Blood Adiponectin Levels Research Articles

Antidiabetic and Antihyperlipidemic Effects of Sulphurenic Acid, a Triterpenoid Compound from Antrodia camphorata, in Streptozotocin-Induced Diabetic Mice.

The present study was designed to evaluate the protective effect of sulphurenic acid (SA), a pure compound from Antrodia camphorata, on diabetes and hyperlipidemia in an animal model study and to clarify the underlying molecular mechanism. Diabetes was induced by daily 55 mg/kg intraperitoneal injections of streptozotocin (STZ) solution over five days. Diabetic mice were randomly divided into six groups and orally gavaged with SA (at three dosages) or glibenclamide (Glib), fenofibrate (Feno) or vehicle for 3 weeks. Our findings showed that STZ-induced diabetic mice had significantly increased fasting blood glucose, glycated hemoglobin (HbA1C), plasma triglyceride (TG), and total cholesterol (TC) levels (p < 0.001, p < 0.001, p < 0.001, and p < 0.05, respectively) but decreased blood insulin, adiponectin, and leptin levels compared to those of the control group (p < 0.001, p < 0.001, and p < 0.001, respectively). Administration of SA to STZ-induced diabetic mice may lower blood glucose but it increased the insulin levels with restoration of the size of the islets of Langerhans cells, implying that SA protected against STZ-induced diabetic states within the pancreas. At the molecular level, SA treatment exerts an increase in skeletal muscle expression levels of membrane glucose transporter 4 (GLUT4) and phospho-Akt to increase the membrane glucose uptake, but the mRNA levels of PEPCK and G6Pase are decreased to inhibit hepatic glucose production, thus leading to its hypoglycemic effect. Moreover, SA may cause hypolipidemic effects not only by enhancing hepatic expression levels of peroxisome proliferator-activated receptor α (PPARα) with increased fatty acid oxidation but also by reducing lipogenic fatty acid synthase (FAS) as well as reducing mRNA levels of sterol regulatory element binding protein (SREBP)1C and SREBP2 to lower blood TG and TC levels. Our findings demonstrated that SA displayed a protective effect against type 1 diabetes and a hyperlipidemic state in STZ-induced diabetic mice.

Evaluation of blood adiponectin levels as an index for subacute ruminal acidosis in cows: a preliminary study

The objective of this study was to evaluate blood levels of various hormones and compounds related to energy metabolism in cows with subacute ruminal acidosis (SARA). We investigated 11 lactating cows presumed to have SARA based on duration of ruminal pH <5.6 and reticulum pH <6.3 in 2015-2016. Kraft pulp (KP) was used to supplement feed of 7 of the cows studied in an effort to reduce SARA. We continuously monitored ruminal pH and measured blood concentrations of hormones and metabolites related to energy metabolism. Blood measurements included glucose (GLU), total cholesterol (TC), free fatty acid (FFA), insulin, adiponectin (ADN), malate dehydrogenase (MDH), and lactate dehydrogenase (LDH). Additionally, we analyzed milk data (milk yield, milk fat percentage, milk protein percentage, milk urea nitrogen, and protein fat ratio) and reproduction data. The results demonstrated that ADN levels at 4weeks post-parturition correlated with the total amount of time that the ruminal or reticulum fluid pH was under the threshold during 1week post-parturition, as well as the numbers of days the cows were diagnosed with SARA (SARA-positive days) up to 30days post-parturition. SARA-positive days in 2016 were higher than those in 2015. In both years, numbers of SARA-positive days for cows supplemented with KP were lower than those for cows without KP. Increased ADN levels may be a compensatory reaction to frequent SARA which modulates the inflammatory response against high LPS levels and improves insulin resistance caused by LPS. ADN may serve as an estimative index for SARA.

