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PubMed2005

Anomalously phosphorylated tau and Abeta fragments in the CSF correlates with cognitive impairment in MCI subjects.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the presence of extracellular amyloid deposits, consisting largely of Abeta peptide and the presence of intraneuronal aggregates of neurofibillary tangles formed by tau. Development of cerebrospinal fluid (CSF) biomarkers has become a rapidly growing research field, considering the need for diagnostic tools for AD, thus allowing therapeutic compounds to have the greatest potential for being effective. We have focused on the relationships between critical biomarkers such as tau and Abeta in the CSF and the cognitive impairment of patients, as assessed by a battery of neuropsychological tests derived from CDR and CERAD, of value in the evaluation of AD patients. As part of a longitudinal study, we analyzed by ELISA and Western blots the levels and molecular patterns of hyperphosphorylated tau in the CSF of three different groups of patients: AD patients between 69- and 73-years-old, a group characterized with mild cognitive impairment (MCI) between 65- and 70-years-old, and a non-demented neurological control group of comparable ages. The levels of AT8-reactive phosphorylated tau were significantly higher (P<0.05) in AD patients (0.604+/-0.078, n=23) as compared with the control group (0.457+/-0.086, n=25). No differences between the levels of AT8-reactive tau of MCI patients (0.510+/-0.090, n=45) and controls were observed. However, when the MCI group was divided on the basis of the total box score (TBS) from CDR, those subjects with a TBS<1.5 presented tau levels (0.456+/-0.032, n=31) similar to controls, whereas those patients with TBS>or=1.5 displayed tau levels (0.590+/-0.086, n=14) comparable with those of AD. Western blot analyses revealed a higher AT8 reactivity in CSF samples of AD patients as compared with MCI and control samples, indicating higher levels of AD tau phosphoepitopes in the CSF. Tau heterogeneity was observed in samples of AD and MCI with higher impairment as compared with controls. As expected from previous reports, levels of Abeta (1-42) were lower (0.052+/-0.005) than controls (0.070+/-0.010), whereas the levels of MCI group were 0.060+/-0.007. The MCI group with a TBS>or=1.5 presented Abeta levels of 0.053+/-0.005 similar to those of AD patients, whereas the MCI group with TBS<1.5 exhibited Abeta levels (0.066+/-0.007) similar to controls. Studies highlight the relationships between anomalously phosphorylated tau markers in CSF with the information from TBS analysis of the different groups of patients.

Aged↗
PubMed2006

Inflammation markers predicting frailty and mortality in the elderly.

Greater numbers of individuals are living to older ages. A major concern at both individual and population levels is how to live these years at a high functional level. If we had physiological markers to identify those at risk for progressive functional decline and impeding death, therapies could be targeted towards these individuals to prevent adverse outcomes. Senescence is presently considered as the consequence of lifelong antigenic stress impinging upon the individual genetic background. We might consider inflammation markers as synthetic measures of lifelong attrition combined with genetic tendency to develop an inflammatory phenotype. Such biomarkers are the most powerful predictors of frailty and mortality in the elderly available today. The aim of this review is to translate results from the research on ageing into a practical view, suggesting new tools for the clinical approach to older people.

Aged↗
PubMed1999

Biological monitoring of exposure to pesticides: current issues.

Biological monitoring is becoming an increasingly important element of field studies designed to assess the risk from occupational pesticide exposure for preventive purposes. Selection of suitable biomarkers of exposure to pesticides, development of detection methods, validation of measurement and interpretation of results are of utmost concern among current issues. This paper provides an overview on the research strategies and application of biological monitoring of pesticide exposure.

Acetylcholinesterase↗
PubMed2002

Biomonitoring of polycyclic aromatic hydrocarbons in human urine.

Measurement of polycyclic aromatic hydrocarbons (PAH) metabolites in human urine is the method of choice to determine occupational and/or environmental exposure of an individual to PAH, in particular, when multiple routes of exposure have to be taken into account. Requirements for methods of biomonitoring PAH metabolites in urine are presented. Studies using 1-hydroxypyrene or phenanthrene metabolites including its phenols and dihydrodiols are summarized. The role of these PAH metabolites as established biomarkers and also more recent developments of PAH biomonitoring are discussed.

Environmental Monitoring↗
PubMedDate not supplied

Characterization of proteins in human pancreatic cancer serum using differential gel electrophoresis and tandem mass spectrometry.

