Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Adiponectin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMed2005

The relationship between insulin sensitivity and serum adiponectin levels in three population groups.

Reduced plasma adiponectin levels are associated with insulin resistance. Black South Africans, like African Americans, are more insulin-resistant than BMI-matched white subjects, as are Asian Indians. We investigated whether this interethnic variation in insulin resistance is due to differences in plasma adiponectin levels. Blood and anthropometric measurements were taken from black, white and Asian-Indian subjects. Serum adiponectin, lipids, glucose and insulin were measured; insulin sensitivity was calculated using HOMA. Black (HOMA = 2.62 +/- 0.99) and Asian-Indian subjects (HOMA = 3.41 +/- 2.85) were more insulin-resistant than BMI-matched white (HOMA = 1.76 +/- 0.63) subjects (p = 0.0001). Furthermore, the white subjects had higher adiponectin levels (8.11 +/- 4.39 microg/ml) compared to black (5.71 +/- 2.50 microg/ml) and Asian Indian (5.86 +/- 2.50 microg/ml) subjects (p = 0.003). When all ethnic groups were combined, multiple regression analysis demonstrated that serum adiponectin levels corrected for BMI and ethnicity did not correlate with HOMA, but did explain 10.0 % of the variance in HDL-cholesterol levels. Within each ethnic group, adiponectin only correlated inversely with HOMA in white subjects. Adiponectin may play a role in determining serum HDL-cholesterol levels, but ethnic variation in insulin sensitivity is not dependent on serum levels of this adipokine. The relationship between adiponectin and insulin resistance varies across ethnic groups.

Adiponectin↗
PubMed2007

Circulating serum adiponectin concentrations do not differ between obese and non-obese caucasians and are unrelated to insulin sensitivity.

Reduced serum levels of adiponectin in obesity and insulin resistance seem paradoxical, since adipose tissue is the only source of adiponectin, and reports on that subject are contradictory. The aim of this study was to investigate the concentrations of adiponectin in non-obese and obese normoglycemic humans, and to determine the correlation between adiponectin and HOMA index of insulin sensitivity. Based on the WHO definition of obesity, 145 obese subjects and 49 non-obese controls (aged 20-55 years) were studied. The serum adiponectin concentrations did not differ between subjects and controls (p=0.6398) and were not correlated with HOMA index (r=-0.0211; p=0.8048, and r=-0.0523; p=0.4757, for subjects and controls, respectively). Adiponectin was not correlated with HOMA index in females (r=-0.0521; p=0.6546, and r=-0.0825; p=0.3981, for female subjects and controls, respectively) as well as in males (r=0.0033; p=0.9791, and r=0.0123; p=0.9131, for male subjects and controls, respectively). These results lead to the conclusion that neither the concentrations of adiponectin differ between obese and non-obese humans, nor does any relationship between adiponectin concentration and insulin sensitivity exist.

Adiponectin↗
PubMed2002

Hydroxylation and glycosylation of the four conserved lysine residues in the collagenous domain of adiponectin. Potential role in the modulation of its insulin-sensitizing activity.

It has recently been shown that the fat-derived hormone adiponectin has the ability to decrease hyperglycemia and to reverse insulin resistance. However, bacterially produced full-length adiponectin is functionally inactive. Here, we show that endogenous adiponectin secreted by adipocytes is post-translationally modified into eight different isoforms, as shown by two-dimensional gel electrophoresis. Carbohydrate detection revealed that six of the adiponectin isoforms are glycosylated. The glycosylation sites were mapped to several lysines (residues 68, 71, 80, and 104) located in the collagenous domain of adiponectin, each having the surrounding motif of GXKGE(D). These four lysines were found to be hydroxylated and subsequently glycosylated. The glycosides attached to each of these four hydroxylated lysines are possibly glucosylgalactosyl groups. Functional analysis revealed that full-length adiponectin produced by mammalian cells is much more potent than bacterially generated adiponectin in enhancing the ability of subphysiological concentrations of insulin to inhibit gluconeogenesis in primary rat hepatocytes, whereas this insulin-sensitizing ability was significantly attenuated when the four glycosylated lysines were substituted with arginines. These results indicate that full-length adiponectin produced by mammalian cells is functionally active as an insulin sensitizer and that hydroxylation and glycosylation of the four lysines in the collagenous domain might contribute to this activity.