Systematic Review and Meta-Analysis of Randomized Controlled Trials on the Effect of SGLT2 Inhibitor on Blood Leptin and Adiponectin Level in Patients with Type 2 Diabetes

Sodium glucose cotransporter 2 (SGLT2) inhibitors are a new kind of hypoglycemic drugs that improve glucose homeostasis by inhibiting renal glucose reabsorption. Recent studies have shown that SGLT2 inhibitors can also mediate body metabolism through regulation of adipokines level, but the effects of SGLT2 inhibitors on the concentration of adipokines (leptin and adiponectin) remains controversial. This meta-analysis was set out to evaluate the changes in circulating leptin and adiponectin levels in patients with type 2 diabetes mellitus (T2DM) receiving SGLT2 inhibitors therapy. Ten randomized controlled trials (RCTs), that evaluated the effects of SGLT2 inhibitors on blood leptin and adiponectin levels in patients with type 2 diabetes, were identified by performing a systematic search of Pubmed, Embase, Cochrane, and Web of science databases through July 2018. Data were calculated using a random-effects model and presented as standardized mean difference (SMD) and 95% confidence interval (CI). Compared with placebo, treatment with SGLT2 inhibitors contributed to a decreased circulating leptin levels (SMD -0.29, 95% CI -0.56, -0.03) and an increased circulating adiponectin levels (SMD 0.30, 95% CI 0.22, 0.38). SGLT2 inhibitor treatment was associated with decreased circulating leptin levels and increased circulating adiponectin levels, which might contribute to the beneficial effects of SGLT2 inhibitors on metabolic homeostasis.

DHA supplementation in women with pregestational obesity does not affect the offspring´s adiposity neither at birth nor at 4 months of age.

Maternal pregestational obesity is a well-known risk factor for offspring obesity, metabolic syndrome, cardiovascular disease and type 2 diabetes. The mechanisms by which maternal obesity can induce alterations in fetal and later neonatal metabolism are not fully elucidated due to its complexity and multifactorial causes. Two adipokines, leptin and adiponectin, are involved in fetal and postnatal growth trajectories, and both are altered in women with pregestational obesity. The placenta synthesizes leptin, which goes mainly to the maternal circulation and in lesser amount to the developing fetus. Maternal pregestational obesity and hyperleptinemia are associated with placental dysfunction and changes in nutrient transporters which directly affect fetal growth and development. By the other side, the embryo can produce its own leptin from early in development, which is associated to fetal weight and adiposity. Adiponectin, an insulin-sensitizing adipokine, is downregulated in maternal obesity. High molecular weight (HMW) adiponectin is the most abundant form and with most biological actions. In maternal obesity lower total and HMW adiponectin levels have been described in the mother, paralleled with high levels in the umbilical cord. Several studies have found that cord blood adiponectin levels are related with postnatal growth trajectories, and it has been suggested that low adiponectin levels in women with pregestational obesity enhance placental insulin sensitivity and activation of placental amino acid transport systems, supporting fetal overgrowth. The possible mechanisms by which maternal pregestational obesity, focusing in the actions of leptin and adiponectin, affects the fetal development and postnatal growth trajectories in their offspring are discussed.

Smoking results in accumulation of ectopic fat in the liver.

ObjectiveAn association between smoking and nonalcoholic fatty liver disease has been reported. However, objective quantification of intrahepatic fat via magnetic resonance spectroscopy (MRS) in relation to smoking has rarely been performed in previous studies. Moreover, the possible pathways via which smoking could induce ectopic fat accumulation have not yet been addressed. The current study aimed to examine the association between smoking status and intrahepatic fat quantity and explore the possible mediating effects of triglycerides (TG) and adiponectin.Subjects and methodsMagnetic resonance imager (MRI) spectra were analyzed to quantify intrahepatic fat in 45 men who were on average 62.3 years of age. Smoking status and alcohol intake were self-reported. Accelerometers were used to record daily total physical activity. Fasting blood TG and adiponectin levels were measured enzymatically. Differences in mean intrahepatic fat values according to smoking status were assessed using analysis of covariance.ResultsA stepwise increase in mean intrahepatic fat was observed between never, former, and current smokers, respectively, independent of age, physical activity, alcohol intake, and body mass index (BMI) (P=0.005). Adjustment for TG and adiponectin significantly attenuated this association (P=0.074).ConclusionCurrent smoking was significantly associated with increased intrahepatic fat, which may be a result of adipocyte dysfunction, manifested as high circulating TG concentrations and low adiponectin levels.

