Hypoadiponectinemia In Patients Research Articles

Mean Adiponectin Levels and Frequency of Hypoadiponectinemia in Gestational Diabetes Mellitus

Background: Insulin resistance, a major pathogenic factor in Gestational Diabetes Mellitus (GDM), has an inverse correlation with adiponectin; therefore, the role of adiponectin in the pathogenesis of GDM has been suggested. The study aimed to determine mean adiponectin levels and the frequency of hypoadiponectinemia in patients with GDM. Methods: The study was carried out at Dr. Ziauddin University Hospital, Karachi from June 2016 to December 2017. A total of 99 women of age group 15-45 years diagnosed with GDM on Oral Glucose Tolerance Test (OGTT) at 24-28 weeks of gestations were included in the study. Patient’s data was recorded on proposed proforma, regarding age, gestational age, parity, ethnicity, Body Mass Index (BMI). Serum samples for quantitative estimation of Adiponectin were collected while performing OGTT and were analyzed on Immunoassay in conjunction with control materials. Mean±Std. was calculated for quantitative variables. Percentages and frequencies were calculated for categorical variables. For significant differences between categories, an independent t-test and Chi-square test were used. Results: High frequency of hypoadiponectinemia was observed in GDM women with mean adiponectin levels of 6.90±2.86 µg/ml (95%CI: 6.33 to 7.47). Out of 99 GDM women, 91(91.92%) had hypoadiponectinemia while 8(8.08%) had normal Adiponectin levels. A significant (p=0.05) association was found between BMI and hypoadiponectinemia. Conclusion: In the majority of GDM females, hypoadiponectinemia was observed. The high frequency of hypoadiponectinemia suggests further large-scale studies, are warranted to ascertain the diagnostic accuracy of adiponectin as a potential biomarker for GDM.

Inverse Correlation between Serum Levels of Selenoprotein P and Adiponectin in Patients with Type 2 Diabetes

BackgroundWe recently identified selenoprotein P (SeP) as a liver-derived secretory protein that causes insulin resistance in the liver and skeletal muscle; however, it is unknown whether and, if so, how SeP acts on adipose tissue. The present study tested the hypothesis that SeP is related to hypoadiponectinemia in patients with type 2 diabetes.Methodology/Principal FindingsWe compared serum levels of SeP with those of adiponectin and other clinical parameters in 36 patients with type 2 diabetes. We also measured levels of blood adiponectin in SeP knockout mice. Circulating SeP levels were positively correlated with fasting plasma glucose (r = 0.35, P = 0.037) and negatively associated with both total and high-molecular adiponectin in patients with type 2 diabetes (r = −0.355, P = 0.034; r = −0.367, P = 0.028). SeP was a predictor of both total and high-molecular adiponectin, independently of age, body weight, and quantitative insulin sensitivity index (β = −0.343, P = 0.022; β = −0.357, P = 0.017). SeP knockout mice exhibited an increase in blood adiponectin levels when fed regular chow or a high sucrose, high fat diet.Conclusions/SignificanceThese results suggest that overproduction of liver-derived secretory protein SeP is connected with hypoadiponectinemia in patients with type 2 diabetes.

Hypoadiponectinemia in Patients With Paroxysmal Atrial Fibrillation

Background and ObjectivesAdiponectin is an adipose tissue-derived hormone that has beneficial effects on cardiac function and has been reported to be associated with lipid metabolism, glucose metabolism, and insulin resistance. Serum levels of adiponectin are reduced in obese individuals compared with non-obese individuals. Obesity is associated with an increased incidence of atrial fibrillation (AF); however, the role of adiponectin in AF is unclear. The aim of this study is to evaluate the relationship between the plasma adiponectin level and AF.Subjects and MethodsSixty-one consecutive patients were prospectively enrolled for this study. Subjects were divided into two groups: patients with AF (n=30) and controls (n=31). Laboratory evaluation, including levels of plasma adiponectin, was performed and echocardiographic parameters were measured.ResultsThe baseline characteristics were not different between the two groups. The plasma adiponectin level of patients in the AF group was significantly lower than in the control group (14.9±7.2 vs. 19.±8.9 µg/mL, p<0.05). In addition, when we divided the AF patients into paroxysmal and chronic AF, the plasma adiponectin level was significantly lower in patients with paroxysmal AF, compared with the control group. In multiple binary logistic regression analysis to evaluate the independent predictors for AF, adiponectin and left atrial diameter were strong independent predictors of AF.ConclusionIn this study a lower plasma adiponectin concentration was significantly associated with that of paroxysmal AF. Hypoadiponectinemia can potentially be an important risk factor for AF.