The purpose of this study was to develop techniques for identifying cancer biomarkers in human serum using differential in-gel electrophoresis (DIGE), and characterizing the protein biomarkers using tandem mass spectrometry (MS/MS). A major problem in profiling protein expression by DIGE comes from the presence of high concentrations of a small number of proteins. Therefore, serum samples were first chromatographed using an immunoaffinity HPLC column (Agilent Technologies), to selectively remove albumin, immunoglobulins, transferrin, haptoglobin, and antitrypsin. Serum samples from three individuals with pancreatic cancer and three individuals without cancer were compared. Serum samples were processed using the immunoaffinity column. Differential protein analysis was performed using DIGE. A total of 56 protein spot-features were found to be significantly increased and 43 significantly decreased in cancer serum samples. These spot features were excised, trypsin digested, and analyzed by MALDI/TOF/TOF (4700 Proteomics Analyzer, Applied Biosystems). We identified 24 unique proteins that were increased and 17 unique proteins that were decreased in cancer serum samples. Western blot analysis confirmed increased levels of several of these proteins in the pancreatic cancer serum samples. In an independent series of serum samples from 20 patients with pancreatic cancer and 14 controls, increased levels of apolipoprotein E, alpha-1-antichymotrypsin, and inter-alpha-trypsin inhibitor were found to be associated with pancreatic cancer. These results suggest that affinity column enrichment and 2-D DIGE can be used to identify numerous proteins differentially expressed in serum from individuals with pancreatic cancer.

Adult↗
PubMed2000

Influence of total IgE and seasonal increase of eosinophil cationic protein on bronchial hyperreactivity in asthmatic grass-sensitized farmers.

BACKGROUND: This study correlates biomarkers of atopy (serum total and specific IgE) and inflammation (serum eosinophil cationic protein) with bronchial hyperreactivity assessed after the complete end of pollination, in a group of farmers suffering from grass-allergic asthma. METHODS: A total of 28 asthmatic farmers, with allergy to grass pollen, reporting persistent asthma symptoms after grass pollination, were enrolled. An accurate allergologic screening excluded other sensitizations. Analysis of total and grass-specific IgE and eosinophil cationic protein was carried out before (March) and during (May) the following spring. After the complete end of pollination, bronchial hyperreactivity was assessed. RESULTS: Symptoms (cough, wheezing) persisted during the autumn for a mean period of 41 days (range 13-69). Total IgE was moderately high and grass-specific IgE ranged from 9.25 to 41.12 kU/l without significant differences before and during spring. On the contrary, serum ECP levels significantly increased during the pollination period. PD20 methacholine evaluated after the end of grass pollination was negatively significantly correlated with levels of total IgE (r=-0.73; P<0.01) and the increase (from March to May) of serum ECP (r=-0.75; P<0.01). However, PD20 methacholine did not correlate with grass-specific IgE and serum ECP absolute values of both March and May. A positive correlation was found between number of postseasonal days with symptoms and both spring increase of serum ECP (r=0.75; P=0.04) and levels of total IgE (r=0.76; P<0.01). The number of postseasonal days with symptoms inversely correlated with postseason PD20 methacholine (r=-0.76; P<0.01). CONCLUSIONS: The study demonstrates that in grass-sensitized farmers with asthmatic symptoms persisting for several weeks after grass pollination has ceased, the degree of airways hyperreactivity and the duration of postseasonal symptoms are directly related to the spring increase of ECP levels, as well as to the level of total IgE in serum. This allows us to identify two candidate biomarkers for the risk of developing prolonged asthma symptoms, and for the effective monitoring of anti-inflammatory treatment and allergen-specific immunotherapy.

Adult↗
PubMed2006

Androgen receptor mutation (T877A) promotes prostate cancer cell growth and cell survival.

