human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Supplementation with n-3 polyunsaturated fatty acids ( PUFA ) for 6 weeks did not alter plasma leptin concentrations in male smokers . Changes in dietary intake of saturated fatty acids ( FA ) correlated positively , whereas changes in the intake of PUFA correlated negatively to changes in plasma leptin levels . A 3-week n-3 PUFA-enriched diet , as compared with a 3-week lard-enriched diet , induced lower plasma leptin concentration and reduced leptin mRNA expression in rat epididymal adipose tissue . In the human trophoblast cell line ( BeWo ) , n-3 PUFA had a dose- and time-dependent effect on leptin expression . One mM of eicosapentaenoic acid or docosahexaenoic acid ( DHA ) reduced leptin expression by 71 % and 78 % , respectively , as compared with control , after 72 h. There was no effect on expression of the signal transducing form of the leptin receptor . In BeWo cells transfected with the human leptin promoter , we found that n-3 PUFA reduced leptin promoter activity ; in contrast saturated and monounsaturated FA had no effect on leptin promoter activity . The transcription factors peroxysomal proliferator activated receptor gamma and sterol regulatory element binding protein-1 mRNAs were reduced after incubation with n-3 PUFA , whereas the expression of CCAAT/enhancer binding protein alpha was unchanged . DHA-reduced leptin expression was abolished in BeWo cells grown in cholesterol-free medium . In conclusion , n-3 FA decreased leptin gene expression both in vivo and in vitro . The direct effects of PUFA on leptin promoter activity indicate a specific regulatory action of FA on leptin expression BACKGROUND Information is lacking on the potential effect of n-3 polyunsaturated fatty acids ( PUFAs ) on the adipose tissue of patients with type 2 diabetes . OBJECTIVE We evaluated whether n-3 PUFAs have additional effects on adiposity , insulin sensitivity , adipose tissue function ( production of adipokines and inflammatory and atherogenic factors ) , and gene expression in type 2 diabetes . DESIGN Twenty-seven women with type 2 diabetes without hypertriglyceridemia were r and omly allocated in a double-blind parallel design to 2 mo of 3 g/d of either fish oil ( 1.8 g n-3 PUFAs ) or placebo ( paraffin oil ) . RESULTS Although body weight and energy intake measured by use of a food diary were unchanged , total fat mass ( P < 0.019 ) and subcutaneous adipocyte diameter ( P < 0.0018 ) were lower in the fish oil group than in the placebo group . Insulin sensitivity was not significantly different between the 2 groups ( measured by homeostasis model assessment in all patients and by euglycemic-hyperinsulinemic clamp in a subgroup of 5 patients per group ) . By contrast , atherogenic risk factors , including plasma triacylglycerol ( P < 0.03 ) , the ratio of triacylglycerol to HDL cholesterol ( atherogenic index , P < 0.03 ) , and plasma plasminogen activator inhibitor-1 ( P < 0.01 ) , were lower in the fish oil group than in the placebo group . In addition , a subset of inflammation-related genes was reduced in subcutaneous adipose tissue after the fish oil , but not the placebo , treatment . CONCLUSIONS A moderate dose of n-3 PUFAs for 2 mo reduced adiposity and atherogenic markers without deterioration of insulin sensitivity in subjects with type 2 diabetes . Some adipose tissue inflammation-related genes were also reduced . These beneficial effects could be linked to morphologic and inflammatory changes in adipose tissue . This trial was registered at clinical trials.gov as NCT0037 The study was design ed to evaluate the chronic regulation of plasma leptin by dietary ( n-3 ) polyunsaturated fatty acids ( PUFA ) in insulin-resistant , sucrose-fed rats . Male Sprague-Dawley rats were r and omly assigned to consume for 3 or 6 wk a diet containing 57.5 % ( g/100 g ) sucrose and 14 % lipids as either fish oil ( SF ) or control oils ( SC ) . After 3 and 6 wk of consuming the SF diet , plasma leptin was 70 % ( P < 0.001 ) and 75 % ( P < 0.05 ) greater , respectively , than in rats fed the SC diet . The same result was found when plasma leptin was adjusted by total fat mass , as measured by dual-energy X-ray absorptiometry . Despite high leptin levels , food intake of rats fed the SF diet was greater than in SC-fed rats without any difference in body weight or total fat mass . After 3 wk , accumulated leptin in epididymal and retroperitoneal adipose tissue was higher in the SF-fed rats than in the SC-fed rats . However , after 6 wk , tissue leptin in the SF-fed rats did not differ from that of the SC-fed rats . The SF diet increased adipose tissue glucose transporter-4 protein quantity and prevented the sucrose-induced elevations in plasma triglycerides and free fatty acids . When all SC- and SF-fed rats ( both diets and feeding duration s ) were considered , plasma leptin levels were positively correlated with body weight ( r = 0.5 , P < 0.0001 ) and with total fat mass ( r = 0.5 , P < 0.0005 ) . These results suggest that plasma leptin at a given time could be inappropriately high for a given fat mass in insulin-sensitive rats fed ( n-3 ) PUFA Introduction There is evidence that n-3 polyunsaturated fatty acids ( n-3 PUFAs ) exert beneficial effects to improve type 2 diabetes mellitus ( T2DM ) , but its complications remain poorly understood . Hypoadiponectinemia is one of the important mechanisms responsible for T2DM which necessitates developing novel therapeutic strategies . We aim ed to determine the effect of n-3 PUFA supplementation on circulating adiponectin and mRNA expression of adiponectin receptors ( AdipoR1 , AdipoR2 ) and Sirt-1 in T2DM patients . Material and methods A r and omized , double-blind , placebo-controlled trial of 10-week follow-up of n-3 PUFAs ( 2.7 g/day ) vs. placebo in T2DM patients ( n = 88 ) was conducted . In detail , T2DM patients ( n = 44 ) were treated with n-3 PUFAs and the remainder received placebo .  Anthropometric and metabolic characteristics were assessed in all participants .  Circulating level of adiponectin and mRNA expression of AdipoR1 , AdipoR2 and Sirt-1 were measured in peripheral blood mononuclear cells ( P BMC ) using real-time polymerase chain reaction before and after the intervention . Results It was found that n-3 PUFAs  increased AdipoR1 gene expression ( fold change = 1.321 in n-3 PUFAs vs. 1.037 in placebo ) and AdipoR2 mRNA ( fold change = 1.338 in n-3 PUFAs vs. 1.034 in placebo ) . No significant changes were observed for Sirt-1 expression . The serum level of adiponectin significantly ( p = 0.035 ) increased in n-3 PUFAs ( 5.09 to 5.58 μg/ml ) but remained unchanged in the placebo group . Conclusions Daily supplementation with n-3 PUFAs ( 2.7 g ) was effective to significantly improve gene expression of AdipoR1 and AdipoR2 and the serum level of adiponectin in T2DM patients . Therefore , n-3 PUFAs might emerge as an adjuvant for current antidiabetic therapies . However , confirmatory long-term studies are required BACKGROUND : Visfatin is an adipocytokine which is secreted from adipose tissue and can affect on the diabetes inflammatory reaction and also serum lipids level . On the other h and , Omega-3 can also prevent formation of insulin resistance . In the present study , the effect of Omega-3 on the serum visfatin concentration was evaluated . METHODS : 71 women with type II diabetes were r and omly assigned to the group that took Omega-3 capsules or control group with placebo capsules . In the first step , study subjects filled a question naire collecting their age , height , weight , waist circumference , and hip circumference . Also their blood sample s were taken for blood tests . In the second step , the intervention was done for 8 weeks and in the third step the aforementioned were collected again . In the blood sample s visfatin and lipid profiles ( low density lipoprotein [ LDL ] , high density lipoprotein [ HDL ] , triglyceride [ TG ] , and cholesterol ) , glucose and HbA1c were measured . RESULTS : There was no significant difference in serum visfatin level between Omega-3 and placebo groups