Lower circulating levels of CTRP12 and CTRP13 in polycystic ovarian syndrome: Irrespective of obesity
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Altered production of adipokines is suggested to play a pivotal role in the pathogenesis of polycystic ovarian syndrome (PCOS). C1q/TNF-related proteins (CTRPs) play diverse roles in regulation of metabolism in physiologic and pathologic conditions. In the present study, we assessed serum concentrations of adiponectin, CTRP12, and CTRP13 in individuals with PCOS and those without PCOS. We also evaluated the possible association of these adipokines with metabolic and hormonal variables. A total of 171 premenopausal women (86 with PCOS and 85 without PCOS) enrolled in this study. Serum levels of adiponectin, CTRP12, and CTRP13 were measured. The results showed significantly lower serum concentrations of adiponectin, CTRP12, and CTRP13 in PCOS women compared to non-PCOS women. This difference remained significant after controlling for age, body mass index (BMI), and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). However, we did not observe any significant differences in serum levels of adiponectin, CTRP12, and CTRP13 between the overweight/obese and normal weight subgroups in PCOS and non-PCOS women. Multiple linear regression analysis showed associations of CTRP12 with adiponectin and BMI with CTRP13 in both the PCOS and non-PCOS groups. CTRP12 was significantly associated with BMI and adiponectin in the non-PCOS group, and fasting blood glucose (FBG) and CTRP13 in the PCOS group. Our results indicated that decreased adiponectin, CTRP12, and CTRP13 levels, regardless of obesity, could independently predict PCOS. This finding suggested a novel link between adipokines and PCOS.The aim of this study was to investigate whether recurrent pregnancy loss (RPL) is associated with adipokine gene polymorphisms (namely the leptin -2548 (G/A), adiponectin 276 (G/T), and adiponectin 45 (T/G) polymorphisms) and/or adipokine serum levels.A total of 145 women participated in the study. For the analysis of serum adipokine levels, 19 healthy fertile women (control group) and 60 women suffering from RPL were included. For the polymorphism analysis, 126 women suffering from RPL were included. Serum adipokine levels were determined using a commercial radioimmunoassay kit. Adipokine polymorphisms were analyzed using an allele-specific polymerase chain reaction (PCR).Our immunoassays revealed that serum leptin levels were similar in control and RPL groups (17.34 and 20.16 ng/mL, respectively). In contrast, serum adiponectin levels were significantly higher in women with RPL than in controls (9.83 and 6.89 μg/mL, respectively; P < 0.05). Unfortunately, our allele-specific PCR experiments did not reveal any significant differences in allele frequency between women with RPL and NCBI allele frequencies.This study demonstrates that adiponectinemia is increased in patients suffering from RPL. However, association of adiponectin with adverse pregnancy outcomes remains to be elucidated.
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Adipose tissue has been identified as an endocrine organ secreting adipokines involved in metabolic and inflammatory pathways. Adiponectin, an anti-inflammatory adipokine, is reduced in sepsis. High Molecular Weight (HMW) adiponectin, the biologically most relevant molecule, has been investigated very little in human sepsis. Zinc-alpha2-glycoprotein (ZAG) is a novel adipokine and its expression in adipose tissue is positively correlated with adiponectin expression. It is not yet known whether ZAG has a role in sepsis. In this study we assessed levels of HMW adiponectin and ZAG during different stages of sepsis. A prospective observational pilot study was carried out on 21 septic patients. Serum samples were taken on day 1 and 2 post ICU admission and on day of discharge. Samples were analysed for total and HMW adiponectin, HMW/total adiponectin ratio, and ZAG. Results were correlated with clinical and metabolic data. There were no differences in total adiponectin, HMW adiponectin and ZAG plasma concentrations between day 1 (admission) and day 2 of the sepsis episode. Compared to admission, a significant increase in total and HMW adiponectin and ZAG was observed on the day of discharge when clinical improvement had been achieved. There was also an increase in the HMW/total adiponectin ratio at that time. Our data demonstrate an increase in both HMW adiponectin and total adiponectin in patients who had clinically recovered from sepsis. The increase in HMW/total adiponectin ratio with improvement of the clinical condition suggests that HMW adiponectin may have a greater role in the inflammatory process and insulin resistance seen in sepsis. In this pilot study, we have also demonstrated a significant increase in ZAG in critically ill patients temporally related to recovery from sepsis.