Oral Administration of Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032 with Cinnamomi Ramulus Extract Reduces Diet-Induced Obesity and Modulates Gut Microbiota.

Obesity is a major health issue worldwide, and is associated with many diseases including type 2 diabetes. In this study, we evaluated the anti-obesity effects of combinations of two lactic acid bacteria (LAB), Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032, and Cinnamomi Ramulus (CR) extract, and explored the mechanism through which they modulate gut microbiota using diet-induced obese mice. Male C57BL/6J mice were randomly divided into five groups that received a high-fat diet (HFD), HFD and LAB (HFD+LAB), HFD and CR extract (HFD+CR), HFD with LAB and CR extract (HFD+LAB+CR), or normal diet for 10 weeks. The mice in the HFD+LAB+CR group showed significant reductions in body weight gain, in particular epididymal fat and liver, blood leptin levels, and an increase in the levels of blood adiponectin. In addition, the LAB and CR extract altered the gut microbiota, mainly increasing the alpha diversity. These results demonstrate that a mixture of two LAB (Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032) and CR extracts alleviate HFD-induced obesity, and has potential of being used as a strategy for the treatment of obesity.

Antidiabetic and Hypolipidemic Effects of a Novel Dual Peroxisome Proliferator-Activated Receptor (PPAR) α/γ Agonist, E3030, in db/db Mice and Beagle Dogs

We investigated the antidiabetic effects of E3030, which is a potent dual activator of peroxisome proliferator-activated receptor (PPAR) α and PPARγ, in an animal model of diabetes, C57BL/KsJ-db/db mice (db/db mice), and the lipidemic effects of E3030 in beagle dogs, whose PPARα and PPARγ transactivation responses to E3030 were similar to those of humans. E3030 activated human PPARα, mouse PPARα, dog PPARα, human PPARγ, mouse PPARγ, and dog PPARγ with EC50 values of 65, 920, 87, 34, 73, and 34 nM, respectively, in the chimeric GAL4-PPAR receptor transactivation reporter assay. In db/db mice orally administered E3030 decreased blood glucose, triglyceride (TG), non-esterified fatty acids (NEFA), and insulin levels and increased blood adiponectin levels during a 14-day experimental period. Significant effects on blood glucose and adiponectin levels were observed at a dose of 3 mg/kg or greater. Furthermore, significant effects on blood TG, NEFA, and insulin levels were observed at doses of 1 mg/kg or more. An oral glucose tolerance test (OGTT) performed on Day 15 showed that E3030 at 3 mg/kg improved glucose tolerance in this model. Fourteen days of oral treatment with E3030 at a dose of 0.03 mg/kg or greater showed remarkable TG- and non high-density lipoprotein (non-HDL) cholesterol–lowering effects in beagle dogs. These results were similar to those observed for the PPARα agonist fenofibrate. E3030 also reduced apo C-III levels on Days 7 and 14, and elevated lipoprotein lipase (LPL) levels on Day 15. These results indicate that the TG- and non-HDL cholesterol-lowering actions of E3030 involve combined effects on reduction of apo C-III and elevation of LPL, resulting in increased lipolysis. The experimental results in animals suggest that E3030 has potential for use in the treatment of various aspects of metabolic dysfunction in type 2 diabetes, including dyslipidemia, hyperglycemia, hyperinsulinemia, and impaired glucose disposal.