3T3 Cells↗
PubMed2006

Serum adiponectin levels in normal and hypertensive pregnancy.

OBJECTIVE: The aim of this study was to quantify adiponectin levels in women with normal and hypertensive pregnancies to determine whether there is an independent association, while controlling for body fat and insulin sensitivity. METHODS: A cross-sectional study was conducted in the following categories: 12 normotensive non-pregnant women, 10 normotensive, 12 gestational hypertensive, 13 essential hypertensive, and 12 preeclamptic women. All subjects underwent measurements of body fat by bio-impedance analysis and blood sampling. RESULTS: Percentage of body fat and insulin resistance were greater in all pregnant groups compared with non-pregnant women. Adiponectin concentrations were significantly lower in women with normal pregnancies (18.6 +/- 1.4 microg/mL, p = 0.02) compared with non-pregnant women (24.0 +/- 1.5 microg/mL). However, adiponectin levels were not significantly different among normal pregnancy, gestational hypertension (19.0 +/- 3.1 microg/mL), essential hypertension (24.0 +/- 3.7 microg/mL) and pre-eclampsia (22.4 +/- 2.5 microg/mL) groups. Adiponectin levels were inversely related to percent body fat and insulin resistance. When adiponectin levels were corrected for percent body fat and insulin resistance, no significant differences were seen among the study groups. CONCLUSIONS: Adiponectin levels are decreased in normal pregnancy, however this difference disappears when adiponectin levels are corrected for the pregnancy-related increases in body fat and insulin resistance. Adiponectin levels are not altered significantly in states of hypertension in pregnancy compared with normal pregnancy.

Adiponectin↗
PubMed2004

IRIS II Study: Sensitivity and specificity of intact proinsulin, adiponectin, and the proinsulin/adiponectin ratio as markers for insulin resistance.

OBJECTIVE: This study was performed to compare the specificity and sensitivity of intact proinsulin, adiponectin, and their ratio (proinsulin/adiponectin) in the prediction of insulin resistance as assessed by the homeostasis model assessment (HOMA) score (> or =2 = resistant). RESEARCH DESIGN AND METHODS: Using a cross-sectional approach, 500 orally treated patients with type 2 diabetes (272 women, 238 men; mean +/- SD age, 64.8 +/- 11.6 years; hemoglobin A1c, 7.0 +/- 1.5%; disease duration, 5.8 +/- 6.1 years) were investigated. Various cutoffs for body mass index-adjusted adiponectin and proinsulin/adiponectin were compared with the established cutoff value of 10 pmol/L for fasting proinsulin. RESULTS: Fasting proinsulin correlated more closely with the HOMA score (r = 0.560, P < 0.001) than fasting adiponectin (r = -0.204, P < 0.001) or proinsulin/adiponectin (r = 0.355, P < 0.001). For proinsulin, specificity and sensitivity for insulin resistance in correlation to the HOMA score results were 96% and 70%, respectively. At a comparable specificity level to proinsulin, adiponectin did not reach a comparable sensitivity (14%), while the proinsulin/adiponectin ratio almost reached the same sensitivity (65%). Overall, patients with elevated proinsulin had a higher prevalence of micro- and macrovascular disease [odds ratio 1.47 (adiponectin, 1.08; proinsulin/ adiponectin, 1.48) and 1.34 (adiponectin, 1.32; proinsulin/adiponectin, 1.27), respectively]. CONCLUSIONS: Elevation of fasting intact proinsulin seems to be the more specific marker for insulin resistance and increased cardiovascular risk than suppression of fasting adiponectin. Formation of the ratio does not lead to a further increase in the predictive value.

Adiponectin↗
PubMed2004

Association of the T45G polymorphism in exon 2 of the adiponectin gene with polycystic ovary syndrome: role of Delta4-androstenedione.