Alteration of the AR functions due to amplification, overexpression and somatic mutation of the AR itself or altered interaction of AR with other cell growth regulatory proteins, may contribute to a significant subset of advanced prostate cancer (CaP). Very little is known about the pathways impacted by AR dysfunctions, although CaP associated AR alterations suggest the biological role of the AR dysfunction in disease progression. Comparative evaluations of wild type (wt) AR and mutant (mt) ARs in appropriate experimental models should provide a better understanding of the functional impact of AR alterations in CaP. Here, we provide direct evidence showing cell growth/cell survival promoting effects of the widely studied CaP associated AR mutation (T877A). In contrast to Ad-wtAR or Ad-control infected LNCaP or LAPC4 cells, Ad-mtAR (T877A) infected LNCaP or LAPC4 cells continued to grow in the androgen-deprived medium and exhibited an androgen independent AR-transcription factor activity. Further, Ad-mtAR (T877A) infected LNCaP or LAPC4 cells exhibited enhanced cell growth in the presence of lower concentrations of the synthetic androgen, R1881. Of note, Ad-mtAR (T877A) infected LNCaP cells showed striking resistance to cell growth inhibition/apoptosis mediated by the wt p53. Taken together, these findings provide novel insights into the AR dysfunctions resulting from the T877A mutation and functionally similar AR alterations may provide selective cell growth/survival advantage for CaP progression. These observations have important implications for developing biology-based prognostic biomarkers and therapeutic strategies for CaP showing such AR dysfunctions.

Apoptosis↗
PubMed2006

Post-translational modifications regulating the activity and function of the nuclear factor kappa B pathway.

The diverse cellular and biological functions of the nuclear factor kappa B (NF-kappaB) pathway, together with the catastrophic consequences of its aberrant regulation, demand specific and highly regulated control of its activity. As described in this review, regulation of the NF-kappaB pathway is brought about through multiple post-translational modifications that control the activity of the core components of NF-kappaB signaling: the IkappaB kinase (IKK) complex, the IkappaB proteins and the NF-kappaB subunits themselves. These regulatory modifications, which include phosphorylation, ubiquitination, acetylation, sumoylation and nitrosylation, can vary, depending on the nature of the NF-kappaB-inducing stimulus. Moreover, they frequently have distinct, sometimes antagonistic, functional consequences and the same modification can have different effects depending on the context. Given the important role of NF-kappaB in human health and disease, understanding these pathways will not only provide valuable insights into mechanism and function, but could also lead to new drug targets and the development of diagnostic and prognostic biomarkers for many pathological conditions.

Animals↗
PubMed2000

One year growth hormone replacement therapy does not alter colonic epithelial cell proliferation in growth hormone deficient adults.

OBJECTIVE: Increased colonic epithelial cell proliferation has been found in various conditions associated with increased risk of colorectal cancer including acromegaly. In a placebo-controlled study we determined the effect of growth hormone (GH) replacement therapy in GH deficient adults on the colonic epithelial proliferation rate. PATIENTS AND DESIGN: Sixteen GH deficient adults were randomised to low dose GH therapy (1 U (0.5 mg) subcutaneously per day, n = 5), high dose GH therapy (2 U daily, n = 5) or placebo (n = 6) during 6 months. Thereafter, all patients were treated with 2 U of GH daily during a 6-months open extension period. MEASUREMENTS: Plasma Insulin-like growth hormone I (IGF-I) and IGF binding protein 3 (IGF BP3) concentrations were measured using commercial RIA kits. The colonic epithelial proliferation rate, expressed as overall crypt labelling index (LI) using 5-bromo-2'-deoxyuridine (BrdU) immunostaining, was determined at baseline, after 6 months treatment and at the end of the 6 months open extension period. RESULTS: IGF-I rose from 8.9 +/- 6.7 to 34.6 +/- 20.0 nmol/l after 6 months in 8 GH treated patients (P < 0.01 from baseline; P < 0.01 from change with placebo). In the extension study, plasma IGF-I was also increased in the patients who previously received placebo (P < 0.02, n = 5). LI was evaluable in 14 biopsies at baseline, in 16 after 6 months and in 14 after 12 months. Overall crypt LI did not change in 8 GH treated patients after 6 months (P > 0.40 from baseline; P > 0.80 from change with placebo). In the extension study, overall crypt LI was also unchanged in those patients who received GH after placebo (n = 5, P > 0.40) and in those who continued GH replacement (n = 9, P > 0.60; P > 0.80 from change in initially placebo treated patients). Separate evaluation of the LI at the basal, mid and luminal portions of the colonic crypts also did not reveal any effect of GH treatment on BrdU labelling. CONCLUSIONS: Six to 12 months of GH replacement therapy, aimed to increase plasma IGF-I into the (high) physiological range, does not adversely affect colonic epithelial cell proliferation as a biomarker for the risk of development of colorectal cancer.

Adult↗
PubMed2001

Gastrin-releasing peptide is a potent vasodilator in humans.