Biological and pathophysiological role of adiponectin

Adipose tissue is now recognized as an important endocrine organ that secretes numerous protein hormones, including leptin, adiponectin, and resistin. Adiponectin is a hormone that is produced by white adipose tissue. Adiponectin has been isolated independently by several groups of scientists. In humans, this protein is encoded by the ADIPOQ gene. Adiponectin receptors are widely distributed in many organs and tissues including liver, heart, pancreas, kidneys, muscles and many other cell types. A serum concentration of adipocin correlates with body mass index (BMI). Decreased level of adiponectin leads to obesity, the development of gestational complications in pregnant women, as well as a high risk of diabetes mellitus development and atherosclerosis. A high concentration of this hormone has anti-inflammatory, antiatherogenic, antiproliferative and cancer-defense mechanisms. Adiponectin strongly suppresses hepatic gluconeogenesis by inhibiting genes involved in glucose production. Obese people have lower blood levels of adiponectin than normal weight individuals. Adiponectin’s anti-inflammatory and anti-apoptotic properties result in protection of the blood vessels, heart, lungs, and colon. Adiponectin, an abundant adipocyte-secreted factor with a wide-range of biological activities, improves insulin sensitivity in insulin target tissues, modulates inflammatory responses, and plays a crucial role in the regulation of energy metabolism.

Blood levels of adiponectin and IL-1Ra could facilitate earlier detection of PDAC by distinguishing individuals with type 3c diabetes from those with type 2 diabetes

Combined portal vein (PV) resection is performed for pancreatic head cancer to achieve clear resection margins. This can be complicated by the formation of varices due to sinistral portal hypertension after pancreaticoduodenectomy (PD) with combined PV resection. However, clinical strategies to prevent varices formation due to sinistral portal hypertension remain controversial. Moreover, the critical vein among splenic vein (SPV), inferior mesenteric vein, left gastric vein, or middle colonic vein requiring preservation to prevent the development of varices remains unclear.We retrospectively analyzed patients with pancreatic cancer who underwent PD with combined PV resection over 18 years at our institution. Varices were evaluated using enhanced computed tomography (CT) and endoscopy. Preoperative types of porto-mesenterico-splenic confluence, venous drainage, and venous resection types were determined by operative records and CT findings.Of the 108 subjects, the incidence of postoperative varices was observed in 24.1% of cases over 5.6 months. These varices were classified into five types based on location, as pancreaticojejunostomy anastomotic (11.5%), gastrojejunostomy anastomotic (11.5%), esophageal (11.5%), splenic hilar-gastric (23.1%), and right colonic (65.4%) varices. No case of variceal bleeding occurred. Multivariate analysis showed SPV ligation as the greatest risk factor of varices (P < 0.001), with a higher incidence of left-sided varices in patients with all the SPV venous drainage sacrificed (60%) than in the others (16.7%). Therefore, sacrificing all the SPV venous drainage was the only independent risk factor of varices (P = 0.049).Preservation of SPV venous drainage should be considered during SPV ligation to prevent post-PD varices.

Effects of Hypobaric Hypoxia on Endothelial Function and Adiponectin Levels in Airforce Aviators.

Background: Hypobaric hypoxia (HH) increases the risk of high altitude-related illnesses (HARI). The pathophysiological mechanism(s) involved are still partially unknown. Altered vascular reactivity as consequence of endothelial dysfunction during HH might play a role in this phenomenon. Adiponectin exerts protective effect on cardiovascular system since it modulates NO release, antagonizing endothelial dysfunction. Aims of this study, performed in a selected population of airforce aviators, were (1) to investigate whether exposure to acute HH might be associated with endothelial dysfunction and (2) to evaluate whether adiponectin might be involved in modulating this phenomenon. Methods: Twenty aviators were exposed to acute HH in a hypobaric chamber by simulating altitude of 8000 and then 6000 m for 2 hours. Vascular reactivity was evaluated by the EndoPAT test immediately before and after the HH; salivary and blood adiponectin levels were measured. Results: EndoPAT performed immediately after HH divided pilots in two groups: 12 pilots with preserved vascular reactivity and 8 pilots with reduction of vascular reactivity, indicating that HH exposure might cause endothelial dysfunction. Salivary and blood adiponectin levels increased post-HH in a time-dependent manner in all aviators, but the significant increase was observed only in those with preserved vascular reactivity suggesting that HH stimulated release of adiponectin that, in turn, by exerting a protective effect, might reduce endothelial dysfunction. Conclusions: Acute HH may cause endothelial dysfunction due, at least in part, to reduced release of adiponectin. This phenomenon might be involved in pathophysiology of HARI.

