Lower Serum Adiponectin Levels Research Articles

Low Serum Adiponectin Levels in Korean Children with a Family History of Type 2 Diabetes Mellitus

Background/Aims: The current worldwide increases of type 2 diabetes mellitus (T2DM) in children coincide with increases in the prevalence of obesity. We investigated the insulin resistance and adiponectin levels of children and adolescents with a family history of T2DM (FHD). Methods: Our sample included 131 children and adolescents aged 8–15 years. Fasting plasma glucose, lipids, fasting insulin, adiponectin levels and HOMA-IR were analyzed according to FHD and obesity. Oral glucose tolerance tests were performed in all subjects except non-obese subjects without FHD. Results: Adiponectin levels of subjects with FHD were significantly lower than those of subjects without FHD in both the obese and nonobese groups. HOMA-IR was significantly higher in obese subjects with FHD than in those without FHD. Adiponectin levels were found to be independently associated with FHD and Matsuda index. The frequency of impaired glucose tolerance in obese subjects with FHD was more than four times higher compared to obese subjects without FHD. Conclusion: Our results suggest that FHD could be a risk factor of T2DM in obese Korean children, especially with low serum levels of adiponectin.

Relationship among Gensini score and levels of glucose and adiponectin in patients with stable angina pectoris

Objectives: Adiponectin is an adipocyte-secreted protein that modulates insulin sensitivity and whose low circulating concentration is associated with insulin resistance. We evaluated the association between serum adiponectin and blood glucose levels with coronary artery disease severity on the angiogram in patients with stable angina pectoris. Materials and methods: The study included 160 patients (82 males) with stable angina pectoris. The patients were divided into three groups according to the blood glucose levels on admission; thus, 24 had normal glucose group, 53 had impaired glucose tolerance group, and 53 had diabetes mellitus (DM) group. The severity of coronary lesions was assessed using the Gensini score. Serum adiponectin levels were measured in the all group. Results: The hypertension, hyperlipidemia, obesity, and insulin resistance were significantly higher in the DM group. Patients with DM significantly lower serum levels of adiponectin (13.55±7.16, p=0.002). The mean Gensini score was 40.84± 37.25 in the DM group (p=0.006). Conclusion: Serum adiponectin levels may be a clue for severity coronary artery disease in patients with stable angina pectoris.

Metabolic syndrome correlates intracoronary stenosis detected by multislice computed tomography in male subjects with sleep-disordered breathing

BackgroundSleep-disordered breathing (SDB), especially obstructive sleep apnea (OSA), has frequent complications include hypertension, dyslipidemia and insulin resistance based on abdominal obesity or excess visceral fat (called Syndrome Z). OSA is a potential risk factor for cardiovascular diseases. The clinical characteristics of Japanese OSA subjects with OSA remain unclear. The present study investigated prevalence and predictive factors of intracoronary stenosis detected by multislice computed tomography (MSCT) in Japanese male subjects with SDB/OSA.FindingsThe study (O-VFStudy) subjects were 39 Japanese men with SDB/OSA who underwent all-night cardiorespiratory monitoring with fully attended polysomnography, and moreover both fat computed tomography (CT) scan and 64-row MSCT coronary angiography. The prevalence of coronary stenosis in this selected population with SDB/OSA was 15%. Logistic regression analysis showed a significant relationship between age-adjusted CAD and metabolic syndrome (p < 0.05), but not serum adiponectin levels and nocturnal fall in adiponectin. Subjects with the metabolic syndrome had significantly higher prevalence of CAD (31.3 versus 4.3%, p = 0.033), and lower levels of serum adiponectin (4.5 ± 0.6 versus 6.4 ± 0.6 μg/mL, p = 0.014), compared with groups without the metabolic syndrome.ConclusionsThe present study describes that the prevalence of greater than 50% intracoronary stenotic lesions detected by MSCT was 15% and the metabolic syndrome was correlated with intracoronary stenosis detected by MSCT in Japanese SDB/OSA subjects.Trial RegistrationUMIN 000002997https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&type=summary&recptno=R000003633&language=E.

