obese [ MHO ] ) in the overall population was 3.5 % and 8.8 % , respectively . According to Kaplan-Meier curves , rates of freedom from CKD in the MHO and MONW obesity phenotypes were 75.3 % and 60.6 % , respectively ( p < 0.0001 ) . Age- and sex-adjusted ( model 1 ) hazard ratios for participants with MHO or MONW obesity phenotype were 1.14 ( 95 % confidence interval [ CI ] , 0.91–1.43 ) and 1.43 ( 95 % CI , 1.09–1.88 ) , respectively . After further adjustment for confounder variables ( model 2 ) , multivariate-adjusted hazard ratios for CKD for participants with MHO or MONW obesity phenotypes were 1.23 ( 95 % CI , 0.93–1.62 ) and 1.43 ( 95 % CI , 1.08–1.90 ) , respectively . Conclusion : Adults with the MONW obesity phenotype compared to those with MHO obesity phenotype have a higher risk for incidence of CKD . The results indicate that having a normal weight is not the only factor to protect against incidence of CKD We aim ed to evaluate the therapeutic efficacy on weight control by different bariatric surgeries and investigate the ghrelin and obestatin changes after these surgeries in obesity and nonobese type 2 diabetes mellitus ( T2DM ) rats . Obese rats were r and omly assigned to receive sleeve gastrectomy ( SG , n = 8) , minigastric bypass ( MGBP , n = 8) , roux-en-Y gastric bypass ( RYGBP , n = 8) , and sham operation ( SO , n = 4 ) . Another 4 rats served as control . Besides , Goto-Kakisaki ( GK ) rats were also r and omly divided into similar groups except for total gastrectomy ( TG , n = 8) group . The results showed that in obese rats , weigh loss in RYGBP group was similar to that in MGBP group but larger than that in SG group . Ghrelin significantly increased in RYGB group , but obestatin increased in MGBP group . Ghrelin/obestatin ratio significantly decreased in SG group . In GK rats , weight loss was most obvious in TG group . Postoperatively , ghrelin was significantly increased in MGBP and RYGB groups but decreased in TG group . Obestatin also showed an increase in MGBP and RYGB groups . Ghrelin/obestatin in TG group decreased significantly . In conclusion , RYGB and MGBP may be more suitable for obese rats , but TG may be the best strategy for T2DM rats to control weight with different mechanisms Background : Human adipose tissue expresses and releases proinflammatory cytokines and these measures of chronic inflammation have recently been associated with obesity . Hypothesis : To test whether the proinflammatory state is reversible in subjects undergoing weight loss by surgical measures .Subjects and Methods : Twenty morbidly obese women participated in this prospect i ve study . Subjects were examined for fat mass , high-sensitive C-reactive protein ( hs-CRP ) , interleukin 6 ( IL-6 ) and tumor necrosis factor-alpha ( TNF-α ) before and 1 y after Swedish adjustable gastric b and ing . Results : Anthropometric measures displayed a significant reduction of the body mass index ( BMI ) from 41.6±5.4 to 30.8±6.1 kg/m2 and the fat mass from 53.9±10.3 to 29.8±12.1 kg ( mean±s.d . ) . Hs-CRP levels decreased significantly from 1.33±1.21 mg/dl in pre-gastric b and ing subjects to 0.40±0.61 mg/dl in post-gastric b and ing subjects , respectively . IL-6 and TNF-α levels did not differ significantly between pre- and post-gastric b and ing subjects . Conclusions : We speculate that in these patients the marked reduction in C-reactive protein might be beneficial in reducing their cardiovascular risk and is not solely mediated by IL-6 and TNF-α Background : In obesity , metabolic stress and inflammation in injured tissues could favour enhanced shedding of procoagulant microparticles ( MPs ) . At sites of endothelium injury , the swift recruitment of procoagulant leukocyte-derived MPs enables the initiation of blood coagulation and thrombus growth . Objectives : In obese females , we sought to evaluate the impact of a very low-calorie diet ( VLCD ) on procoagulant MP levels , fibrinolytic status , inflammation and endothelium damage . Methods : Circulating biomarkers of vascular damage , fibrinolytic status , platelet activation and inflammation were measured before , 30 and 90 days after starting a short-term VLCD . MPs were measured by flow cytometry and capture assays . Their procoagulant potential was quantified using functional prothrombinase assays and their cellular origin were determined using flow cytometry ( endothelium , platelet , leukocyte , lymphocyte and erythrocyte-derived MP ) or capture assays . Results : A total of 24 obese females ( 39±10 years ) with a mean body mass index of 35±4 kg m−2 were prospect ively enroled . Procoagulant leukocyte-derived MPs were associated with the waist circumference at baseline ( r=0.534 ; P=0.010 ) and at 90 days follow-up ( r=0.487 ; P=0.021 ) . At 90 days , weight reduction ( −9.8 % ) was associated with a lowering of blood pressure , improvement of metabolic parameters and a significant reduction of plasminogen activator inhibitor-1 ( PAI-1 ) ( −38 % ) , procoagulant platelet-derived MPs ( −43 % ) , leukocyte-derived MPs ( −28 % ) and leptin ( −32 % ) levels . Conclusion : In obese females  , a short-term VLCD results in an overall improvement of the haemostatic balance characterized by the reduction of PAI-levels , diminished release of platelet and leukocyte-derived MPs and a reduction in leptin levels , an adipocyte-derived cytokine Background —Visceral fat is a key regulator site for the process of inflammation , and atherosclerotic lesions are essentially an inflammatory response . Methods and Results —Fifty-six healthy premenopausal obese women ( age range 25 to 44 years , body mass index 37.2±2.2 , waist to hip ratio range 0.78 to 0.92 ) and 40 age-matched normal weight women were studied . Compared with nonobese women , obese women had increased basal concentrations of tumor necrosis factor-&agr ; ( TNF-&agr ; , P < 0.01 ) , interleukin-6 ( IL-6 , P < 0.01 ) , P-selectin ( P < 0.01 ) , intercellular adhesion molecule-1 ( ICAM-1 , P < 0.02 ) , and vascular adhesion molecule-1 ( VCAM-1 , P < 0.05 ) . Vascular responses to l-arginine ( 3 g IV ) , the natural precursor of nitric oxide , were impaired in obese women : reductions in mean blood pressure ( P < 0.02 ) , platelet aggregation to adenosine diphosphate ( P < 0.05 ) , and blood viscosity ( P < 0.05 ) were significantly lower as compared with those in the nonobese group . Concentrations of TNF-&agr ; and IL-6 were related ( P < 0.01 ) to visceral obesity , as well as to adhesin levels and responses to l-arginine . After 1 year of a multidisciplinary program of weight reduction ( diet , exercise , behavioral counseling ) , all obese women  lost at least 10 % of their original weight ( 9.8±1.5 kg , range 7.5 to 13 kg ) . Compared with baseline , sustained weight loss was associated with reduction of cytokine ( P < 0.01 ) and adhesin ( P < 0.02 ) concentrations and with improvement of vascular responses to l-arginine . Conclusion —In obese women , endothelial activation correlates with visceral body fat , possibly through inappropriate secretion of cytokines . Weight loss represents a safe method for downregulating the inflammatory state and ameliorating endothelial dysfunction in obese women Different hormones and peptides involved in inflammation have been studied in and related to obesity . The aim of our work is to assess the variations of different molecules related to inflammation in obese patients during the first year following sleeve gastrectomy .  This was a prospect i ve study on patients who underwent sleeve gastrectomy .  The variations in different clinical , anthropometric , and analytical parameters related to inflammation were determined and analysed in all patients at the preoperative visit and at the first and fifth days , first and sixth months , and 1 year following surgery . We enrolled 20 patients to the study . The median body mass index ( BMI ) before intervention was 48.5 kg/m2 . With respect to comorbidities , 70 % of the patients had obstructive sleep apnoea syndrome ( OSA ) , 65 % high blood pressure , 45 % dyslipidaemia , and 40 % diabetes mellitus ( DM ) . The median percentage of BMI lost ( % BMI L ) 1 year after the intervention was 71 % . The dyslipidaemia healing or improvement rate was 100 % , whereas it was 87.5 % for diabetes , 84.6 % for hypertension , and 57.1 % for OSA . During the 1-year postintervention period , the average levels of adiponectin increased , although not significantly , whereas those of leptin significantly decreased . In addition , the blood levels of MCP-1 , IL-6 , CRP , ferritin , and PAI-1 significantly decreased in that period . Sleeve gastrectomy is a surgical technique that is associated with improvements in body weight and comorbid conditions from the first postoperative months , which lead to significant variations in the levels of different inflammation-related parameters and a decrease in the levels of leptin , IL-6 , CRP , MCP-1 , ferritin , and serpin ( PAI-1 ) BACKGROUND To our knowledge , no single investigation concerning the long-term effects of overweight status on the risk for hypertension , hypercholesterolemia , diabetes mellitus , and cardiovascular sequelae has been reported . METHODS Relations between categories of body mass index ( BMI ) , cardiovascular disease risk factors , and vascular disease end points were examined prospect ively in Framingham Heart Study participants aged 35 to 75 years , who were followed up to 44 years . The primary outcome was new cardiovascular disease , which included angina pectoris , myocardial infa rct ion , coronary heart disease , or stroke . Analyses compared  overweight ( BMI [ calculated as weight in kilograms divided by the square of height in meters ] , 25.0 - 29.9 ) and obese persons ( BMI > or = 30 )  to a  referent group of normal-weight persons ( BMI , 18.5 - 24.9 ) . RESULTS The age-adjusted relative risk ( RR ) for new hypertension was highly associated with overweight status ( men : RR , 1.46 ; women : RR , 1.75 ) . New hypercholesterolemia and diabetes mellitus were less highly associated with excess adiposity . The age-adjusted RR ( confidence interval [ CI ] ) for cardiovascular disease was increased among those who were overweight ( men : 1.21 [ 1.05 - 1.40 ] ; women : 1.20 [ 1.03 - 1.41 ] ) and the obese ( men : 1.46 [ 1.20 - 1.77 ] ; women : 1.64 [ 1.37 - 1.98 ] ) . High population attributable risks were related to excess weight ( BMI > or = 25 ) for the outcomes hypertension ( 26 % men ; 28 % women ) , angina pectoris ( 26 % men ; 22 % women ) , and coronary heart disease ( 23 % men ; 15 % women ) . CONCLUSIONS The overweight category is associated with increased relative and population attributable risk for hypertension and cardiovascular sequelae . Interventions to reduce adiposity and avoid excess weight may have large effects on the development of risk factors and cardiovascular disease at an individual and population level Objective : To evaluate the physiologic importance of the satiety gut hormones . Background : Controversy surrounds the physiologic role of gut hormones in the control of appetite . Bariatric surgery remains the most effective treatment option for obesity , and gut hormones are implicated in the reduction of appetite and weight after Roux-en-Y gastric bypass . Methods : We correlated peptide YY ( PYY ) and glucagon-like peptide 1 ( GLP-1 ) changes within the first week after gastric bypass with changes in appetite . We also evaluated the gut hormone responses of patients with good or poor weight loss after gastric bypass .  Finally , we inhibited the gut hormone responses in gastric bypass patients and then evaluated appetite and food intake . Results : Postpr and ial PYY and GLP-1 profiles start rising as early as 2 days after gastric bypass ( P < 0.05 ) . Changes in appetite are evident within days after gastric bypass surgery ( P < 0.05 ) , and unlike other operations , the reduced appetite continues . However , in patients with poor weight loss after gastric bypass associated with increased appetite , the postpr and ial PYY and GLP-1 responses are attenuated compared with patients with good weight loss ( P < 0.05 ) . Inhibiting gut hormone responses , including PYY and GLP-1 after gastric bypass , results in return of appetite and increased food intake ( P < 0.05 ) . Conclusion : The attenuated appetite after gastric bypass is associated with elevated PYY and GLP-1 concentrations , and appetite returns when the release of gut hormones is inhibited . The results suggest a role for gut hormones in the mechanism of weight loss after gastric bypass and may have implication s for the treatment of obesity
target: Results Insulin resistance indicators were significantly improved after bariatric surgery .
  Leptin was also significantly decreased while adiponectin was significantly increased .
  Although the level of metabolic hormones changed after bariatric surgery , they were not statistically significant .
  Inflammation indicators were significantly decreased .
  Significant reduction was also detected in PAI-1 and sICAM-1 .
  Conclusions Bariatric surgery is beneficial in morbidly obese patients .
  Although treating obesity in a surgical way may cause some complications , the weight loss is generally safe and effective
background: Background Considering conflicting results on the consequences of all types of obesity surgery , we were to summarize them via a systematic review .