Levels Of Low Molecular Weight Adiponectin Research Articles

Relationship between adiponectin multimer levels and subtypes of cerebral infarction.

Serum adiponectin levels are decreased in patients with cerebral infarction. Adiponectin in circulation exists in three isoforms: high molecular weight (HMW), medium molecular weight (MMW), and low molecular weight (LMW) adiponectin. We measured serum levels of total adiponectin and adiponectin multimers (HMW, MMW, and LMW) in patients with cerebral infarction and compared the serum levels of the three adiponectin multimers in stroke subtypes. We also evaluated the clinical value of adiponectin multimer levels as a biomarker for cerebral infarction. We assessed a total of 132 patients with cerebral infarctions. The serum levels of total and adiponectin multimers were measured using enzyme-linked immunosorbent assay (ELISA). The total and HMW adiponectin levels were significantly lower in atherothrombotic infarction (AI) than in cerebral embolism (CE) (total, p < 0.05; HMW, p < 0.05). In male patients, the MMW adiponectin level was significantly lower in the lacunar infarction (LI) group than in the AI group (p < 0.05). The LMW adiponectin level was significantly lower in the AI group than in the LI and CE groups (LI, p < 0.001; CE, p = 0.001). However, there were no significant differences in adiponectin multimer levels among the stroke subtypes in female subjects. Additionally, in female patients with AI and LI, the LMW adiponectin levels were negatively associated with C-reactive protein (CRP; AI, p < 0.05; LI, p < 0.05). These findings suggest that a decrease in adiponectin is associated with AI and that serum LMW adiponectin level represents a potential biomarker for AI.

Adiponectin multimers in patients with Barrett’s Oesophagus

Barrett’s oesophagus is associated with abdominal obesity. Adiponectin is a peptide that is secreted from adipocytes and circulates in three multimeric forms: low molecular weight (LMW), middle molecular weight (MMW), and high molecular weight (HMW). The anti- inflammatory effects of adiponectin are specific to individual multimers, with the LMW being most anti-inflammatory. We investigated the possibility that circulating levels of adiponectin and its multimers would be associated with the risk of Barrett’s oesophagus. Subjects and methods This study comprised patients diagnosed to have Barrett’s oesophagus, and control subjects diagnosed to have gastrooesophageal reflux disease (GORD), all were diagnosed in the gastroenterology and endoscopy unit, King Fahd hospital, Riyadh, Saudi Arabia. Plasma adiponectin levels and its multimers were evaluated for patients with Barrett’s oesophagus and controls with GORD. Results There were 120 cases of Barrett’s oesophagus and 250 GORD controls. Total adiponectin was not significantly associated with Barrett’s oesophagus; low levels of LMW adiponectin and low LMW/total ratio were significantly present in patients with Barrett’s oesophagus. Conclusion Low levels of LMW adiponectin are significantly associated with Barrett’s oesophagus.

Changes in the Composition of Adiponectin Fractions over a 3-Year Period in Children: A Population-Based Cohort Study.

Little information is available regarding changes in adiponectin fractions. The objective of this study was to examine changes in the composition of differing adiponectin fractions using a population-based, prospective pediatric cohort. A total of 358 fourth graders (9-10 years old) from Ina town in Saitama, Japan, were followed up for 3 years. BMI and total adiponectin (TAD), high-molecular weight adiponectin (HAD), medium-molecular weight adiponectin, and low-molecular weight adiponectin levels were measured in these subjects at baseline and at the end of the follow-up. Of the fourth graders participating in the study, 326 (172 boys and 154 girls; follow-up rate, 91.1%) became available for follow-up. No significant changes were observed in TAD values after 3 years. HAD values were significantly decreased in both the boys (2.4 to 2.2 μg/mL: p < 0.001) and girls (3.1 to 2.7 μg/mL: p = 0.005). All values in the parameters examined at baseline and after 3 years were significantly correlated. A negative correlation was found between the ratios of follow-up compared to baseline values for BMI and those for TAD (boys, r = -0.322, p < 0.001; girls, r = -0.433, p < 0.001) as well as those for HAD (boys, r = -0.353, p < 0.001; girls, r = -0.351, p < 0.001). HAD had the most robust correlation between its values at baseline and those after 3 years in both boys and girls. The changes in HAD also had the most robust correlation between the changes in BMI in 3 years.

Low-molecular-weight adiponectin is more closely associated with disease activity of rheumatoid arthritis than other adiponectin multimeric forms.