Protective role of adiponectin against ethanol-induced gastric injury in mice

Adiponectin is an anti-inflammatory molecule released from adipocytes, and serum adiponectin concentrations are reduced in obesity. We previously reported that gastric erosion occurs in association with obesity and low serum adiponectin levels. In the present study, we examined adiponectin-knockout (APN-KO) mice to elucidate the role of adiponectin in gastric mucosal injury. Gastric injury was induced by oral administration of ethanol in wild-type (WT) and APN-KO mice. Ethanol treatment induced severe gastric injury in APN-KO mice compared with WT mice. In APN-KO mice, increased apoptotic cells and decreased expression of prostaglandin E(2) (PGE(2)) were detected in the injured stomach. We next assessed the effect of adiponectin on the cellular response to ethanol treatment and wound repair in rat gastric mucosal cells (RGM1). Adiponectin induced the expression of PGE(2) and cyclooxygenase 2 (COX-2) in ethanol-treated RGM1 cells. RGM1 cells exhibited efficient wound repair accompanied by increased PGE(2) expression in the presence of adiponectin. Coadministration of adiponectin with celecoxib, a COX-2 inhibitor, inhibited efficient wound repair. These findings indicate that adiponectin has a protective role against ethanol-induced gastric mucosal injury in mice. This effect may be partially mediated by the efficient wound repair of epithelial cells via increased PGE(2) expression.

Associations between Adiponectin and Two Different Cancers: Breast and Colon

Breast and colon cancer are neoplasms well known to be related to obesity. Adiponectin, a protein that increases in obesity, seems to be involved in the relationship but clinical data are limited. In this study, we therefore evaluated the serum adiponectin levels in 87 breast and 27 colon cancer patients and assessed the relation with BMI, menopausal status, receptor status and stage of disease. Serum adiponectin levels were lower in cancer cases (8583 ± 2095 ng/ml for breast cancer, 9513 ± 2276 for colon cancer) than in controls (13905 ± 3263). A low serum adiponectin level may be associated with both breast and colon cancer, and that this association is not statistically significant for either receptor or menopausal status in breast cancer groups.

Hyperadiponectinemia protects against premature death in metabolic syndrome model mice by inhibiting AKT signaling and chronic inflammation

We previously reported that transgenic (Tg) expression of adiponectin significantly prolonged the lifespan of normal mice. The aim of this study was to elucidate the mechanism involved in the longevity effects of adiponectin using KK/Ta mice, a murine model of metabolic syndrome. We established a Tg line of KK/Ta (Tg-KK/Ta) mice expressing human adiponectin in the liver, and assessed their lifespan. The cause of death was determined by macroscopic and microscopic examinations immediately after death. The expressions of SIRT1, C-reactive protein (CRP), inflammatory cytokines, AMPK, and AKT were measured by quantitative real-time PCR, ELISAs, and/or western blotting. KK/Ta mice had lower serum adiponectin levels and shorter lifespan (57.6±13.9 vs 106.5±18.3 weeks, P<0.0001) than C57BL/6N mice. Tg adiponectin expression significantly extended the lifespan of KK/Ta mice (73.6±16.6 weeks, P<0.001) without affecting body weight, daily food consumption, or plasma glucose levels. Neoplasms were observed in only three of 22 KK/Ta mice that died spontaneously because of tumors. Atherosclerotic lesions were not detected in any mice. SIRT1 levels were not significantly different between KK/Ta and Tg-KK/Ta mice. Gene expressions of Crp, Tnfα, Il6, and Nfκb were increased in KK/Ta mice, but they were significantly attenuated in Tg-KK/Ta mice. Phosphorylated AMPK levels were increased and phosphorylated AKT levels were decreased in Tg-KK/Ta mice. The anti-inflammatory effects of adiponectin, achieved by inhibiting the AKT signaling pathway, may explain how adiponectin slows the accelerated aging process associated with the metabolic syndrome.