Combination of Niacin and Fenofibrate with Lifestyle Changes Improves Dyslipidemia and Hypoadiponectinemia in HIV Patients on Antiretroviral Therapy: Results of “Heart Positive,” a Randomized, Controlled Trial

HIV patients on antiretroviral therapy (ART) have a unique dyslipidemia [elevated triglycerides and non-high-density lipoprotein-cholesterol (HDL-C), low HDL-C] with insulin resistance (characterized by hypoadiponectinemia). The aim was to test a targeted, comprehensive, additive approach to treating the dyslipidemia. We conducted a randomized, double-blind, placebo-controlled, 24-wk trial of lifestyle modification, fenofibrate, and niacin in multiethnic HIV clinics at an academic center. Hypertriglyceridemic adult patients were stratified on three combinations of ART classes. Subjects retained at the first measurement (2 wk) after entry were included in the analysis (n = 191). Subjects were randomized into five treatment groups: usual care (group 1); low-saturated-fat diet and exercise (D/E; group 2); D/E + fenofibrate (group 3); D/E + niacin (group 4); or D/E + fenofibrate + niacin (group 5). We measured changes in fasting triglycerides, HDL-C, and non-HDL-C (primary), and in insulin sensitivity, glycemia, adiponectin, C-reactive protein, energy expenditure, and body composition (secondary). Data were analyzed as a factorial set of treatment combinations using a mixed repeated measures model, last observation carried forward, and complete case approaches (groups 2-5), and as an unstructured set of treatments (groups 1-5). Fenofibrate improved triglycerides (P = 0.002), total cholesterol (P = 0.02), and non-HDL-C (P = 0.003), whereas niacin improved HDL-C (P = 0.03), and both drugs decreased the total cholesterol-to-HDL-C ratio (P = 0.005-0.01). The combination of D/E, fenofibrate, and niacin provided maximal benefit, markedly reducing triglycerides (-52% compared to usual care; P = 0.003), increasing HDL-C (+12%; P < 0.001), and decreasing non-HDL-C (-18.5%; P = 0.003) and total cholesterol-to-HDL-C ratio (-24.5%; P < 0.001). Niacin doubled adiponectin levels. A combination of fenofibrate and niacin with low-saturated-fat D/E is effective and safe in increasing HDL-C, decreasing non-HDL-C and hypertriglyceridemia, and ameliorating hypoadiponectinemia in patients with HIV/ART-associated dyslipidemia.

Systemic Adiponectin Malfunction as a Risk Factor for Cardiovascular Disease

Adiponectin (Ad) is an abundant protein hormone regulatory of numerous metabolic processes. The 30 kDa protein originates from adipose tissue, with full-length and globular domain circulatory forms. A collagenous domain within Ad leads to spontaneous self-assemblage into various oligomeric isoforms, including trimers, hexamers, and high-molecular-weight multimers. Two membrane-spanning receptors for Ad have been identified, with differing concentration distribution in various body tissues. The major intracellular pathway activated by Ad includes phosphorylation of AMP-activated protein kinase, which is responsible for many of Ad's metabolic regulatory, anti-inflammatory, vascular protective, and anti-ischemic properties. Additionally, several AMP-activated protein kinase-independent mechanisms responsible for Ad's anti-inflammatory and anti-ischemic (resulting in cardioprotective) effects have also been discovered. Since its 1995 discovery, Ad has garnered considerable attention for its role in diabetic and cardiovascular pathology. Clinical observations have demonstrated the association of hypoadiponectinemia in patients with obesity, cardiovascular disease, and insulin resistance. In this review, we elaborate currently known information about Ad malfunction and deficiency pertaining to cardiovascular disease risk (including atherosclerosis, endothelial dysfunction, and cardiac injury), as well as review evidence supporting Ad resistance as a novel risk factor for cardiovascular injury, providing insight about the future of Ad research and the protein's potential therapeutic benefits.