Adiponectin is divided into high-molecular-weight (HMW), medium-molecular-weight (MMW), and low-molecular-weight (LMW) forms. These forms differ not only in the number of adiponectin molecules but also in their biological activity. There are conflicting findings regarding the role of adiponectin in rheumatoid arthritis (RA). Moreover, few reports have described the relationships between serum adiponectin multimers levels and RA. Therefore, we examined the association of total adiponectin and its multimers with RA. Two study groups were examined: 180 recently diagnosed untreated RA patients with disease duration less than 1 year (RA group) and 160 age- and sex-matched control subjects (control group). RA-related factors, blood pressure, body mass index, glucose, complete lipid profile, and adiponectin multimers were measured. The levels of total adiponectin and each multimer of adiponectin were significantly lower in the RA than in the control (P < 0.01). Serum levels of total, HMW, MMW, and LMW were positively correlated with triglycerides levels and negatively correlated with the Disease Activity Score for 28 joints (DAS28). Multivariate regression analysis showed that total, HMW, and MMW adiponectin were independently associated with serum triglycerides level. LMW adiponectin was independently correlated with serum triglycerides level and DAS28. The decreased LMW adiponectin levels may be associated with disease activity of RA.

Roles of the ALDH2 and ADH1B genotypes on the association between alcohol intake and serum adiponectin levels among Japanese male workers.

Adiponectin secreted from adipose tissue is assumed to mediate protective effects on development of metabolic syndrome (MetS) and MetS-related diseases such as cardiovascular diseases and cancer. Relationship between alcohol intake and circulating adiponectin levels is not consistent among the several previous studies. In the present study, we investigated effects of alcohol intake and the alcohol-related polymorphisms on serum adiponectin levels among Japanese male workers. We conducted a cross-sectional design study with 541 male workers aged 51.5 ± 5.9 (mean ± SD) years in a Japanese plant. Information on alcohol intake and other lifestyles was obtained by a self-administered questionnaire. Serum total adiponectin (T-Ad), high-molecular-weight adiponectin (HMW-Ad), medium-molecular-weight adiponectin (MMW-Ad), and low-molecular-weight adiponectin (LMW-Ad) levels were measured by the enzyme-linked immune assay system kit. Two genotypes in the alcohol dehydrogenase-1B (ADH1B) and aldehyde dehydrogenase-2 (ALDH2) genes were determined using blood sample. In multivariate regression analyses, we adjusted for age, body mass index, smoking, and physical exercise. Among all subjects, high alcohol consumption of 12 units (1 unit contains 22.9 g of ethanol) a week or more was negatively associated with T-Ad levels in the multivariate model, although not significant. When we performed analyses separately for each genotype, high alcohol consumption was negatively associated with T-Ad, HMW-Ad, and LMW-Ad levels only in those with ADH1B *2/*2. Such relationships were not observed in each ALDH2 genotype group. High alcohol consumption was inversely associated with T-Ad, HMW-Ad, and LMW-Ad levels in those with ADH1B *2/*2 genotype, but not in those with the other ADH1B genotypes. To our knowledge, this is the first study that reports combined effects of the alcohol-related polymorphisms and alcohol intake on serum adiponectin levels. Additional studies are required to confirm the present finding.

Low-molecular-weight adiponectin is more closely associated with episodes of asthma than high-molecular-weight adiponectin

Adiponectin is divided into high-molecular-weight (HMW), middle-molecular-weight (MMW) and low-molecular-weight (LMW) types. While HMW adiponectin has been studied by many researchers, the roles of MMW and LMW adiponectin have not yet been sufficiently elucidated. In addition, there are conflicting findings regarding the role of adiponectin in chronic inflammatory diseases, especially asthma. Therefore, we compared patients who suffered episodes of asthma in the past (=asthmatics) with those who did not (=non-asthmatics) in order to investigate the relationship between asthma and HMW, MMW and LMW adiponectin. The subjects in this study included 76 university students. None of the subjects were smokers, on regular medications or seeing a doctor regularly at the time. Fourteen subjects reported past histories of asthma. We also measured and compared the levels of leptin and ghrelin to that of adiponectin, as these hormones are connected with inflammatory conditions. Although the physical data of the asthmatics were similar to those of the non-asthmatics, the levels of ghrelin and all fractions of adiponectin tended to be lower in the asthmatics than in the non-asthmatics. While the levels of MMW and LMW adiponectin in the asthmatics were found to be significantly low, the levels of ghrelin and HMW adiponectin were not clear. According to a multivariate regression analysis of the MMW and LMW adiponectin levels, asthma was found to be more significantly associated with the LMW adiponectin level than age, waist circumference or HDL-C. The results suggest that LMW adiponectin may be associated with episodes of asthma in males.