High prevalence of gastroesophageal reflux symptoms in type 2 diabetics with hypoadiponectinemia and metabolic syndrome

BackgroundThe prevalence of gastroesophageal reflux disease (GERD) has been increasing worldwide. Abdominal obesity or visceral fat accumulation rather than simple obesity is associated with GERD. Previous reports demonstrated the association between GERD and type 2 diabetes mellitus (T2DM). Signification of visceral fat accumulation and adiponectin in T2DM patients with GERD remains unclear. The present study investigated the relationships between GERD symptoms, visceral fat accumulation and adiponectin in subjects with T2DM.FindingsThe study (ADMIT study) subjects were 66 Japanese T2DM outpatients, who answered the questionnaire regarding GERD symptoms in Frequency Scale for the Symptoms of GERD (FSSG), and were measured visceral fat area by bioelectrical impedance analysis. Patients with FSSG scores of more than 8 were considered as positive. The prevalence of FSSG score ≥ 8 and average FSSG score in T2DM subjects with the metabolic syndrome (Mets) were significantly higher compared to those without Mets. The prevalence of FSSG score ≥ 8 and average FSSG score in T2DM subjects with low levels of serum adiponectin were significantly higher compared to those with high levels of serum adiponectin. Moreover, the combination of Mets and hypoadiponectinemia had a multiplicative effect on GERD symptom score (p = 0.047).ConclusionsOur study showed that the coexistence of MetS and low levels of serum adiponectin was associated with the higher prevalence of FSSG score ≥ 8 and the higher scores of GERD symptom in subjects with T2DM.Trial RegistrationUMIN 000002271.

Adiponectin inhibits oxidative stress in human prostate carcinoma cells

Emerging data suggest that obesity increases the risk of aggressive prostate cancer (PC), but the mechanisms underlying this relationship remain to be fully elucidated. Oxidative stress (OS) is a key process in the development and progression of PC. Adiponectin, an adipocyte-specific hormone, circulates at relatively high levels in healthy humans, but at reduced levels in obese subjects. Moreover, case-control studies also document lower levels of serum adiponectin in PC patients compared with healthy individuals. Human 22Rv1 and DU-145 PC cell lines were examined for the generation of OS and detoxification of reactive oxygen species after treatment with adiponectin. Normality was confirmed using the Shapiro-Wilk test and results were analyzed using a one-way analysis of variance. We demonstrate that adiponectin increased cellular anti-oxidative defense mechanisms and inhibited OS in a significant and dose-dependent manner. We show that adiponectin treatment decreased the generation of superoxide anion in both cell lines, whereas the transcript levels of NADPH oxidase (NOX)2 and NOX4 increased. We also found indications of an overall anti-oxidative effect, as the total anti-oxidative potential, catalase activity and protein levels, and manganese superoxide dismutase protein levels increased significantly (P<0.05) in both cell lines after treatment with adiponectin. Lower levels of adiponectin in obese individuals may result in higher levels of prostatic OS, which may explain the clinical association between obesity, hypoadiponectinemia and PC.

Low serum adiponectin level is predictor of arterial stiffness in new onset diabetes after renal transplantation

Background: The purpose of this study was to determine whether the level of adiponectin in serum of renal transplant patients is associated with arterial stiffness related to new onset diabetes after transplantation (NODAT). Methods: A total of 90 previously non-diabetic patients who underwent renal transplantation between 1999 and 2009 were enrolled. We evaluated their diabetic risk factors, lipid profiles, brachial-ankle pulse wave velocity (baPWV), ankle-brachial blood pressure index (ABPI) and serum adiponectin level before and after transplantation. Results: Eleven (12.2%) patients were diagnosed with NODAT and 79 (87.8%) without (non-NO-DAT). The mean post-transplant serum adiponectin level in NODAT patients was significantly lower than that in non-NODAT patients (11.9 vs. 16.4 μg/ml, p = 0.01), whereas the mean baPWV level in NODAT patients was significantly higher (1686 vs. 1468 cm/s, p = 0.016). We found a significant inverse correlation between mean pre-transplant serum adiponectin and baPWV level (r = -0.27, p = 0.011). Furthermore, patients with lower pretransplant serum adiponectin levels (<20 μg/ml) developed NODAT significantly more frequently than those with higher levels (p = 0.038) and the mean baPWV level in the former was also significantly higher (1520 vs. 1412 cm/s, p = 0.047). Conclusion: Our results indicate that low pre-transplant serum adiponectin level is associated with arterial stiffness in development of NODAT in patients who undergo renal transplantation.