Comparative analysis of glucose metabolism responses of large yellow croaker Larimichthys crocea fed diet with fish oil and palm oil.

In order to study the effects of dietary fatty acid compositions on glucose metabolism, large yellow croaker juveniles Larimichthys crocea (initial weight, 36.80 ± 0.39g) were fed with two experiment diets for 12weeks. The two diets contained 6.5% of fish oil (FO) and palm oil (PO), respectively. Results showed that the contents of saturated fatty acids in liver and muscle, levels of glucose, triglyceride (TG), non-esterified fatty acid (NEFA), and leptin in blood were significantly higher in PO group, while the hepatic glycogen and muscle glycogen significantly decreased (P <0.05). There were no significant differences in blood insulin and adiponectin levels between the two groups (P >0.05). Compared with the FO group, the expressions of glucokinase (GK), glucose-6-phosphate dehydrogenase, glycogen synthase (GYS), glucose transporter 2 (GLUT2), insulin receptor 1 (IR1), insulin receptor substrate 1 (IRS1), insulin receptor substrate (IRS2), and protein kinase B (AKT2) were significantly decreased, and the expressions of phosphoenolpyruvate carboxykinase (PEPCK) in liver were significantly increased in the PO group. Meanwhile, the expressions of GK, phosphofructokinase, GYS, GLUT4, and insulin receptor 2 (IR2) were significantly reduced, and the expressions PEPCK, fructose-1 and 6-diphosphatase in muscle were significantly increased in the PO group. In conclusion, palm oil in diet could inhibit the utilization of glucose and promote the endogenous glucose production in large yellow croaker by reducing the sensitivity of insulin, so as to increase the blood glucose level.

Sex differences in the expression of lipid oxidation and glucose uptake genes in muscles of fasted mice

Fasting has become increasingly popular for treatment and prevention of obesity. Sex differences in the mechanisms of adaptation to fasting may contribute to choosing a therapeutic strategy for correction of metabolic disorders. Hepatokine fibroblast growth factor 21 (FGF21) is involved in the adaptation to fasting. Muscles are assumed to be the main energy-consuming tissue in the body, as muscle metabolism plays an important role in the adaptation to nutritional deficit. However, there is still little information on sex differences in muscle and FGF21 physiological response to fasting. Our aim was to find out whether there were sex differences in hormonal regulation and the expression of genes controlling glucose and lipid metabolism in skeletal muscles in response to fasting. We estimated the effect of 24-hour fasting on the expression of genes involved in lipid (Ucp3, Cpt1) and carbohydrate (Slc2a4) metabolism in muscles and evaluated changes in body weight and blood plasma levels of glucose, insulin, free fatty acids (FFA), adiponectin, and FGF21 in male and female C57BL/6J mice. None of the genes studied (Ucp3, Cpt1 and Slc2a4) showed sex-related changes at mRNA levels in control groups, but females exposed to fasting demonstrated a significant increase in the expression of all genes as compared to control. Fasting significantly decreased body weight and glucose blood plasma levels in animals of both sexes but exerted no effect on the levels of insulin or FFA. The adiponectin and FGF21 levels were increased in response to fasting, the increase in females being significant. We were first to show sex dimorphism in muscle gene expression and FGF21 blood level in response to fasting. In females, the greater increase in FGF21 and adiponectin blood levels was positively associated with the greater upregulation of lipid oxidation and glucose uptake gene expression.

Association of cord blood bisphenol A (BPA) with cord blood adiponectin, leptin, fetal growth; adiposity and neoantal complications in a newborn cohort