OBJECTIVES: Our objective was to characterize the local vascular effects of gastrin-releasing peptide in forearm resistance vessels as a biomarker to aid the clinical development of broad-spectrum neuropeptide antagonists as anticancer agents. METHODS: On different occasions, 7 healthy male volunteers received brachial artery infusions of gastrin-releasing peptide, and forearm blood flow was measured by venous occlusion plethysmography. Dose-finding studies identified a range of pharmacologically active doses of gastrin-releasing peptide (3 to 450 pmol/min) for use in dose response and tachyphylaxis studies. The nitric oxide clamp method was used for the assessment of the contribution of nitric oxide to the vasodilatory effect shown. RESULTS AND CONCLUSIONS: Gastrin-releasing peptide proved to be a potent, dose-dependent arteriolar vasodilator. The time to onset and offset of effect was rapid, within minutes, and marked tachyphylaxis was shown, with recovery by approximately 20 minutes. The contribution of nitric oxide to this vasodilatation was minimal. Forearm blood flow studies with the use of gastrin-releasing peptide may be usefully incorporated into the further clinical development of broad-spectrum neuropeptide growth factor antagonists.

Adult↗
PubMed1997

Age-related association of tail tendon break time with tissue pentosidine in DBA/2 vs C57BL/6 mice: the effect of dietary restriction.

In recent years, there has been a growing interest in the development of a panel of biomarkers useful in the evaluation of interventions on aging processes. An ideal marker should change with age, be related to species longevity, and respond to the effects of dietary restriction, which is the only intervention currently known to increase species longevity. In the present study; we compared parameters of collagen aging (i.e., tail tendon break time [TBT] and the glycoxidation product pentosidine) in tendon, ear, and skin of two species of rodents with different life spans: the shorter-lived DBA/2 versus the longer-lived C57BL/6 mouse strain. Both TBT and tissue pentosidine significantly increased with age in both strains of mice. The rate of increase for TBT And pentosidine occurred faster for the DBA/2 compared with the C57BL/6 strain. Dietary restriction significantly inhibited the age-related increase of TBT and pentosidine formation rte in DBA/2 mice. In C57BL/6 mice, the age-related increase of TBT was significantly inhibited by dietary restriction. However, except for tendon at 24 months, pentosidine level was not affected by dietary restriction. These studies show that the rate of collagen aging, as reflected by TBT and glycoxidation, increases proportionally with age, and that these rate increases are related to longevity in two strains of mice. Pentosidine can be monitored with age just as well in a piece of easily accessible ear tissue as in skin or tendon. Thus, pentosidine is expected to be a useful and easily measurable noninvasive marker in future intervention studies on aging.

Aging↗
PubMed2001

Gene expression profiles for monitoring radiation exposure.

Previous demonstrations that the dose, dose rate, radiation quality, and elapsed time since ionising radiation exposure result in variations in the response of stress genes suggest that gene expression signatures may be informative markers of radiation exposure. Defining sets of genes that ate specific for different outcomes of interest will be key to such an approach. A generalised post-exposure prolile may identify exposed individuals within a population, while more specific fingerprints may reveal details of a radiation exposure. Changes in gene expression in human cell lines occur after as little as 0.02 Gy rays, and in peripheral blood lymphocytes alter as little as 0.2 Gy. Diverse genes are also elevated in vivo in mice 24 h after 0.2 Gy irradiation. Ongoing microarray analyses meanwhile continue to identify large numbers of potential biomarkers from varied irradiation protocols. Development of computation-intensive informatics analysis methods will be needed for management of the complex gene expression profiles resulting from such experiments. Although the preliminary data are encouraging, significant work remains before meaningful correlations with risk or practical assessment of exposure can be made by gene expression profiling.

Gene Expression↗
PubMed2000

Extraction and quantification by ELISA of eggshell organic matrix proteins (ovocleidin-17, ovalbumin, ovotransferrin) in shell from young and old hens.

