Total Adiponectin (total + adiponectin)

Distribution by Scientific Domains


Selected Abstracts


Altered distribution of adiponectin isoforms in children with Prader,Willi syndrome (PWS): association with insulin sensitivity and circulating satiety peptide hormones

CLINICAL ENDOCRINOLOGY, Issue 6 2007
Andrea M. Haqq
Summary Objective, Prader,Willi syndrome (PWS) is a genetic syndrome characterized by relative hypoinsulinaemia and normal or increased insulin sensitivity despite profound obesity. We hypothesized that this increased insulin sensitivity is mediated by increased levels of total and high molecular weight adiponectin and associated with changes in levels of satiety hormones. Design, patients and measurements, We measured total adiponectin and its isoforms [high molecular weight (HMW), middle molecular weight (MMW) and low molecular weight (LMW) adiponectin] and satiety hormones in 14 children with PWS [median age 1135 years, body mass index (BMI) Z- score 215] and 14 BMI-matched controls (median age 1197 years, BMI Z- score 234). Results, Despite comparable BMI Z- scores and leptin levels, the PWS children exhibited lower fasting insulin and HOMA-IR (homeostasis model assessment of insulin resistance) scores compared to obese controls. For any given BMI Z- score, the PWS children showed higher concentrations of fasting total and HMW adiponectin and higher HMW/total adiponectin ratios. The HMW/total adioponectin ratio was preserved in children with PWS at high degrees of obesity. In PWS children, fasting plasma total adiponectin, HMW adiponectin and HMW/total adiponectin ratio correlated negatively with age (P < 005), HOMA-IR (P < 001), BMI Z- score (P < 005), insulin (P < 001) and leptin (P < 005). In addition to higher fasting ghrelin concentrations, the PWS children showed significantly higher fasting levels of total peptide YY (PYY) and gastric inhibitory polypeptide (GIP) compared to obese controls. Conclusions, Relative to controls of similar age and BMI Z- score, the PWS children had significantly higher levels of total and HMW adiponectin, and increased ratios of HMW/total adiponectin. These findings may explain in part the heightened insulin sensitivity of PWS children relative to BMI-matched controls. [source]


Adiponectin changes in HCV-Genotype 4: relation to liver histology and response to treatment

JOURNAL OF VIRAL HEPATITIS, Issue 10 2009
M. Derbala
Summary., Recently, attention has been focussed on adiponectin and its changes in different types of chronic liver disease. Its relation to hepatic fibrosis and insulin resistance in post-hepatitis liver disease is not clear. The aim of this study was to clarify the adiponectin changes in genotype 4 hepatitis C virus (HCV)-infected patient in relation to liver histology and insulin resistance, and its usefulness as a predictor of hepatic fibrosis and response to treatment. Total adiponectin and its high molecular weight (HMW) form as well as insulin levels were studied in 92 chronic HCV, genotype 4 and 66 healthy control volunteers. Neither total adiponectin (r = 0.101, P = 0.220) nor HMW adiponectin (r = 0.081, P = 0.328) correlated with viral load. Total and not HMW adiponectin was significantly correlated with hepatic fibrosis and inflammation (r = 0.267, P = 0.002, r = 0.278, P < 0.001, respectively). In addition, total adiponectin (r = 0.224, P = 0.002) and HMW adiponectin (r = 0.266, P < 0.0006) significantly correlated with insulin resistance. As fibrosis did not correlate with insulin resistance (r = 0.081, P = 0.204), the correlation between total adiponectin and fibrosis was not mediated by insulin resistance. Multivariable regression analysis, (including pretreatment cases and controls) revealed that total adiponectin was significantly associated with gender, being lower among male subjects (X2 = 13.04, P = 0.0001). The multivariable regression model supported the lack of association between insulin resistance and total adiponectin levels (X2 = 1.88, P = 0.171), while non cirrhotics had significantly lower total adiponectin levels than cirrhotics (X2 = 10.90, P = 0.004) and lower level of inflammation significantly lower total adiponectin levels than more severe inflammation (X2 = 8.95, P = 0.003). Total or HMW adiponectin did not yield receiver operating characteristic (ROC) curves with area under the curve (AUC) >75%, thus the cutoff points have poor sensitivity/specificity as predictors of fibrosis. However, as a predictor of end-of-treatment response, the ROC curve of adiponectin index gave yield an AUC = 81.4%. We can conclude that total adiponectin level, in HCV genotype 4 patients, increases with progression of hepatic fibrosis regardless of insulin resistance. Its high molecular form does not have such correlation. The adiponectin changes are not related to viral load, insulin resistance or other demographic data suggesting that this change is histologically related. In spite of this, no adiponectin cutoff level had reasonable sensitivity/specificity for predicting hepatic fibrosis stage, while this may be used as a predictor for antiviral response possibly reflecting improvement in hepatic inflammation post treatment. [source]