Impact of artificial sunlight therapy on the progress of non-alcoholic fatty liver disease in rats

Non-alcoholic steatohepatitis (NASH) is recognized as the most severe form of non-alcoholic fatty liver disease, with likely progression to liver cirrhosis and hepatocellular carcinoma. However, there is no unified standard for diagnosis and therapeutics. This study aimed to characterize lipid transfer/metabolic proteins as non-invasive diagnostic markers, and to evaluate the therapeutic effects of phototherapy on the progression of NASH in rats. Lewis rats given a choline-deficient and iron-supplemented l-amino acid-defined (CDAA) diet and Zucker fa/fa rats were used as a diet-induced and an obesity-related NASH models, respectively, with or without phototherapy. Serum apolipoprotein E and low molecular weight-adiponectin levels were gradually reduced and reached the lowest level at fatty liver/NASH stage both in CDAA diet-induced NASH model and in genetically obese model. Total-adiponectin levels were dramatically elevated after NASH was established in CDAA diet-induced NASH model. Phototherapy ameliorated hepatocyte apoptosis, inflammation, fibrosis, and insulin/leptin resistance caused by CDAA diet with alteration of the levels of lipid transfer/metabolic proteins and elevation of the circulating active form of vitamin D(3). Vitamin D(3) supplementation ameliorated NASH progression in CDAA diet-induced NASH model. However, phototherapy failed to ameliorate the obesity and steatosis, suggesting that phototherapy may possess anti-inflammatory/fibrotic activity rather than anti-obesity/steatotic activity. These results suggest that serum lipid transfer/metabolic proteins and vitamin D(3) status may be effective biomarkers for non-invasive diagnosis of NASH progression, and that phototherapy may be a good complementary therapy for NASH because of its regulation of lipid transfer/metabolic proteins and vitamin D(3).

Association of adiponectin multimers with Barrett’s oesophagus

Objective:Barrett’s oesophagus is associated with abdominal obesity. Adiponectin is a peptide that is secreted from adipocytes and circulates in three multimeric forms: low molecular weight (LMW), middle molecular weight (MMW),...

Adiponectin Oligomers and Ectopic Fat in Liver and Skeletal Muscle in Humans

We aimed at determining which circulating forms of the adipokine adiponectin that increases lipid oxidation in liver and skeletal muscle are related to ectopic fat in these depots in humans. Plasma total-, high-molecular weight (HMW)-, middle-molecular weight (MMW)-, and low-molecular weight (LMW) adiponectin were quantified by an enzyme-linked immunosorbent assay. Their relationships with liver- and intramyocellular fat, measured using (1)H magnetic resonance spectroscopy, were investigated in 54 whites without type 2 diabetes. Liver fat, adjusted for gender, age, and total body fat, was associated only with HMW adiponectin (r = -0.35, P = 0.012), but not with total-, MMW-, or LMW adiponectin. In addition, subjects with fatty liver (liver fat > or =5.56%, n = 15) had significantly lower HMW- (P = 0.04), but not total-, MMW-, or LMW adiponectin levels, compared to controls (n = 39). Similarly, intramyocellular fat correlated only with HMW (r = -0.32, P = 0.039), but not with the other circulating forms of adiponectin. These data indicate that, among circulating forms of adiponectin, HMW is strongly related to ectopic fat, thus possibly representing the form of adiponectin regulating lipid oxidation in liver and skeletal muscle.

Clinical Significance of High-Molecular Weight Form of Adiponectin in Male Patients With Coronary Artery Disease

It has been reported previously that the measurement of plasma total adiponectin level is clinically useful to estimate the risk of coronary artery disease (CAD). Here, the relevance of high molecular weight (HMW) adiponectin with risk factors for atherosclerosis is investigated A total of 186 consecutive male CAD patients participated in the study and were categorized into quartiles based on their total adiponectin level. The interquartile cut-off points were 4.0, 5.5 and 7.0 microg/ml. The HMW adiponectin levels were significantly lower in the quartile of lower total adiponectin levels both in non-diabetic and diabetic patients. In contrast, low molecular weight adiponectin levels (which were calculated as the Total - HMW) were constant. In univariate analysis, total adiponectin correlated negatively with body mass index and hemoglobin (Hb) A1c, and HMW adiponectin correlated negatively with HbA1c in non-diabetic patients. On the other hand, total and HMW adiponectin correlated positively with high-density lipoprotein-cholesterol (HDL-C) in diabetic patients. Multiple regression analysis revealed that HMW adiponectin correlated negatively with HbA1c in non-diabetic patients, and total and HMW adiponectin correlated positively with HDL-C in diabetic patients. Change in the HMW isoform reflects a change in total adiponectin level. Measurement of total and HMW adiponectin were equally useful in assessing metabolic risk in CAD patients.