before the intervention ( p = 0.14 ) , while after the intervention , the mean serum visfatin level in the Omega-3 group was significantly higher ( p < 0.001 ) . In addition , the mean difference between the serum visfatin level before and after the intervention in both groups was significant ( p < 0.001 ) . CONCLUSIONS : This study showed an increase in visfatin level following consuming Omega-3 fats but according to controversial issues on insulin-like function of visfatin , the effects of Omega-3 on diabetes should be studied more in further studies Objectives —Fish oil rich in n-3 polyunsaturated fatty acids ( PUFAs ) or n-3 PUFAs have been shown to reduce the incidence of coronary heart disease . Here we investigated the effect of highly purified eicosapentaenoic acid ( EPA ) on production of adiponectin , the only established antiatherogenic and antiinflammatory adipocytokine , in rodent models of obesity and human obese subjects . Methods and Results —We demonstrated that EPA increases adiponectin secretion in genetically obese ob/ob mice and high-fat diet – induced obese mice . In the in vitro coculture of adipocytes and macrophages , EPA reversed the coculture-induced decrease in adiponectin secretion at least in part through downregulation of tumor necrosis factor-&agr ; in macrophages . We also showed significant increase in plasma adiponectin concentrations in human obese subjects after a 3-month treatment with EPA ( 1.8 g daily ) . Multivariate regression analysis revealed that EPA treatment is the only independent determinant of plasma adiponectin concentrations . Conclusion —This study demonstrates that EPA increases adiponectin secretion in rodent models of obesity and human obese subjects , possibly through the improvement of the inflammatory changes in obese adipose tissue . Because EPA has reduced the risk of major coronary events in a large-scale , prospect i ve , r and omized clinical trial , this study provides important insight into its therapeutic implication in obesity-related metabolic sequelae Recent evidence suggests that omega-3 polyunsaturated fatty acids [ n-3 PUFAs : eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) ] , improve insulin sensitivity in humans . In a double-blind , placebo-controlled , r and omized , crossover study , we investigated the effects of EPA/DHA on paraoxonase-1 activity as well as fasting and postpr and ial levels of circulating adiponectin and leptin in 34 subjects with type 2 diabetes mellitus who received daily for 6 weeks either 2 g purified EPA/DHA or olive oil ( placebo ) , separated by a 6 weeks washout . At the end of each treatment , measurements were performed in fasting state and 2 , 4 , and 6 h following a st and ardized high-fat meal ( 600 kcal ) . No significant differences in fasting and postpr and ial circulating adiponectin , leptin , and paraoxonase-1 activity were seen between n-3 PUFAs and placebo . Our data do not support an insulin sensitizing effect of n-3 PUFAs by means of influencing circulating adipocytokines in this population . Clinical Trial Register Number : NCT00328536 Background Energy restriction affects circulating  leptin and ghrelin concentrations . The aim of this study To investigate whether seafood consumption affects fasting leptin and ghrelin concentrations in addition to weight loss . Methods In this 8-week dietary intervention , subjects ( 324 Icel and ic , Spanish and Irish subjects , 20–40 years , BMI 27.5–32.5 kg/m2 ) were r  and omized to energy-restricted diets ( −30 % ) of identical macronutrient composition but different amount of seafood : control ( no seafood ) ; lean fish ( 150 g cod , three times per week ) ; fatty fish ( 150 g salmon , three times per week ) ; EPA&DHA [ daily docosahexaenoic (DHA)/eicosapentaenoic acid ( EPA ) capsules ] . Anthropometric data , ghrelin , leptin , and insul 
    Output:
    
agent
Conclusion Plant and marine sources of n-3 PUFAs can modify serum leptin and adiponectin levels by increasing adiponectin and decreasing leptin levels in patients with type 2 diabetes .