Hepatitis C and Metabolic Disorders: Genetics, Mechanism, and Therapies (Clinical and Experimental)

Hepatitis C and Metabolic Disorders: Genetics, Mechanism, and Therapies (Clinical and Experimental)

Adipocytokines and ischemic stroke: Differential associations between stroke subtypes

Objective Experimental studies have indicated that adipocytokines are associated with vascular diseases with regard to the pathology of atherosclerotic plaque. We hypothesized that the strength of the associations between adipocytokines and stroke would differ between ischemic stroke subtypes. Methods A total of 96 acute ischemic stroke patients (within 5 days from onset) and 48 non-stroke subjects were analyzed in this study. Stroke patients were comprised of 26 strokes due to large artery atherosclerosis (LAA) and 72 non-LAA strokes. Venous blood from all participants was drawn after an overnight fast, and serum levels of leptin, adiponectin and resistin were measured by multiple sandwich immunoassay techniques. Results Compared with non-LAA strokes, patients with LAA strokes had lower levels of serum adiponectin (6.4 ± 3.1 vs. 8.5 ± 3.9 μg/mL; P = 0.04), and a higher level of leptin-to-adiponectin ratio (L:A ratio; 1.6 ± 1.4 vs. 0.9 ± 0.9; P < 0.01). Multinomial logistic regression analyses showed that, although none of the adipocytokines was associated with non-LAA strokes, lower adiponectin (adjusted OR, 0.79 per 1-μg/mL increase; 95% CI, 0.64–0.98), higher leptin (aOR, 1.12 per 1-ng/mL increase; 95% CI, 1.004–1.25) and higher L:A ratio (aOR, 2.93 per 1-quartile increase; 95% CI, 1.39–6.15) showed significant associations with increased odds of having LAA stroke, compared to non-stroke subjects. Conclusion From our study, we documented that leptin and adiponectin had differential association patterns with ischemic stroke according to the stroke subtype. Careful consideration of the heterogeneity of stroke subtypes would be warranted in studying the utility of biomarkers including adipocytokines.

Hypoadiponectinemia in Middle-aged Men with Type 2 Diabetes Mellitus is Associated with Left Atrium Enlargement

Background: Diabetes mellitus is frequently associated with a progression of left ventricular diastolic dysfunction and a decrease of serum adiponectin level. Left atrium (LA) enlargement is also associated with a functional impairment in diastolic heart failure. We investigated whether serum adiponectin level may be associated with LA size in type 2 diabetic patient. Methods and Results: Thirty-three male type 2 diabetic patients who did not have organic heart disease were categorized into a low adiponectin group (<5.0μg/mL, n=17, 58±8 years) or a preserved adiponectin group (≥5.0μg/mL, n=16, 60±11 years). Conventional echocardiographic assessment was performed in all patients. When compared with preserved adiponectin group, LA diameter (40±4 vs. 36±4 mm, p<0.05), plasma insulin concentration (8.1±2.5 vs. 5.9±1.6μU/mL, p<0.01) and the homeostasis model assessment index (3.1±1.0 vs. 2.0±0.5, p<0.001) were greater in low adiponectin group. Univariate correlation analysis revealed that LA diameter positively correlated with diastolic blood pressure (p<0.05), fasting plasma glucose concentration (p<0.05), while it negatively correlated with serum adiponectin level (p<0.01). Stepwise multiple regression analysis revealed that increase in LA diameter was independently predicted by low serum adiponectin level (F=7.53) and high diastolic blood pressure (F=4.12).

Association of low serum adiponectin levels with erosive esophagitis in men: an analysis of 2405 subjects undergoing physical check-ups

Obesity is a risk factor for gastro-esophageal reflux disease (GERD). It is generally considered that intra-abdominal pressure in obese subjects is involved in the pathogenesis of GERD through acid exposure to the esophagus. Recently, visceral fat has been recognized as an endocrine organ that secretes various adipocytokines including adiponectin. The aim of this study was to elucidate the relation between adiponectin and erosive esophagitis. This was a cross-sectional retrospective observational study: 2405 consecutive subjects who underwent screening esophago-gastro-duodenoscopy with serum adiponectin measurement as part of their physical check-up programs were analyzed. Clinical factors were compared between subjects with and without erosive esophagitis. The association between adiponectin and erosive esophagitis was assessed using a bootstrapping re-sampling method after adjustment for factors that tended to be different in univariate analysis. Serum adiponectin levels were significantly lower in those with erosive esophagitis (8.17 μg/ml) than in those without (10.1). The erosive esophagitis group had a greater body mass index (BMI) and waist circumference (WC) and a higher prevalence of hiatal hernia. Using the bootstrap method, with a lower adiponectin cut-off value of 3-7 μg/ml, the lower limit of the 95% confidence interval of the adjusted odds ratio consistently exceeded 1 after adjustment for BMI and hiatal hernia in men. When adjusting for WC instead of BMI, the effect of adiponectin was reduced but remained significant at a lower cut-off value (3-3.5 μg/ml). Low serum adiponectin levels may be associated with an increased risk for erosive esophagitis in men.