Total and high molecular weight adiponectin concentrations in plasma of patients with end-stage renal disease before and after peritoneal dialysis

NEPHROLOGY, Issue 3 2008
JAE-HO PARK
SUMMARY: Background: Adiponectin is an antiatherogenic adipocyte-derived proteins. The level of plasma adiponectin is inversely correlated to cardiovascular risk in patients with end-stage renal disease (ESRD). The aim of this study was to elucidate the changes of adiponectin concentrations in newly diagnosed ESRD patients after peritoneal dialysis. Methods: In 16 newly diagnosed ESRD patients, total concentrations of adiponectin and high molecular weight (HMW) adiponectin, the HMW ratio (HMWR; ratio of the plasma level of HMW adiponectin to that of total adiponectin), the body mass index (BMI), insulin concentrations, blood glucose and estimation of the insulin sensitivity index by the homeostasis model assessment (HOMRIR) were compared before and after 1 year of peritoneal dialysis. Results: Plasma total adiponectin was decreased from 15.52 9.35 ,g/mL to 11.80 6.84 ,g/mL (P = 0.046), HMW adiponectin was decreased from 9.05 6.48 ,g/mL to 4.83 4.15 ,g/mL (P = 0.009), and HMWR was decreased from 0.51 0.18 to 0.35 0.20 (P = 0.008). Total and HMW adiponectin/BMI ratio was decreased. The BMI was increased from 25.2 5.7 to 25.8 6.2 (P = 0.036). The HOMRIR, insulin level and lipid profile were not changed. Conclusion: Total adiponectin, HMW adiponectin and HMWR were decreased in newly diagnosed ESRD patients after 1 year of peritoneal dialysis. The factors that influence the decrease of the level of adiponectin should be studied in a larger prospective study. [source]


Adiponectin changes in HCV-Genotype 4: relation to liver histology and response to treatment

JOURNAL OF VIRAL HEPATITIS, Issue 10 2009
M. Derbala
Summary., Recently, attention has been focussed on adiponectin and its changes in different types of chronic liver disease. Its relation to hepatic fibrosis and insulin resistance in post-hepatitis liver disease is not clear. The aim of this study was to clarify the adiponectin changes in genotype 4 hepatitis C virus (HCV)-infected patient in relation to liver histology and insulin resistance, and its usefulness as a predictor of hepatic fibrosis and response to treatment. Total adiponectin and its high molecular weight (HMW) form as well as insulin levels were studied in 92 chronic HCV, genotype 4 and 66 healthy control volunteers. Neither total adiponectin (r = 0.101, P = 0.220) nor HMW adiponectin (r = 0.081, P = 0.328) correlated with viral load. Total and not HMW adiponectin was significantly correlated with hepatic fibrosis and inflammation (r = 0.267, P = 0.002, r = 0.278, P < 0.001, respectively). In addition, total adiponectin (r = 0.224, P = 0.002) and HMW adiponectin (r = 0.266, P < 0.0006) significantly correlated with insulin resistance. As fibrosis did not correlate with insulin resistance (r = 0.081, P = 0.204), the correlation between total adiponectin and fibrosis was not mediated by insulin resistance. Multivariable regression analysis, (including pretreatment cases and controls) revealed that total adiponectin was significantly associated with gender, being lower among male subjects (X2 = 13.04, P = 0.0001). The multivariable regression model supported the lack of association between insulin resistance and total adiponectin levels (X2 = 1.88, P = 0.171), while non cirrhotics had significantly lower total adiponectin levels than cirrhotics (X2 = 10.90, P = 0.004) and lower level of inflammation significantly lower total adiponectin levels than more severe inflammation (X2 = 8.95, P = 0.003). Total or HMW adiponectin did not yield receiver operating characteristic (ROC) curves with area under the curve (AUC) >75%, thus the cutoff points have poor sensitivity/specificity as predictors of fibrosis. However, as a predictor of end-of-treatment response, the ROC curve of adiponectin index gave yield an AUC = 81.4%. We can conclude that total adiponectin level, in HCV genotype 4 patients, increases with progression of hepatic fibrosis regardless of insulin resistance. Its high molecular form does not have such correlation. The adiponectin changes are not related to viral load, insulin resistance or other demographic data suggesting that this change is histologically related. In spite of this, no adiponectin cutoff level had reasonable sensitivity/specificity for predicting hepatic fibrosis stage, while this may be used as a predictor for antiviral response possibly reflecting improvement in hepatic inflammation post treatment. [source]