Objective: To evaluate the relation between cord blood bisphenol A (BPA), leptin, adiponectin, birth weight, height, skin thickness, and postnatal results.Method: This study was performed in near East University Medical Faculty, Nicosia, Cyprus with 150 healthy newborns. Cord blood leptin, adiponectin, BPA levels were measured by ELISA and birth weight, heights and back, waist, and arm skin thickness were measured and postnatal problems noted.Results: One hundred eighty-seven newborns were included in the study. Mean ± SD of BPA, adiponectin, leptin levels were 48.3 ± 2.22 ng/mL, 65.60 ± 15.29 µg/mL and 3.08 ± 2.08 ng/mL. Mean birth weight, height, head circumferences were 3156.76 ± 493.45 g, 48.28 ± 2.04 cm, 34.14 ± 1.74 cm. The association anthropometric measurements, BPA, leptin, and adiponectin levels were not statistically significant (p>.05). The relation between cord blood leptin, adiponectin, and BPA levels and small for gestation, large for gestation and average for gestation groups were not significant (p>.05). Moreover, relation between back, waist and arm skin thickness and BPA, leptin, and adiponectin were not statistically significant (p>.05). However, newborns who were hospitalized and had newborn jaundice had higher BPA levels (p<.05).Conclusion: In previous studies, higher BPA levels were associated with small for gestational age (SGA) birth, however, this relation was not noted in our study. Furthermore, there is no relation between skin thickness, BPA, leptin, and adiponectin. This difference may be as a result of higher cord BPA levels compared with previous studies.

EFFECTS OF TYPE 2 DIABETES MELLITUS ON CLINICAL AND LABORATORY STATUS OF WOMEN WITH ARTERIAL HYPERTENSION, OBESITY, AND LEFT VENTRICULAR DIASTOLIC DYSFUNCTION

Patients with type 2 diabetes mellitus (DM) may develop cardiomyopathy independently of such risk factors as arterial hypertension and coronary heart disease. Myocardial dysfunction in diabetes mellitus may vary from subclinical forms of left ventricular dysfunction to heart failure. It was suggested that diastolic left ventricular dysfunction is one of the earliest signs of myocardial injury in diabetes mellitus and plays a key role in the formation of diabetic cardiomyopathy. The aim of our study was to evaluate the effect of diabetes on the clinical and laboratory status of women with hypertension, obesity, and left ventricular diastolic dysfunction (LVDD). Materials and methods. We examined 80 patients aged 40 to 60 years with stage 2, grade II and grade III hypertension, class I–III obesity, grade 1 LVDD and preserved ejection fraction. Depending on the presence or absence of diabetes, the cohort of patients was divided into two groups: patients with diabetes were assigned to group 1 and non-diabetes patients ­­– to group 2. Statistical processing was performed using Statistica for Windows version 6.0. Results. Patients had tendency to increased body mass index (BMI) in the DM group, but without significant differences. The results of the 6-minute walk test showed a tendency to decreased distance in the group of patients with diabetes. There was an increase in leptin levels and a decrease in adiponectin in patients with diabetes without significant differences. Levels of IL-6, glycosylated hemoglobin, and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) index were significantly higher in the cohort of patients with diabetes (p &lt;0.05). Conclusions. Women aged 40–60 years with LVDD with hypertension, class I–III obesity and type 2 diabetes mellitus differ from similar cohorts of patients without diabetes with a tendency to increased BMI levels, leptinemia, and decrease in distance of 6-minute walk test, LV ejection fraction and blood adiponectin level; they have significantly higher blood levels of interleukin-6, glycosylated hemoglobin (HbA1c) and HOMA-IR; indicators of diastolic function in the group of patients with diabetes tend to worsen the parameters of diastolic filling of the LV even in grade 1 DD.

Association between Peripheral Leptin and Adiponectin Levels and Cognitive Decline in Patients with Neurocognitive Disorders ≥65 Years.