Serum adiponectin and leptin as predictors of the presence and degree of coronary atherosclerosis

The association of adipocyte-derived proteins, adiponectin and leptin, with the degree of coronary atherosclerosis has not been not been well elucidated. This study aimed to determine the relationship between serum adiponectin and leptin with the presence and degree of coronary atherosclerosis. Seventy patients and 20 matched controls were recruited. Angiographic evaluation of coronary atherosclerosis was carried out by assessing three atherosclerotic indices, severity (transverse disease), extent (longitudinal disease), and pattern (lesion complexity). The independent predictors of atherosclerosis severity were larger waist/hip ratio, followed by higher low-density lipoprotein-cholesterol, low serum adiponectin level, older age, higher leptin level, current unstable angina, and finally previous myocardial infarction (MI). This model is a good one as indicated by the model-adjusted r (50%). For extent index, lower serum adiponectin level was by far the most important independent predictor, followed by higher low-density lipoprotein-cholesterol, older age, and previous MI, whereas higher serum leptin level was only a univariate predictor. The model-adjusted r was 65%. For pattern index, the independent predictors were previous MI, lower serum adiponectin level, larger waist/hip ratio, higher serum leptin level, older age, and higher fasting blood glucose level. The model-adjusted r was 62%. Both serum adiponectin and leptin might play an important pathogenic role not only in the occurrence but also in the severity, extent, and lesion complexity in coronary artery disease patients.

Genetic variants in ADIPOQ gene and the risk of type 2 diabetes: a case–control study of Chinese Han population

This study was to evaluate the association between ADIPOQ gene variants and type 2 diabetes mellitus (T2DM). TaqMan(®) assay was performed to test the genotypes in T2DM patients (n=1,105) and normal control subjects (n=1,107). Serum adiponectin concentration was measured by ELISA kit. The variant genotypes rs7649121AT and rs7649121AT/TT, compared with the AA genotype, were associated with a significantly decreased risk of T2DM [Adjusted OR (95% CI)=0.79(0.66-0.95), 0.80(0.67-0.96), respectively]. In stratified analysis, rs2241767AG genotype increased the risk of T2DM in obesity group [Adjusted OR (95% CI)=1.32(1.03-1.69)]. Patients with genotype AG/GG of rs2241767 had lower levels of serum adiponectin than those with the genotype AA (P=0.044). Haplotype analyses were not significant. Crossover analysis of rs7649121 and environmental risk factor (obesity) indicated that the protect effect of rs7649121AT/TT maybe offset by the environmental risk. Those who exposed to environmental risk factor (obesity) had a chance to attack T2DM compared with those who did not expose to the two factors [Adjusted OR (95% CI)=1.64(1.30-2.06)]. This study suggested that the ADIPOQ gene polymorphisms were associated with the risk of T2DM in a Chinese Han population.

&amp;lt;italic&amp;gt;ADIPOQ&amp;lt;/italic&amp;gt; Gene Variants Associated with Susceptibility to Obesity and Low Serum Adiponectin Levels in Healthy Koreans

OBJECTIVESThis study aimed to measure the association between the adiponectin, C1Q and collagen domain-containing (ADIPOQ) gene variants and obesity in Koreans.METHODSThree single nucleotide polymorphisms located in the ADIPOQ gene were genotyped in a population-based cross-sectional study of 986 healthy Koreans. Three different case-control groups (i.e. G1, G2, and G3) were defined according to body mass index (BMI) and serum adiponectin levels. Allelic and genotypic associations of this gene with obesity were measured using multivariate logistic regression analyses in each group.RESULTSThe G allele of -11377C>G, a polymorphism located in the promoter region of the ADIPOQ gene (odds ratio (OR), 1.48; 95% confidence interval, 1.13-1.94) and most haplotypes including this allele significantly increased the risk for obesity. However, the OR decreased from 3.98 (G1 group) to 2.90 (G2 group) and 2.30 (G3 group) when a less strict definition of obesity was used. Most haplotypes, including this allele, significantly increased the risk of obesity. The statistical evidence from the GG genotype of -11377C>G (OR, 3.98) and the GT/GT diplotype composed of -11377G>C and +45T>G (OR, 5.20) confirmed the contribution of the G allele toward a predisposition for obesity.CONCLUSIONThese results suggest the contribution of the ADIPOQ gene toward susceptibility to obesity in healthy Koreans. The high-risk genotypes and haplotypes identified here may provide more information for identifying individuals who are at risk of obesity.