The eggshell matrix is mainly composed of proteins that are thought to influence shell formation and calcification and, thus, modify the resulting properties of the shell. We investigated the potential of some of these proteins as biomarkers of eggshell quality by developing a competitive indirect ELISA for quantifying ovotransferrin, ovalbumin, and ovocleidin-17 in eggshell extract. Eggshell fragments were demineralized in acetic acid (20%) and freeze-dried. The micro-extraction yield was markedly increased (>50%) when Tween 20 was added to the subsequent extraction and dialysis milieus. Microplates were coated with ovotransferrin and ovalbumin in a 0.1M carbonate-bicarbonate buffer, but ovocleidin-17 was fixed with acetone (-20 C, 20 min). Optimal dilutions of the monoclonal (ovotransferrin) and polyclonal (ovalbumin and ovocleidin-17) antibodies were 1/3,000, 1/25,000 and 1/4,000, respectively. The inhibition curves were optimized by preincubating the antibodies and proteins overnight. The intraassay coefficient (<5%), parallelism of the standards and samples curves, and recovery (101%) were satisfactory for ovotransferrin. Measurements of ovalbumin were less precise because of higher interassay variation and differences between the slopes of standard and sample inhibition curves. Ovocleidin-17 assays showed similar slopes for standard and eggshell extracts. Although the total protein in soluble matrix extracts was not affected by age, the concentrations of these proteins were higher in eggshell extracts from older hens compared with those from young hens: 1.98x for ovotransferrin, 1.86x for ovalbumin, and 1.58x for ovocleidin-17. The quantification of specific eggshell matrix proteins in shell of differing quality is, therefore, a promising tool for analyzing the origin of eggshell faults and may provide useful information for breeding programs.

Aging↗
PubMed2004

Protease-activated receptor signaling in the regulation of inflammation.

OBJECTIVE: To discuss recent studies addressing the relationship between protease-activated receptor signaling, coagulation, and inflammation. DATA EXTRACTION AND SYNTHESIS: This review article covers relevant original articles published until October 2003 dealing with animal models, clinical trial data, and in vitro experiments. CONCLUSIONS: Although activation of protease-activated receptors has been implicated in the proinflammatory effects of the coagulation cascade, current data provide evidence that protease-activated receptor signaling plays a more complex role in the regulation of inflammation and endothelial homeostasis. Sensitive assays for coagulation activation have provided clear evidence that targeting the coagulation pathway effectively reduces the coagulopathy in sepsis. However, the effect of these anticoagulant agents on sepsis-associated inflammation is less clear. Further insight into this question will require the development or use of additional biomarkers for assessing pharmacologic interference with coagulation-related cell-signaling pathways.

Animals↗
PubMedDate not supplied

The role of biomarkers in clinical trials for Alzheimer disease.

Biomarkers are likely to be important in the study of Alzheimer disease (AD) for a variety of reasons. A clinical diagnosis of Alzheimer disease is inaccurate even among experienced investigators in about 10% to 15% of cases, and biomarkers might improve the accuracy of diagnosis. Importantly for the development of putative disease-modifying drugs for Alzheimer disease, biomarkers might also serve as indirect measures of disease severity. When used in this way, sample sizes of clinical trials might be reduced, and a change in biomarker could be considered supporting evidence of disease modification. This review summarizes a meeting of the Alzheimer's Association's Research Roundtable, during which existing and emerging biomarkers for AD were evaluated. Imaging biomarkers including volumetric magnetic resonance imaging and positron emission tomography assessing either glucose utilization or ligands binding to amyloid plaque are discussed. Additionally, biochemical biomarkers in blood or cerebrospinal fluid are assessed. Currently appropriate uses of biomarkers in the study of Alzheimer disease, and areas where additional work is needed, are discussed.

Alzheimer Disease↗
PubMed2000

An interpretation for the ROC curve and inference using GLM procedures.

The accuracy of a medical diagnostic test is often summarized in a receiver operating characteristic (ROC) curve. This paper puts forth an interpretation for each point on the ROC curve as being a conditional probability of a test result from a random diseased subject exceeding that from a random nondiseased subject. This interpretation gives rise to new methods for making inference about ROC curves. It is shown that inference can be achieved with binary regression techniques applied to indicator variables constructed from pairs of test results, one component of the pair being from a diseased subject and the other from a nondiseased subject. Within the generalized linear model (GLM) binary regression framework, ROC curves can be estimated, and we highlight a new semiparametric estimator. Covariate effects can also be evaluated with the GLM models. The methodology is applied to a pancreatic cancer dataset where we use the regression framework to compare two different serum biomarkers. Asymptotic distribution theory is developed to facilitate inference and to provide insight into factors influencing variability of estimated model parameters.

