Home About us Contact
|
Home About us Contact | ||
|
|
||
Serum Adiponectin (serum + adiponectin)
Terms modified by Serum Adiponectin Selected AbstractsSerum adiponectin and resistin levels in major depressive disorderACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2010S. M. Lehto Lehto SM, Huotari A, Niskanen L, Tolmunen T, Koivumaa-Honkanen H, Honkalampi K, Ruotsalainen H, Herzig K-H, Viinamäki H, Hintikka J. Serum adiponectin and resistin levels in major depressive disorder. Objective:, To examine the role of the adipose-tissue-derived low-grade inflammation markers adiponectin and resistin in major depressive disorder (MDD) in a population-based sample. Method:, Serum levels of adiponectin and resistin were measured from 70 DSM-IV MDD subjects and 70 healthy controls. Depression severity was assessed with the 29-item Hamilton Depression Rating Scale. Results:, The MDD group had lowered serum adiponectin levels. Regression modelling with adjustments for age, gender, overweight, several socioeconomic and lifestyle factors, coronary heart disease and metabolic syndrome showed that each 5.0 ,g/ml decrease in serum adiponectin increased the likelihood of MDD by approximately 20% (P = 0.01). The resistin levels correlated with atypical (P = 0.02), but not with typical depressive symptoms (P = 0.12). Conclusion:, Our findings suggest that the lowered adiponectin levels in MDD are depression-specific and not explained by conventional low adiponectin-related factors such as such as coronary heart disease and metabolic disorders. [source] Relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomiaJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 3 2010Jing Wang Abstract Aim:, Adiponectin and resistin are novel hormones secreted by human adipocytes and mononuclear cells, which have been postulated to play roles in the regulation of energy metabolism during pregnancy. However, correlations between adiponectin and resistin levels in umbilical and maternal serum and fetal macrosomia remain poorly understood. The purpose of this study was to clarify the relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomia. Methods:, Serum adiponectin and resistin levels were prospectively measured by enzyme immunoassay in 70 mothers and their 70 neonates. The study group included 30 neonates with macrosomia and the control group included 40 neonates that were appropriate for gestational age. The correlations of cord serum adiponectin and resistin with maternal serum adiponectin and resistin, birth weight, body mass index (BMI), and placental weight were analyzed. Results:, Serum adiponectin and resistin levels were significantly decreased in macrosomic mothers compared with those in control women. The levels of adiponectin and resistin were diminished in macrosomic babies in comparison with control newborns. Umbilical serum adiponectin levels were inversely correlated with birth weight, newborn BMI, and placental weight, but not with maternal serum adiponectin levels. Umbilical serum resistin levels had a positive correlation with maternal serum resistin and a negative correlation with birth weight, newborn BMI, and placental weight. In addition, maternal serum resistin levels were inversely correlated with newborn birth weight. Conclusion:, It is suggested that adiponectin and resistin play important roles in controlling body weight and may be related to the occurrence of fetal macrosomia. [source] S -Adenosylmethionine Attenuates Hepatic Lipid Synthesis in Micropigs Fed Ethanol With a Folate-Deficient DietALCOHOLISM, Issue 7 2007Farah Esfandiari Background: To demonstrate a causative role of abnormal methionine metabolism in the pathogenesis of alcoholic steatosis, we measured the effects on hepatic lipid synthesis of supplementing ethanol and folate-deficient diets with S -adenosylmethionine (SAM), a metabolite that regulates methionine metabolism. Methods: Yucatan micropigs were fed folate-deficient diets as control, with ethanol at 40% of kcal, and with ethanol supplemented with SAM at 0.4 g/1,000 kcal for 14 weeks. Histopathology, triglyceride levels and transcripts, and protein levels of the regulatory signals of hepatic lipid synthesis were measured in terminal omental adipose and liver samples. Results: Feeding ethanol at 40% of kcal with folate-deficient diets for 14 weeks increased and supplemental SAM maintained control levels of liver and plasma triglyceride. Serum adiponectin, liver transcripts of adiponectin receptor-1 (AdipoR1), and phosphorylated adenosine monophosphate kinase- , (p-AMPK,) were each reduced by ethanol feeding and were sustained at normal levels by SAM supplementation of the ethanol diets. Ethanol feeding activated and SAM supplementation maintained control levels of ER stress-induced transcription factor sterol regulatory element-binding protein-1c (SREBP-1c) and its targeted transcripts of lipid synthesizing enzymes acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and glycerol-3-phosphate acyltransferase (GPAT). Conclusions: Ethanol feeding with a folate-deficient diet stimulates hepatic lipid synthesis by down-regulating adiponectin-mediated pathways of p-AMPK to increase the expression of nSREBP-1c and its targeted lipogenic enzymes. Preventing abnormal hepatic methionine metabolism by supplementing ethanol diets with SAM reduces liver triglyceride levels by up-regulation of adiponectin-mediated pathways to decrease fatty acid and triglyceride synthesis. This study demonstrates that ethanol-induced hepatic lipid synthesis is mediated in part by abnormal methionine metabolism, and strengthens the concept that altered methionine metabolism plays an integral role in the pathogenesis of steatosis. [source] Serum adiponectin acutely after an ischemic stroke: implications for a long-lasting, suppressed anti-inflammatory roleACTA NEUROLOGICA SCANDINAVICA, Issue 4 2010S. Marousi Marousi S, Theodorou G, Karakantza M, Papathanasopoulos P, Ellul J. Serum adiponectin acutely after an ischemic stroke: implications for a long-lasting, suppressed anti-inflammatory role. Acta Neurol Scand: 2010: 121: 277,284. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objective,,, Past ischemic stroke (IS) patients display suppressed adiponectin (ADPN) levels a few months after disease onset. It is still unclear whether hypoadiponectinemia is already present by the early stages of stroke or occurs as a delayed effect of the acute ischemic reaction. In the present study we investigated ADPN levels acutely after an IS. Materials and methods,,, Serum ADPN was measured in 82 consecutive acute IS patients, and 30 stroke-free subjects of similar age and sex distributions. Results,,, Patients had significantly lower ADPN levels than controls. Higher ADPN was significantly associated with reduced odds for IS accounting for age, sex and high-density lipoproteins. This association was strengthened after further adjustments for potential confounders. ADPN levels remained suppressed even 6 months after stroke. Conclusions,,, ADPN is significantly suppressed already by the early phases of stroke, and remains unchanged 6 months later. We propose a stable-over-time anti-inflammatory role of ADPN in IS, unrelated to the acute ischemic reaction. [source] Serum adiponectin and resistin levels in major depressive disorderACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2010S. M. Lehto Lehto SM, Huotari A, Niskanen L, Tolmunen T, Koivumaa-Honkanen H, Honkalampi K, Ruotsalainen H, Herzig K-H, Viinamäki H, Hintikka J. Serum adiponectin and resistin levels in major depressive disorder. Objective:, To examine the role of the adipose-tissue-derived low-grade inflammation markers adiponectin and resistin in major depressive disorder (MDD) in a population-based sample. Method:, Serum levels of adiponectin and resistin were measured from 70 DSM-IV MDD subjects and 70 healthy controls. Depression severity was assessed with the 29-item Hamilton Depression Rating Scale. Results:, The MDD group had lowered serum adiponectin levels. Regression modelling with adjustments for age, gender, overweight, several socioeconomic and lifestyle factors, coronary heart disease and metabolic syndrome showed that each 5.0 ,g/ml decrease in serum adiponectin increased the likelihood of MDD by approximately 20% (P = 0.01). The resistin levels correlated with atypical (P = 0.02), but not with typical depressive symptoms (P = 0.12). Conclusion:, Our findings suggest that the lowered adiponectin levels in MDD are depression-specific and not explained by conventional low adiponectin-related factors such as such as coronary heart disease and metabolic disorders. [source] The effect of thiazolidinediones on adiponectin serum level: a meta-analysisDIABETES OBESITY & METABOLISM, Issue 5 2008N. Riera-Guardia Background and aims:, Adiponectin is a hormone mainly produced by white adipose tissue. Decreased levels of adiponectin are linked with visceral obesity, insulin resistance states, and cardiovascular diseases. Recently, several studies have pointed out an increase in adiponectin serum levels in subjects undergoing treatment with thiazolidinediones (TZD). The aim of this study is to systematically review the current state of evidence of the effect of TZD on adiponectin serum level with special attention to avoid publication bias. Materials and methods:, An extensive literature search was performed. Meta Analysis Version 2.0 computer program was used to calculate statistical differences in means and 95% confidence interval (CI). Publication bias was assessed using different statistical approaches. Results:, In the meta-analysis including 19 studies the overall standardized mean difference was 0.94 (95% CI, 0.81,1.06) which means that subjects treated with TZDs on average had means of adiponectin concentration that were about 1 standard deviation higher than the comparison groups even after controlling for possible biases. Conclusions:, The results obtained agree with a moderate increase of serum adiponectin. The results clearly reveal an increase of endogenous serum adiponectin levels by intake of TZDs and may point to a potential new option to manage obesity-related diseases. [source] Improved myocardial perfusion in chronic diabetic mice by the up-regulation of pLKB1 and AMPK signalingJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2010Claudia Kusmic Abstract Previous studies related impaired myocardial microcirculation in diabetes to oxidative stress and endothelial dysfunction. Thus, this study was aimed to determine the effect of up-regulating pAMPK-pAKT signaling on coronary microvascular reactivity in the isolated heart of diabetic mice. We measured coronary resistance in wild-type and streptozotocin (STZ)-treated mice, during perfusion pressure changes. Glucose, insulin, and adiponectin levels in plasma and superoxide formation, NOx levels and heme oxygenase (HO) activity in myocardial tissue were determined. In addition, the expression of HO-1, 3-nitrotyrosine, pLKB1, pAMPK, pAKT, and peNOS proteins in control and diabetic hearts were measured. Coronary response