Protective Role of Adiponectin Against Ethanol Induced Gastric Injury in Mice

19 Adiponectin is an anti-inflammatory molecule released from adipocytes, and serum adiponectin 20 concentrations are reduced in obesity. We previously reported that gastric erosion occurs in 21 association with obesity and low serum adiponectin levels. In the present study, we examined 22 adiponectin-knockout (APN-KO) mice to elucidate the role of adiponectin in gastric mucosal 23 injury. Gastric injury was induced by oral administration of ethanol in wild-type (WT) and 24 APN-KO mice. Ethanol treatment induced severe gastric injury in APN-KO mice compared with 25 WT mice. In APN-KO mice, increased apoptotic cells and decreased expression of prostaglandin 26 E2 (PGE2) were detected in the injured stomach. We next assessed the effect of adiponectin on 27 the cellular response to ethanol treatment and wound repair in rat gastric mucosal cells (RGM1). 28 Adiponectin induced the expression of PGE2 and cyclooxygenase 2 (COX-2) in ethanol-treated 29 RGM1 cells. RGM1 cells exhibited efficient wound repair accompanied by increased PGE2 30 expression in the presence of adiponectin. Co-administration of adiponectin with celecoxib, a 31 COX-2 inhibitor, inhibited efficient wound repair. These findings indicate that adiponectin has a 32 protective role against ethanol-induced gastric mucosal injury in mice. This effect may be 33 partially mediated by the efficient wound repair of epithelial cells via increased PGE2 expression. 34 35

Endoscopic Gastritis: What Does It Mean?

One can confidently assume that there is no evidence of endoscopic gastritis when the gastric mucosa has a regular pinkish color without discoloration or structural alteration, the gastric rugae are not thicker than 5 mm, and if the gastric mucosa expands well upon inflation with air. However, inflammatory changes induce subsequent apoptosis and gland damage, which can lead to regeneration, fibrosis, or metaplasia [1]. Inflammatory changes such as color and/or structural changes are noted in endoscopic findings, and are thus labeled endoscopic gastritis. Endoscopic gastritis can be classified into seven types: (a) superficial, (b) hemorrhagic, (c) erosive, (d) verrucous, (e) atrophic, (f) metaplastic, and (g) hypertrophic [2]. Erosive gastritis is diagnosed when endoscopy reveals small elevations with central umbilication, mimicking octopus’ suckers, which are usually observed in the antrum. It can also be defined as a flat or minimally depressed white spot surrounded by a reddish area that is sometimes accompanied by small superficial bleeding [3]. Since the distinction between erosion and tiny shallow ulcer is arbitrary, the latter might be included under the term ‘‘erosion.’’ When the erosion is elevated, it is generally defined as verrucous gastritis or gastritis varioliformis rather than as erosive gastritis. In this issue of Digestive Diseases and Sciences, Yamamoto et al. [3] provide an interesting finding that lower serum levels of adiponectin are associated with an increased risk of endoscopic erosive gastritis, independently of body mass index (BMI). BMI is known to be associated with abnormal upper endoscopic findings, such as erosive gastritis, gastric ulcer, duodenal ulcer, and reflux esophagitis [4]. Interestingly, when Yamamoto et al. analyzed factors including age, sex, alcohol habits, smoking habits, BMI, blood pressure, cholesterol, triglyceride, glucose, and insulin in 2,400 participants, BMI was significantly higher and the serum adiponectin level was significantly lower in gastritis-positive participants than in gastritis-negative participants. That study indicated a possible role of hypoadiponectinemia in erosive gastritis, in addition to a previous study that showed a link between low plasma adiponectin levels and gastric cancer [5]. Erosive gastritis has been considered relatively less significant than Helicobacter pylori-related endoscopic gastritis, since H. pylori infection involves a multistep progression from gastritis to glandular atrophy, intestinal metaplasia (IM), dysplasia, and ultimately to intestinaltype gastric cancer [6]. We have recently shown that the endoscopic diagnosis of open-type atrophic gastritis is related to the histological diagnosis of IM and Cdx2 expression [7]. Higher levels of Cdx2 expression are related to open-type atrophic gastritis and metaplastic gastritis, but not to closed-type atrophic gastritis and nonatrophic/ nonmetaplastic cases. The location of the atrophic gastric border was found to be strongly related to histological IM and Cdx2 expression. Our findings suggest that Cdx2 expression is an early change that is correlated with the presence of histological IM, and which occurs before endoscopic metaplastic gastritis, and that the risk of development of intestinal-type gastric cancer will continue to remain high during the process of gastric carcinogenesis in open-type atrophic gastritis and metaplastic gastritis, but not in closed-type atrophic gastritis and nonatrophic/ S.-Y. Lee (&) Department of Internal Medicine, Konkuk University School of Medicine, Seoul 143-729, Korea e-mail: sunyoung@kuh.ac.kr