Humans↗
PubMed2006

Magnetic resonance spectroscopy for measuring the biodistribution and in situ in vivo pharmacokinetics of fluorinated compounds: validation using an investigation of liver and heart disposition of tecastemizole.

BACKGROUND AND OBJECTIVE: The study of biodistribution and in situ pharmacokinetics is a challenging, but sometimes very important, aspect of premarketing characterization of drugs. We aimed to develop a non-invasive fluorine magnetic resonance (MR) spectroscopic method for the absolute quantitation of a mono-fluorinated compound and of its metabolites in the heart and liver of healthy subjects for this purpose. METHOD: We used fluorine MR spectroscopy (MRS) at 4 T (Tesla) and external standardization in an open label multiple-dose study. Twenty-three healthy adult subjects were enrolled in the study. The surface coil localized fluorine MR spectrum was monitored in the heart and liver at baseline and after oral administration of multiple doses of tecastemizole. Steady-state measurements were made at set time points that depended upon dose, and washout measurements were made only on subjects in which in vivo fluorine signal was observed. RESULTS AND DISCUSSION: At 4 T, under the given experimental conditions, the method had a lower limit of quantitation (LLOQ) of about 2.6 microm and a limit of detection (LOD) of about 0.3 microm for solution state samples (linewidth approximately 15 Hz). The measurement reproducibility was 6.4% using a 50 microm phantom. The effect of MR operator and spectral analyst on the calculated calibration curve slope was small, with inter-rater correlation coefficients of 0.999 and 0.998 respectively. MR signal from fluorine-containing tecastemizole-related moieties was observed in situ only at day 8 in the liver of three of five subjects dosed at 270 mg/day. The average in situ concentration was estimated to be 58+/-22 microm, with an average test-retest reproducibility of 216%. Extrapolating the in vitro results to human measurements, with an approximate linewidth of 250 Hz, predicts in situ LOD and LLOQ values of approximately 6 and 44 microm respectively. However, the human study had a fluorine MRS LOD of approximately 20 microm. The decrease in sensitivity and the increase in variability of the in vivo, in situ measurements compared with the validation study most likely arose from coil placement and incomplete rephasing of the MR signal by the respiratory phase compensation method. CONCLUSION: The measured concentrations were the lowest ever recorded for a multi-dose exogenous mono-fluorinated compound in the human liver using a validated fluorine MR quantitation method. The proposed non-invasive MR method for studying the biodistribution and in situ pharmacokinetics of mono-fluorinated compounds in the liver and heart should have broader application to the development of non-invasive biomarkers.

Adult↗
PubMed2005

Association between lifestyle factors and plasma adiponectin levels in Japanese men.

BACKGROUND: Adiponectin is an adipocyte-specific protein that plays a role in obesity, insulin resistant, lipid metabolism, and anti-inflammation. Hypoadiponectinemia may be associated with a higher risk for type 2 diabetes and cardiovascular disease. Some studies suggest that adiponectin levels are modulated by lifestyle factors, but little is known about the associations between lifestyle factors and plasma adiponectin levels in Japanese people. We therefore investigated the associations between lifestyle factors and plasma adiponectin levels in general Japanese men. METHODS: The subjects were 202 Japanese male workers who participated in an annual health check. They provided details about anthropometrical data, blood collection, their use of prescribed medication, and the clinical history of their families. They also completed a self-administered questionnaire about their lifestyles. RESULTS: Subjects with plasma adiponectin levels below 4.0 microg/ml had significantly lower levels of HDL cholesterol and higher levels of BMI, SBP, DBP, total cholesterol, FBG, and platelets than did subjects with higher adiponectin levels. In multiple logistic regression after multiple adjustment, a plasma adiponectin level below 4.0 microg/ml was significantly associated with smoking (odds ratio [OR] = 2.08, 95% confidence interval [CI] = 1.01-4.30), a daily diet rich in deep-yellow vegetables (OR = 0.25, 95% CI= 0.07-0.91), frequent eating out (OR = 2.45, 95% CI = 1.19-5.08), and physical exercise two or more times a week (OR = 0.21, 95% CI = 0.06-0.74). CONCLUSION: Our findings show that adiponectin levels in general Japanese men are independently related to smoking, dietary factors, and physical exercise. We think that lifestyle habits might independently modulate adiponectin levels and that adiponectin might be the useful biomarker helping people to avoid developing type 2 diabetes and cardiovascular disease by modifying their lifestyles.

Adiponectin↗