Background:There is evidence that adipokines have roles in brain functioning and cognitive decline.Objective:Assess the role of leptin and adiponectin levels in predicting changes in neuro-cognitive disorders (NCD).Methods:The study included 205 patients over 65 years of age presenting for a one-day hospitalization for current assessment of cognitive function. Peripheral blood leptin and adiponectin levels were measured at admission. Demographic variables, body mass index (BMI), and history of hypertension were also recorded. Cognitive function was assessed by the Mini-Mental State Examination (MMSE) at admission and at later scheduled visits over a median follow-up period of 14.5 months. Conventional univariate comparisons were made between diagnosis groups (Alzheimer’s disease (AD), mild NCD, vascular/mixed dementia). Changes in MMSE scores over time were examined with regard to the above variables using a linear mixed model.Results:The mean BMI was significantly lower (by 2 kg/m2, p = 0.01) in patients with AD than in patients with either mild-NCD or vascular/mixed dementia. Leptin levels were significantly higher (p = 0.043) and adiponectin levels significantly lower (p = 0.045) in patients with mild-NCD than in patients with major-NCD (AD or vascular/mixed dementia). However, the mixed model suggested no influence of the baseline levels of these two biomarkers on the course of cognitive decline.Conclusion:The present study confirms the associations between leptin and adiponectin and AD or AD-related disorders but did not confirm that these peptides may be used as predictive biomarkers of cognitive decline.

Blood adiponectin levels are not associated with risk of cardiovascular events in patients with type 2 diabetes.

We examined whether circulating adiponectin levels are associated with further cardiovascular events in patients with type 2 diabetes. Between December 2004 and February 2005, 349 patients with type 2 diabetes were enrolled and followed-up until December 2015. Blood levels of total, middle-molecular weight and high-molecular weight adiponectin were measured at baseline. The primary composite outcome was the occurrence of the following events: cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or hospitalization for unstable angina and heart failure. During a median follow-up of 9 years, cardiovascular events occurred in 14% of patients (50/349, 1.9% per year). Median blood levels of total, middle-molecular weight and high-molecular weight adiponectin were 4.8, 3.2 and 1.8 μg/mL, respectively. The cumulative incidence of cardiovascular events was not significantly different between the three groups based on total, middle-molecular weight, high-molecular weight or high-molecular weight/total adiponectin. After adjustment for potential confounding factors, blood adiponectin levels were positively associated with an increased number of cardiovascular events, but between tertiles, there was no significant difference. This observational cohort study suggested that blood adiponectin levels are not related to further cardiovascular events in patients with type 2 diabetes.

Analysis of changes on adiponectin levels and abdominal obesity after smoking cessation.

PurposeThe blood levels of Adiponectin, anti-inflammatory and anti-arteriosclerotic adipocytokine, decrease due to smoking and obesity. Cigarette smokers are generally known to gain weight after smoking cessation (SC). Nevertheless, precise changes in serum adiponectin levels after SC and specific effects of abdominal obesity on those changes remain unknown. The objective of this study was to elucidate the changes in serum adiponectin levels after SC and the effects of abdominal obesity on those changes.MethodsIn 86 patients (56 males and 30 females) who had successfully quit smoking, serum adiponectin levels were measured using an enzyme-linked immunosorbent assay at baseline and 1 year after beginning SC.ResultsBody mass index and waist circumference (WC) were significantly increased 1 year after beginning SC. Adiponectin levels, however, did not change after SC. Using the median ΔWC (+2.8%) as the cutoff point, patients were then divided into two groups. The percent change in adiponectin levels from baseline to 1 year was significantly greater in the ΔWC < median group (−1.1%) than in the ΔWC ≥ median group (+8.1%) (p = 0.011).ConclusionsDespite weight gain and increased abdominal obesity, serum adiponectin levels did not decrease after SC. Therefore, the beneficial effect of SC may eliminate the adverse effects of subsequent weight gain. Conversely, patients with less abdominal obesity had increased adiponectin levels 1 year after SC. Therefore, in such patients, the beneficial effect of SC on adiponectin levels is apparent.

A relationship between chronic obstructive pulmonary disease, obesity and melatonin level

This is a review of experimental and clinical studies investigated effects of obesity on clinical course of chronic obstructive pulmonary disease (COPD); pathophysiological mechanisms of this effect, and relationships between melatonin level and the course of COPD have been also discussed. Associations between severity of COPD, rate of exacerbations and blood levels of most important adipokines, such as leptin and adiponectin, and relationships between melatonin levels and those adipokines were published. Conflicting results were obtained in studies of effects of obesity on clinical course of COPD. The "obesity paradox", that is a reduction in mortality and milder bronchial obstruction in obese COPD patients, has been identified in several studies. Despite contradictory results, obesity is likely to improve prognosis of COPD due to decrease in the systemic inflammation. Levels of leptin and adiponectin increase in acute exacerbation of COPD and then decrease to the baseline. Moreover, melatonin is suggested to play a great role for COPD course, mostly due to antiinflammatory and antioxidant activities. According to results of several studies, melatonin could affect blood levels of adiponectin and lectin; this could indirectly influence on the systemic inflammation in COPD. Further studies are needed to elicit these relationships.