BACKGROUND: Insulin resistance is a prominent feature of polycystic ovary syndrome (PCOS), independent of obesity. It is possible that insulin resistance in PCOS is genetically determined. Adiponectin is a protein that modulates insulin action and is regarded as a possible link between adiposity and insulin resistance. The objective of this study was to examine the role of the adiponectin gene T45G polymorphism, located in exon 2, in PCOS, since this polymorphism has been shown to be associated with obesity and insulin resistance. SUBJECTS AND METHODS: Two hundred and thirty-two women were studied, and were classified as follows: 132 women with PCOS [62 with body mass index (BMI) > 25 kg/m2 and 70 with BMI < 25 kg/m2] and 100 ovulating women without hyperandrogenemia (controls: 19 with BMI > 25 kg/m2 and 81 with BMI < 25 kg/m2). From all subjects a whole-blood sample was taken and was used for isolation of peripheral blood leukocytes. The adiponectin T45G polymorphism, located in exon 2, was genotyped by amplification of genomic DNA. In all subjects, serum gonadotropin, androgen, 17-OH-progesterone, fasting glucose, insulin and adiponectin levels were measured between the third and sixth day of the menstrual cycle. RESULTS: A statistically significant difference was observed in the frequency of GG and TG genotypes between women with PCOS (40/132; 30.3%) and controls (19/100; 19.0%). In a subgroup of PCOS women with high Delta4-androstenedione levels (Delta4A > 3.11 ng/ml), a statistically significant difference between the frequencies of the genotypes was also noticed compared with the control group, in contrast to the subgroup with relatively low Delta4-androstenedione levels (Delta4A < 3.11 ng/ml). No significant associations were found between this adiponectin polymorphism and BMI, testosterone level, adiponectin levels and glucose-to-insulin ratio. CONCLUSIONS: Our study suggests that adiponectin polymorphisms are not causatively involved in the metabolic disturbances of PCOS, but that an interaction between adiponectin and steroid synthesis or action might exist.

Adiponectin↗
PubMed2005

Low plasma adiponectin levels and risk of colorectal cancer in men: a prospective study.

BACKGROUND: Adiponectin is an insulin-sensitizing hormone secreted by adipocytes. Levels of adiponectin are inversely associated with adiposity and insulin resistance. Because both adiposity and insulin resistance have been associated with risk of colorectal cancer, we hypothesized that adiponectin is associated with colorectal carcinogenesis. METHODS: We evaluated the association between adiponectin and colorectal cancer among 18 225 men in the Health Professionals Follow-up Study who provided blood samples in 1994. Between blood collection and January 31, 2002, 179 incident colorectal cancer cases occurred. Each case patient was matched to two control subjects on year of birth and date of blood draw. Information on lifestyle factors and diet was collected using biennial questionnaires and food frequency questionnaires. Logistic regression models were used to estimate relative risks (RRs) and confidence intervals (CIs). All statistical tests were two-sided. RESULTS: We observed a statistically significant inverse association between plasma adiponectin levels and risk of colorectal cancer (for the highest quintile [Q5] versus the lowest quintile [Q1], RR = 0.42, 95% CI = 0.23 to 0.78; P(trend) = .01). The association was only slightly attenuated after adjustment for body mass index (Q5 versus Q1, RR = 0.48, 95% CI = 0.25 to 0.90; P(trend) = .04) or for body mass index and other major risk factors for colorectal cancer (family history, physical activity, multivitamin use, smoking, alcohol, aspirin use, history of endoscopy, dietary calcium, folate, vitamin E, and vitamin D; Q5 versus Q1, multivariable RR = 0.50, 95% CI = 0.26 to 0.97; P(trend) = .08). Relative risks were not linear in any of the analyses; the second quintile had a lower relative risk than the lowest quintile, but further decreases in risk were not evident with increasing levels of adiponectin. CONCLUSIONS: In this prospective nested case-control study, men with low plasma adiponectin levels had a higher risk of colorectal cancer than men with higher levels. More prospective observational studies, particularly in women, and mechanistic studies are required to fully understand the relationship between adiponectin and carcinogenesis.

Adiponectin↗
PubMed2005

Plasma adiponectin concentration in early pregnancy and subsequent risk of hypertensive disorders.