Hypoadiponectinemia in Patients with Cerebral Infarction: Comparison with Other Atherosclerotic Disorders

The present study was undertaken to determine serum adiponectin level in patients with cerebral infarction and to further analyze any difference in serum adiponectin levels among atherosclerotic disorders. One hundred fifty-two subjects with atherosclerotic disorders were enrolled, 110 males and 42 females, with the age of 67.0 +/- 9.9 years (mean +/- SD). They were divided into 62 patients with cerebral infarction, 48 patients with ischemic heart disease, and 42 patients with arteriosclerosis obliterans. Thirty-two subjects matched by age, gender, and body mass index served as controls. Serum adiponectin levels were 7.2 +/- 0.6 microg/mL (mean +/- SE) in the patients with cerebral infarction, 7.2 +/- 0.8 microg/mL in those with ischemic heart disease, and 6.9 +/- 0.9 microg/mL in those with arteriosclerosis obliterans. They were significantly less than the level of 12.6 +/- 1.9 microg/mL in the control group (P < 0.01). However, there was no difference in serum adiponectin level among three groups of atherosclerotic disorders. In the patients with acute cerebral infarction, serum adiponectin level was temporarily reduced from 7.3 +/- 0.9 to 6.2 +/- 0.8 microg/mL 14 days after the hospitalization (P < 0.01), followed by recovery to the basal value. The present findings indicate that serum adiponectin levels are equivalently reduced in patients with atherosclerotic disorders, and that serum adiponectin is changeable under acute phase of cerebral infarction.

Decreased serum adiponectin in adolescents and young adults with familial primary hypercholesterolemia

Decreased serum adiponectin is associated with dyslipidemia. However, serum adiponectin status has never before been studied in patients with familial-related severe primary hypercholesterolemia (FRSPH). The aim of this study is to measure serum adiponectin level in a group of young patients with FRSPH and determine its correlation with insulin-resistant status. Twenty-three patients with FRSPH [average LDL-cholesterol (LDL-C) = 250.8 (190-610) mg/dL] without clinical manifestations of metabolic syndrome as well as 46 healthy (control) adolescents and young adults (<30 yr old) were included. The serum adiponectin, fasting sugar, insulin, lipids, systolic and diastolic blood pressure (SBP and DBP), and anthropometrical indices such as body mass index and waist circumference were obtained. The homeostasis model assessment (HOMA) was calculated to estimate the insulin resistant status. Compared with healthy controls, patients with FRSPH had a significantly lower mean serum adiponectin level (7.7+/-1.8 microg/mL vs. 10.1+/-4.3 microg/mL, P= 0.013). After adjustment for HOMA and associated covariates, multiple linear regression analysis showed that patients with FRSPH are significantly associated with hypoadiponectinemia. Compared with healthy controls, patients with FRSPH had a significantly lower mean serum adiponectin level (7.7 +/-1.8 microg/mL vs. 10.1+/-4.3 microg/mL, P = 0.013). After adjustment for HOMA and associated covariates, multiple linear regression analysis showed that patients with FRSPH are significantly associated with hypoadiponectinemia. The serum adiponectin levels are lower in young patients with FRSPH without clinical manifestations of metabolic syndrome. The mechanism of hypoadiponectinemia in patients with FRSPH is probably independent of insulin resistance.