Large-for-Gestational-Age May Be Associated With Lower Fetal Insulin Sensitivity and β-Cell Function Linked to Leptin.

Fetal overgrowth is associated with increased risk for type 2 diabetes in adulthood. It is unclear whether there are alterations in insulin sensitivity and β-cell function in early life. To determine whether large-for-gestational-age (LGA) (birth weight > 90th percentile), an indicator of fetal overgrowth, is associated with altered fetal insulin sensitivity and β-cell function. In the Design, Development, and Discover birth cohort in Canada, we studied 106 pairs of LGA and optimal-for-gestational-age (OGA; birth weight, 25th to 75th percentiles) infants matched by maternal ethnicity, smoking status, and gestational age. Cord plasma glucose-to-insulin ratio was used as an indicator of fetal insulin sensitivity, and proinsulin-to-insulin ratio was used as an indicator of β-cell function. Cord plasma leptin and high-molecular-weight (HMW) adiponectin concentrations were measured. Comparisons of infants who were born LGA vs OGA, adjusted for maternal and newborn characteristics, showed that cord blood insulin, proinsulin, and leptin concentrations were significantly higher, whereas HWM adiponectin concentrations were similar. Glucose-to-insulin ratios were significantly lower (15.4 ± 28.1 vs 22.0 ± 24.9; P = 0.004), and proinsulin-to-insulin ratios significantly higher (0.73 ± 0.82 vs 0.60 ± 0.78; P = 0.005) in LGA vs OGA newborns, indicating lower insulin sensitivity and β-cell function in LGA newborns. These significant differences were almost unchanged after further adjustment for cord blood adiponectin levels but disappeared upon additional adjustment for cord blood leptin levels. This study demonstrates that LGA may be associated with decreases in both fetal insulin sensitivity and β-cell function. The alterations appear to be linked to elevated leptin levels.

Inhibition of Epidermal Growth Factor Receptor Activation Is Associated With Improved Diabetic Nephropathy and Insulin Resistance in Type 2 Diabetes.

Previous studies by us and others have indicated that renal epidermal growth factor receptors (EGFR) are activated in models of diabetic nephropathy (DN) and that inhibition of EGFR activity protects against progressive DN in type 1 diabetes. In this study we examined whether inhibition of EGFR activation would affect the development of DN in a mouse model of accelerated type 2 diabetes (BKS db/db with endothelial nitric oxide knockout [eNOS-/-db/db]). eNOS-/-db/db mice received vehicle or erlotinib, an inhibitor of EGFR tyrosine kinase activity, beginning at 8 weeks of age and were sacrificed at 20 weeks of age. In addition, genetic models inhibiting EGFR activity (waved 2) and transforming growth factor-α (waved 1) were studied in this model of DN in type 2 diabetes. Compared with vehicle-treated mice, erlotinib-treated animals had less albuminuria and glomerulosclerosis, less podocyte loss, and smaller amounts of renal profibrotic and fibrotic components. Erlotinib treatment decreased renal oxidative stress, macrophage and T-lymphocyte infiltration, and the production of proinflammatory cytokines. Erlotinib treatment also preserved pancreas function, and these mice had higher blood insulin levels at 20 weeks, decreased basal blood glucose levels, increased glucose tolerance and insulin sensitivity, and increased blood levels of adiponectin compared with vehicle-treated mice. Similar to the aforementioned results, both waved 1 and waved 2 diabetic mice also had attenuated DN, preserved pancreas function, and decreased basal blood glucose levels. In this mouse model of accelerated DN, inhibition of EGFR signaling led to increased longevity.