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Adiponectin is a hormone-like cytokine (adipokine) mainly released from fat cells. It is believed that adiponectin has anti-inflammatory properties and inversely correlates with body’s adipose tissue, particularly visceral adiposity
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Adiponectin is a most abundant secretory protein produced by adipocytes of white adipose tissue. Adiponectin circulates in blood as three different (high-molecular, middle-molecular, and low-molecular weight) isoforms, gives its effects through AdipoR1 and AdipoR2 receptor. Primary data suggesting that adiponectin has insulin-sensitizing, anti-atherogenic, and anti-inflammatory effects. High serum level of adiponectin is positively associated with inflammation severity and pathological progression in chronic kidney disease, liver disease and inflammatory bowel disease. It has emerged as a valuable biomarker for insulin sensitivity, cardiovascular risk and inflammation. Adiponectin is gaining attention for its therapeutic role in Alzheimer’s disease. Adiponectin appears to play a crucial role not only in glucose and lipid metabolism but also the development and progression of different cancers. Adiponectin also produced locally in the retinas participate in defense of various eye diseases. This review summarizes the role of adiponectin as benevolent adipokine in different disorders.
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Adipocytokines, such as adiponectin, TNF-alpha, and leptin, are cytokines secreted by visceral adipocytes, and they are associated with metabolic syndrome. Adiponectin is one of the adipocytokines, and is a protein comprised of 244 amino acids. It is known as ACRP30, GBP28, and AdipoQ. Adiponectin is secreted by adipocytes, has three different isoforms, including trimers (low-molecular weight: LMW), hexamers (middle-molecular-weight: MMW), and higher-order oligomeric (high-molecular-weight: HMW) structures, and affects the biological activity. Adiponectin is a clinically relevant parameter measured routinely in subjects at risk of type 2 diabetes and metabolic syndrome. We investigated the adiponectin levels using a number of ELISA assay kits.
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Adiponectin (also known as APM1, Acrp 30, AdipoQ or GBP28) is a 30kD circulating plasma protein and is the most abundant adipokine secreted by adipose tissue. In humans, adiponectin accounts for approximately 0.01% of circulating plasma proteins.1 It is thought to have a unique spectrum of properties for an adipokine, many of which are anti-atherosclerotic, and is downregulated in the presence of increasing central adiposity.
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Polycystic ovary syndrome (PCOS) is the most common endocrine disorder associated with metabolic disorders and infertility. Evidence suggests that the adipose tissue secreted products, adipokines, play an important role in the pathophysiology of PCOS. Reciprocally, PCOS influences on the adipokines serum content, also on gene or protein expression of some of them. Finding out of association between serum levels of adipokines and PCOS will help to understand the pathology of PCOS and identify treatment solutions of this syndrome. In this paper, we review the assosiation of several known adipokines with polycystic ovary syndrome.
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Adipose tissue is an active metabolic tissue that secretes multiple metabolically important proteins, known as adipokines. Adiponectin is an important adipokine because of its beneficial effects on glucose and lipid metabolism. Low levels of adiponectin are associated with disease states such as diabetes and cardiovascular disease. Direct administration of adiponectin has been shown to be beneficial in animal models of diabetes, obesity and atherosclerosis. Adiponectin levels in humans can be increased through indirect methods such as weight loss or treatment with thiazolidinediones. This article will review the epidemiology and therapeutic options with adiponectin.
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Adipokines secreted by adipose tissue exert powerful regulatory effects on metabolism and energy balance. The contribution of various fat depots to circulating adipokine concentrations has not been clarified. Moreover, it is unknown whether these adipokines play a role in hepatic steatosis (ST) or progression to portal fibrosis and non-alcoholic steatohepatitis (PT/NASH). The purpose of this study was to explore the relationship between adipokines produced in omental (OM) and subcutaneous (SQ) fat with circulating concentrations, and to examine whether adipokines determine which patients with ST develop PT/NASH. We studied 20 females undergoing bariatric surgery (BMI 48 ± 7 kg/m2; age 40 ± 4 yr) categorized as ST or PF/NASH by liver biopsy. In serum and in OM and SQ fat samples, we quantified the adipokines leptin, resistin, MCP-1, and adiponectin by ELISA. In serum, we also measured high molecular weight (HMW) and low MW (LMW) adiponectin multimers by immunoblot, since we reported that HMW adiponectin was correlated with insulin sensitivity and reduced risk of Metabolic Syndrome. In comparing ST and PT/NASH, there were no differences in serum leptin, resistin, MCP-1, total adiponectin, and HMW and LMW adiponectin. In adipose tissues, OM adiponectin was higher in PF/NASH compared with ST (102.1 ± 8.7 vs. 82.5 ± 19.7 ng/mL; P < 0.05), while SQ adiponectin and tissue leptin levels did not differ between subgroups. OM adiponectin was also correlated with serum HMW adiponectin (r = 0.67, P < 0.05) but not LMW; in contrast, SQ adiponectin did not correlate with either serum HMW or LMW. In conclusion: 1) Serum levels of leptin, resistin, MCP-1, adiponectin, and adiponectin multimers were similar in ST and PT/NASH patients. 2) PT/NASH patients had higher OM adiponectin. 3) OM but not SQ adiponectin was highly correlated with serum HMW, the multimer associated with insulin sensitivity. The data suggest that factors intrinsic to liver, rather than secreted adipokines, determine which patients with hepatic steatosis progress to PT/NASH.
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Steatohepatitis
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