Low serum adiponectin levels in children and adolescents with diabetic retinopathy.

The aim of this study was to elucidate the role of adiponectin, leptin, TNF-α and IL-6 on the early detection of the microvascular complications of type I diabetes. A total of 88 children were included in the study. There were 60 type I diabetic patients and 28 healthy control children. The gender, age, weight, height, BMI and puberty status characteristics were similar in the patient and control groups (p>0.05). The serum leptin, TNF-α and IL-6 levels were similar between the patient and control groups (p>0.05) and the only difference was in the serum adiponectin level which was higher in the patient group (p:0.042). We also found no association between the adiponectin, leptin, TNF-α and IL-6 levels and diabetes duration (p>0.05). Leptin was high in the pubertal period (p:0.016), while adiponectin TNF-α and IL-6 levels were similar in the prepubertal and pubertal periods (p>0.05). The serum leptin level was high in microalbuminuria patients (p<0.041). The serum adiponectin, TNF-α, and IL-6 levels were not different in patients with and without microalbuminuria (p>0.05). The serum adiponectin level was lower in diabetic retinopathy patients (p:0.003), while the serum leptin level was higher (p:0.003). The TNF-α and IL-6 levels were similar in patients with and without retinopathy (p>0.05). We found increased serum adinopectin levels in children and adolescents with type I diabetes mellitus and low levels in diabetic retinopathy patients. Patients with low serum adiponectin levels and high leptin levels should be more closely monitored for chronic complication development and better metabolic control should be aimed for.

Lower Serum Level of Adiponectin Is Associated with Increased Risk of Endoscopic Erosive Gastritis

Obesity is recently known as a risk factor for endoscopic gastritis. Adiponectin is an anti-inflammatory cytokine secreted from fat tissue, and its serum concentrations are reduced in obesity. The relation between adiponectin and gastritis remains unclear. The aim of this study was to determine whether lower serum adiponectin level is associated with the risk of endoscopic gastritis. We analyzed medical records of participants of a routine health check-up examination. Association among endoscopic findings, serum adiponectin level, and other clinical factors including age, sex, alcohol habit, smoking habit, body mass index (BMI), blood pressure, cholesterol, triglyceride, glucose, and insulin were investigated. Endoscopic erosive gastritis was defined as a flat or minimally depressed white spot surrounded by a reddish area or small elevation with central umbilications mimicking octopus' suckers. A total of 2,400 participants were enrolled. BMI was significantly higher in gastritis-positive participants than in gastritis-negative participants. Serum adiponectin levels were significantly lower in gastritis-positive participants than in gastritis-negative participants. Multivariate logistic regression analysis revealed that lower serum adiponectin level (OR 0.96; 95% CI 0.93-0.99), smoking (OR 0.50; 95% CI 0.30-0.80), higher blood pressure (OR 1.02; 95% CI 1.01-1.03), and duodenitis (OR 1.8; 95% CI 1.00-3.09) were significantly associated with endoscopic erosive gastritis. Lower serum level of adiponectin may increase the risk of endoscopic erosive gastritis, independently of BMI. Our findings facilitate further study to clarify the role of hypoadiponectinemia in erosive gastritis.