Total and high molecular weight adiponectin concentrations in plasma of patients with end-stage renal disease before and after peritoneal dialysis

NEPHROLOGY, Issue 3 2008
JAE-HO PARK
SUMMARY: Background: Adiponectin is an antiatherogenic adipocyte-derived proteins. The level of plasma adiponectin is inversely correlated to cardiovascular risk in patients with end-stage renal disease (ESRD). The aim of this study was to elucidate the changes of adiponectin concentrations in newly diagnosed ESRD patients after peritoneal dialysis. Methods: In 16 newly diagnosed ESRD patients, total concentrations of adiponectin and high molecular weight (HMW) adiponectin, the HMW ratio (HMWR; ratio of the plasma level of HMW adiponectin to that of total adiponectin), the body mass index (BMI), insulin concentrations, blood glucose and estimation of the insulin sensitivity index by the homeostasis model assessment (HOMRIR) were compared before and after 1 year of peritoneal dialysis. Results: Plasma total adiponectin was decreased from 15.52 9.35 ,g/mL to 11.80 6.84 ,g/mL (P = 0.046), HMW adiponectin was decreased from 9.05 6.48 ,g/mL to 4.83 4.15 ,g/mL (P = 0.009), and HMWR was decreased from 0.51 0.18 to 0.35 0.20 (P = 0.008). Total and HMW adiponectin/BMI ratio was decreased. The BMI was increased from 25.2 5.7 to 25.8 6.2 (P = 0.036). The HOMRIR, insulin level and lipid profile were not changed. Conclusion: Total adiponectin, HMW adiponectin and HMWR were decreased in newly diagnosed ESRD patients after 1 year of peritoneal dialysis. The factors that influence the decrease of the level of adiponectin should be studied in a larger prospective study. [source]


Altered distribution of adiponectin isoforms in children with Prader,Willi syndrome (PWS): association with insulin sensitivity and circulating satiety peptide hormones

CLINICAL ENDOCRINOLOGY, Issue 6 2007
Andrea M. Haqq
Summary Objective, Prader,Willi syndrome (PWS) is a genetic syndrome characterized by relative hypoinsulinaemia and normal or increased insulin sensitivity despite profound obesity. We hypothesized that this increased insulin sensitivity is mediated by increased levels of total and high molecular weight adiponectin and associated with changes in levels of satiety hormones. Design, patients and measurements, We measured total adiponectin and its isoforms [high molecular weight (HMW), middle molecular weight (MMW) and low molecular weight (LMW) adiponectin] and satiety hormones in 14 children with PWS [median age 1135 years, body mass index (BMI) Z- score 215] and 14 BMI-matched controls (median age 1197 years, BMI Z- score 234). Results, Despite comparable BMI Z- scores and leptin levels, the PWS children exhibited lower fasting insulin and HOMA-IR (homeostasis model assessment of insulin resistance) scores compared to obese controls. For any given BMI Z- score, the PWS children showed higher concentrations of fasting total and HMW adiponectin and higher HMW/total adiponectin ratios. The HMW/total adioponectin ratio was preserved in children with PWS at high degrees of obesity. In PWS children, fasting plasma total adiponectin, HMW adiponectin and HMW/total adiponectin ratio correlated negatively with age (P < 005), HOMA-IR (P < 001), BMI Z- score (P < 005), insulin (P < 001) and leptin (P < 005). In addition to higher fasting ghrelin concentrations, the PWS children showed significantly higher fasting levels of total peptide YY (PYY) and gastric inhibitory polypeptide (GIP) compared to obese controls. Conclusions, Relative to controls of similar age and BMI Z- score, the PWS children had significantly higher levels of total and HMW adiponectin, and increased ratios of HMW/total adiponectin. These findings may explain in part the heightened insulin sensitivity of PWS children relative to BMI-matched controls. [source]