Due to some limitations in this study , further studies are needed to reach a definitive conclusion about the effect of n-3 PUFAs on the levels of leptin and adiponectin in T2DM
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Supplementation with n-3 polyunsaturated fatty acids ( PUFA ) for 6 weeks did not alter plasma leptin concentrations in male smokers . Changes in dietary intake of saturated fatty acids ( FA ) correlated positively , whereas changes in the intake of PUFA correlated negatively to changes in plasma leptin levels . A 3-week n-3 PUFA-enriched diet , as compared with a 3-week lard-enriched diet , induced lower plasma leptin concentration and reduced leptin mRNA expression in rat epididymal adipose tissue . In the human trophoblast cell line ( BeWo ) , n-3 PUFA had a dose- and time-dependent effect on leptin expression . One mM of eicosapentaenoic acid or docosahexaenoic acid ( DHA ) reduced leptin expression by 71 % and 78 % , respectively , as compared with control , after 72 h. There was no effect on expression of the signal transducing form of the leptin receptor . In BeWo cells transfected with the human leptin promoter , we found that n-3 PUFA reduced leptin promoter activity ; in contrast saturated and monounsaturated FA had no effect on leptin promoter activity . The transcription factors peroxysomal proliferator activated receptor gamma and sterol regulatory element binding protein-1 mRNAs were reduced after incubation with n-3 PUFA , whereas the expression of CCAAT/enhancer binding protein alpha was unchanged . DHA-reduced leptin expression was abolished in BeWo cells grown in cholesterol-free medium . In conclusion , n-3 FA decreased leptin gene expression both in vivo and in vitro . The direct effects of PUFA on leptin promoter activity indicate a specific regulatory action of FA on leptin expression BACKGROUND Information is lacking on the potential effect of n-3 polyunsaturated fatty acids ( PUFAs ) on the adipose tissue of patients with type 2 diabetes . OBJECTIVE We evaluated whether n-3 PUFAs have additional effects on adiposity , insulin sensitivity , adipose tissue function ( production of adipokines and inflammatory and atherogenic factors ) , and gene expression in type 2 diabetes . DESIGN Twenty-seven women with type 2 diabetes without hypertriglyceridemia were r and omly allocated in a double-blind parallel design to 2 mo of 3 g/d of either fish oil ( 1.8 g n-3 PUFAs ) or placebo ( paraffin oil ) . RESULTS Although body weight and energy intake measured by use of a food diary were unchanged , total fat mass ( P < 0.019 ) and subcutaneous adipocyte diameter ( P < 0.0018 ) were lower in the fish oil group than in the placebo group . Insulin sensitivity was not significantly different between the 2 groups ( measured by homeostasis model assessment in all patients and by euglycemic-hyperinsulinemic clamp in a subgroup of 5 patients per group ) . By contrast , atherogenic risk factors , including plasma triacylglycerol ( P < 0.03 ) , the ratio of triacylglycerol to HDL cholesterol ( atherogenic index , P < 0.03 ) , and plasma plasminogen activator inhibitor-1 ( P < 0.01 ) , were lower in the fish oil group than in the placebo group . In addition , a subset of inflammation-related genes was reduced in subcutaneous adipose tissue after the fish oil , but not the placebo , treatment . CONCLUSIONS A moderate dose of n-3 PUFAs for 2 mo reduced adiposity and atherogenic markers without deterioration of insulin sensitivity in subjects with type 2 diabetes . Some adipose tissue inflammation-related genes were also reduced . These beneficial effects could be linked to morphologic and inflammatory changes in adipose tissue . This trial was registered at clinical trials.gov as NCT0037 The study was design ed to evaluate the chronic regulation of plasma leptin by dietary ( n-3 ) polyunsaturated fatty acids ( PUFA ) in insulin-resistant , sucrose-fed rats . Male Sprague-Dawley rats were r and omly assigned to consume for 3 or 6 wk a diet containing 57.5 % ( g/100 g ) sucrose and 14 % lipids as either fish oil ( SF ) or control oils ( SC ) . After 3 and 6 wk of consuming the SF diet , plasma leptin was 70 % ( P < 0.001 ) and 75 % ( P < 0.05 ) greater , respectively , than in rats fed the SC diet . The same result was found when plasma leptin was adjusted by total fat mass , as measured by dual-energy X-ray absorptiometry . Despite high leptin levels , food intake of rats fed the SF diet was greater than in SC-fed rats without any difference in body weight or total fat mass . After 3 wk , accumulated leptin in epididymal and retroperitoneal adipose tissue was higher in the SF-fed rats than in the SC-fed rats . However , after 6 wk , tissue leptin in the SF-fed rats did not differ from that of the SC-fed rats . The SF diet increased adipose tissue glucose transporter-4 protein quantity and prevented the sucrose-induced elevations in plasma triglycerides and free fatty acids . When all SC- and SF-fed rats ( both diets and feeding duration s ) were considered , plasma leptin levels were positively correlated with body weight ( r = 0.5 , P < 0.0001 ) and with total fat mass ( r = 0.5 , P < 0.0005 ) . These results suggest that plasma leptin at a given time could be inappropriately high for a given fat mass in insulin-sensitive rats fed ( n-3 ) PUFA Introduction There is evidence that n-3 polyunsaturated fatty acids ( n-3 PUFAs ) exert beneficial effects to improve type 2 diabetes mellitus ( T2DM ) , but its complications remain poorly understood . Hypoadiponectinemia is one of the important mechanisms responsible for T2DM which necessitates developing novel therapeutic strategies . We aim ed to determine the effect of n-3 PUFA supplementation on circulating adiponectin and mRNA expression of adiponectin receptors ( AdipoR1 , AdipoR2 ) and Sirt-1 in T2DM patients . Material and methods A r and omized , double-blind , placebo-controlled trial of 10-week follow-up of n-3 PUFAs ( 2.7 g/day ) vs. placebo in T2DM patients ( n = 88 ) was conducted . In detail , T2DM patients ( n = 44 ) were treated with n-3 PUFAs and the remainder received placebo .  Anthropometric and metabolic characteristics were assessed in all participants .  Circulating level of adiponectin and mRNA expression of AdipoR1 , AdipoR2 and Sirt-1 were measured in peripheral blood mononuclear cells ( P BMC ) using real-time polymerase chain reaction before and after the intervention . Results It was found that n-3 PUFAs  increased AdipoR1 gene expression ( fold change = 1.321 in n-3 PUFAs vs. 1.037 in placebo ) and AdipoR2 mRNA ( fold change = 1.338 in n-3 PUFAs vs. 1.034 in placebo ) . No significant changes were observed for Sirt-1 expression . The serum level of adiponectin significantly ( p = 0.035 ) increased in n-3 PUFAs ( 5.09 to 5.58 μg/ml ) but remained unchanged in the placebo group . Conclusions Daily supplementation with n-3 PUFAs ( 2.7 g ) was effective to significantly improve gene expression of AdipoR1 and AdipoR2 and the serum level of adiponectin in T2DM patients . Therefore , n-3 PUFAs might emerge as an adjuvant for current antidiabetic therapies . However , confirmatory long-term studies are required BACKGROUND : Visfatin is an adipocytokine which is secreted from adipose tissue and can affect on the diabetes inflammatory reaction and also serum lipids level . On the other h and , Omega-3 can also prevent formation of insulin resistance . In the present study , the effect of Omega-3 on the serum visfatin concentration was evaluated . METHODS : 71 women with type II diabetes were r and omly assigned to the group that took Omega-3 capsules or control group with placebo capsules . In the first step , study subjects filled a question naire collecting their age , height , weight , waist circumference , and hip circumference . Also their blood sample s were taken for blood tests . In the second step , the intervention was done for 8 weeks and in the third step the aforementioned were collected again . In the blood sample s visfatin and lipid profiles ( low density lipoprotein [ LDL ] , high density lipoprotein [ HDL ] , triglyceride [ TG ] , and cholesterol ) , glucose and HbA1c were measured . RESULTS : There was no significant difference in serum visfatin level between Omega-3 and placebo groups before the intervention ( p = 0.14 ) , while after the intervention , the mean serum visfatin level in the Omega-3 group was significantly higher ( p < 0.001 ) . In addition , the mean difference between the serum visfatin level before and after the intervention in both groups was significant ( p < 0.001 ) . CONCLUSIONS : This study showed an increase in visfatin level following consuming Omega-3 fats but according to controversial issues on insulin-like function of visfatin , the effects of Omega-3 on diabetes should be studied more in further studies Objectives —Fish oil rich in n-3 polyunsaturated fatty acids ( PUFAs ) or n-3 PUFAs have been shown to reduce the incidence of coronary heart disease . Here we investigated the effect of highly purified eicosapentaenoic acid ( EPA ) on production of adiponectin , the only established antiatherogenic and antiinflammatory adipocytokine , in rodent models of obesity and human obese subjects . Methods and Results —We demonstrated that EPA increases adiponectin secretion in genetically obese ob/ob mice and high-fat diet – induced obese mice . In the in vitro coculture of adipocytes and macrophages , EPA reversed the coculture-induced decrease in adiponectin secretion at least in part through downregulation of tumor necrosis factor-&agr ; in macrophages . We also showed significant increase in plasma adiponectin concentrations in human obese subjects after a 3-month treatment with EPA ( 1.8 g daily ) . Multivariate regression analysis revealed that EPA treatment is the only independent determinant of plasma adiponectin concentrations . Conclusion —This study demonstrates that EPA increases adiponectin secretion in rodent models of obesity and human obese subjects , possibly through the improvement of the inflammatory changes in obese adipose tissue . Because EPA has reduced the risk of major coronary events in a large-scale , prospect i ve , r and omized clinical trial , this study provides important insight into its therapeutic implication in obesity-related metabolic sequelae Recent evidence suggests that omega-3 polyunsaturated fatty acids [ n-3 PUFAs : eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) ] , improve insulin sensitivity in humans . In a double-blind , placebo-controlled , r and omized , crossover study , we investigated the effects of EPA/DHA on paraoxonase-1 activity as well as fasting and postpr and ial levels of circulating adiponectin and leptin in 34 subjects with type 2 diabetes mellitus who received daily for 6 weeks either 2 g purified EPA/DHA or olive oil ( placebo ) , separated by a 6 weeks washout . At the end of each treatment , measurements were performed in fasting state and 2 , 4 , and 6 h following a st and ardized high-fat meal ( 600 kcal ) . No significant differences in fasting and postpr and ial circulating adiponectin , leptin , and paraoxonase-1 activity were seen between n-3 PUFAs and placebo . Our data do not support an insulin sensitizing effect of n-3 PUFAs by means of influencing circulating adipocytokines in this population . Clinical Trial Register Number : NCT00328536 Background Energy restriction affects circulating  leptin and ghrelin concentrations . The aim of this study To investigate whether seafood consumption affects fasting leptin and ghrelin concentrations in addition to weight loss . Methods In this 8-week dietary intervention , subjects ( 324 Icel and ic , Spanish and Irish subjects , 20–40 years , BMI 27.5–32.5 kg/m2 ) were r  and omized to energy-restricted diets ( −30 % ) of identical macronutrient composition but different amount of seafood : control ( no seafood ) ; lean fish ( 150 g cod , three times per week ) ; fatty fish ( 150 g salmon , three times per week ) ; EPA&DHA [ daily docosahexaenoic (DHA)/eicosapentaenoic acid ( EPA ) capsules ] . Anthropometric data , ghrelin , leptin , and insul 
    Output:
    