to changes in perfusion pressure diverged from control in a time-dependent manner following STZ administration. The responses observed at 28 weeks of diabetes (the maximum time examined) were mimicked by L-NAME administration to control animals and were associated with a decrease in serum adiponectin and myocardial pLKB1, pAMPK, pAKT, and pGSK-3 expression. Cobalt protoporphyrin treatment to induce HO-1 expression reversed the microvascular reactivity seen in diabetes towards that of controls. Up-regulation of HO-1 was associated with an increase in adiponectin, pLKB1, pAKT, pAMPK, pGSK-3, and peNOS levels and a decrease in myocardial superoxide and 3-nitrotyrosine levels. In the present study we describe the time course of microvascular functional changes during the development of diabetes and the existence of a unique relationship between the levels of serum adiponectin, pLKB1, pAKT, and pAMPK activation in diabetic hearts. The restoration of microvascular function suggests a new therapeutic approach to even advanced cardiac microvascular derangement in diabetes. J. Cell. Biochem. 109: 1033,1044, 2010. © 2010 Wiley-Liss, Inc. [source] Relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomiaJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 3 2010Jing Wang Abstract Aim:, Adiponectin and resistin are novel hormones secreted by human adipocytes and mononuclear cells, which have been postulated to play roles in the regulation of energy metabolism during pregnancy. However, correlations between adiponectin and resistin levels in umbilical and maternal serum and fetal macrosomia remain poorly understood. The purpose of this study was to clarify the relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomia. Methods:, Serum adiponectin and resistin levels were prospectively measured by enzyme immunoassay in 70 mothers and their 70 neonates. The study group included 30 neonates with macrosomia and the control group included 40 neonates that were appropriate for gestational age. The correlations of cord serum adiponectin and resistin with maternal serum adiponectin and resistin, birth weight, body mass index (BMI), and placental weight were analyzed. Results:, Serum adiponectin and resistin levels were significantly decreased in macrosomic mothers compared with those in control women. The levels of adiponectin and resistin were diminished in macrosomic babies in comparison with control newborns. Umbilical serum adiponectin levels were inversely correlated with birth weight, newborn BMI, and placental weight, but not with maternal serum adiponectin levels. Umbilical serum resistin levels had a positive correlation with maternal serum resistin and a negative correlation with birth weight, newborn BMI, and placental weight. In addition, maternal serum resistin levels were inversely correlated with newborn birth weight. Conclusion:, It is suggested that adiponectin and resistin play important roles in controlling body weight and may be related to the occurrence of fetal macrosomia. [source] The addition of rosiglitazone to insulin in adolescents with type 1 diabetes and poor glycaemic control: a randomized-controlled trialPEDIATRIC DIABETES, Issue 4pt1 2008Monique L Stone Objective:, To evaluate the effect of rosiglitazone, an insulin sensitizer, on glycaemic control and insulin resistance in adolescents with type 1 diabetes mellitus (T1DM) Research design and methods:, Randomized, double-blind, placebo-controlled crossover trial of rosiglitazone (4 mg twice daily) vs. placebo (24 wk each, with a 4 wk washout period). Entry criteria were diabetes duration >1 yr, age 10,18 yr, puberty (,Tanner breast stage 2 or testicular volume >4 mL), insulin dose ,1.1 units/kg/day, and haemoglobin A1c (HbA1c) >8%. Responses to rosiglitazone were compared with placebo using paired t -tests. Results:, Of 36 adolescents recruited (17 males), 28 completed the trial. At baseline, age was 13.6 ± 1.8 yr, HbA1c 8.9 ± 0.96%, body mass index standard deviation scores (BMI-SDS) 0.94 ± 0.74 and insulin dose 1.5 ± 0.3 units/kg/day. Compared with placebo, rosiglitazone resulted in decreased insulin dose (5.8% decrease vs. 9.4% increase, p = 0.02), increased serum adiponectin (84.8% increase vs. 26.0% decrease, p < 0.01), increased cholesterol (+0.5 mmol/L vs. no change, p = 0.02), but no significant change in HbA1c (,0.3 vs. ,0.1, p = 0.57) or BMI-SDS (0.08 vs. 0.04, p = 0.31). Insulin sensitivity was highly variable in the seven subjects who consented to euglycaemic hyperinsulinaemic clamps. There were no major adverse effects attributable to rosiglitazone. Conclusion:, The addition of rosiglitazone to insulin did not improve HbA1c in this group of normal weight adolescents with T1DM. [source] Short communication: A longitudinal study of serum adiponectin during normal pregnancyBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2006Jens Fuglsang Adiponectin is secreted from adipose tissue. Serum adiponectin levels are inversely correlated with body mass index (BMI) and also insulin resistance, independent of the BMI. A role for adiponectin in the development of insulin resistance has been implied in pregnancy. However, no studies have been performed to describe the individual longitudinal course of adiponectin in normal pregnancies. Therefore, we measured serum adiponectin during and after normal pregnancy in 11 healthy women. Serum levels peaked in midpregnancy and the lowest levels were seen in late pregnancy. An inverse association with maternal BMI was observed. [source] | ||||||||||||||||||||||