OBJECTIVE: Adiponectin is an exclusively adipose tissue-derived protein. Low plasma adiponectin levels have been found in hypertensive men. Our objective was to evaluate whether low first-trimester plasma adiponectin values were predictive of hypertensive disorders later in pregnancy. METHODS: A nested case-control study was carried out on a cohort of 1,842 pregnant women who participated in the first-trimester Down syndrome screening program; 34 developed preeclampsia and 48 gestational hypertension. A control group of 82 nonhypertensive uneventful pregnancies was selected. Plasma adiponectin was determined using an enzyme-linked immunosorbent assay (ELISA). RESULTS: Adiponectin median concentrations in the group which subsequently became hypertensive were significantly lower than those in the control group (7.6 versus 13.0 microg/mL) (P < .001). When the 2 hypertensive subgroups were considered, the plasma adiponectin median value in the preeclampsia group was significantly lower than that in the gestational hypertension group (6.6 versus 9.3 microg/mL) (P = .01). Regression analysis showed an inverse correlation between plasma adiponectin concentrations and maternal age, gestational age, body mass index, systolic blood pressure, and proteinuria. Approximately 34% of hypertensive pregnancies, compared with 7% of controls (P < .001), had plasma adiponectin concentrations less than 6.4 microg/mL (mean value of lower quartile of distribution among control patients). After adjusting for maternal age, all these women experienced a 6.6-fold (95% confidence interval 2.5-17.8) increased risk of pregnancy hypertension, compared with those women who had higher concentrations. CONCLUSION: Our findings suggest a strong association between hypoadiponectinemia and the risk of hypertensive disorders in pregnancy, especially with preeclampsia.

Adiponectin↗
PubMed2004

Adiponectin is reduced in gestational diabetes mellitus in normal weight women.

BACKGROUND: Adiponectin is an adipose tissue-derived protein counteracting insulin resistance and inflammation. We have compared women with gestational diabetes mellitus (GDM; n = 22) and normal pregnancies (controls; n = 29) to evaluate whether adiponectin represents a link between endocrine function of adipose tissue and the development of diabetes during pregnancy. METHODS: The participants were categorized according to their prepregnancy body mass index (BMI) into two classes: BMI < 25 and BMI = 25. Plasma concentrations of adiponectin, leptin and insulin were measured by radioimmunoassay (RIA). Total cholesterol, high density lipoprotein (HDL) cholesterol and triacylglycerol were determined by routine enzymatic methods. Expression of adiponectin/glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was determined by real-time reverse transcription polymerase chain reaction (RT-PCR) in subcutaneous adipose tissues obtained by excision at cesarean delivery. RESULTS: Among individuals with GDM and BMI < 25 kg/m2 (n = 8), plasma adiponectin concentration was lower than in the controls (n = 20), 8.1 +/- 1.2 microg/mL vs. 12.2 +/- 1.1 microg/mL; p = 0.04). The mean plasma leptin concentrations did not differ between the GDM and control groups. Plasma concentrations of insulin and C-peptide were significantly higher among GDM than control individuals independent of BMI. For all the women included in the study, we found that plasma adiponectin only correlated negatively with prepregnancy and third-trimester (sampling day) BMI (p = 0.03 vs. p = 0.01). In abdominal subcutaneous adipose tissue of pregnant women, adiponectin mRNA levels were lower in GDM than in control subjects (0.77 +/- 0.18 vs. 1.39 +/- 0.15; p = 0.05). CONCLUSIONS: These results indicate that low plasma adiponectin concentration is associated with GDM. In addition, we found that adiponectin mRNA levels in adipose tissue biopsies from GDM subjects were reduced.

Adiponectin↗
PubMed2004

Plasma adiponectin levels in newborns are higher than those in adults and positively correlated with birth weight.

OBJECTIVE: The aim of this study was to examine plasma adiponectin concentrations during perinatal the period and their correlations with fetal anthropometric parameters and other hormones. DESIGN: Venous cord blood samples were obtained from 59 full-term healthy newborns (36 males and 23 females, gestational age 37.0-41.4 weeks, birth weight 2,146-4,326 g, birth length 44.0-54.5 cm). The blood samples were also obtained from 15 neonates (postnatal day 3-7) whose cord blood had already been collected and the changes in adiponectin concentrations were examined. MEASUREMENTS: The adiponectin concentration was determined by enzyme-linked immunosorbent assay. The leptin concentration was determined by radioimmunoassay. Insulin, GH and IGF-1 concentrations were determined by immunoradiometric assays. RESULTS: The plasma adiponectin concentrations in cord blood ranged from 6.0 to 55.8 microg/ml (median 22.4 microg/ml), which were much higher than those in normal-weight adults (P < 0.0001). In contrast to the findings in adults, these values were positively correlated with birth weight (r = 0.43, P = 0.0005), body mass index (r = 0.44, P = 0.0005), birth weight/birth length ratio (r = 0.46, P = 0.0002) and the leptin concentrations (r = 0.39, P = 0.004). When the effects of fat mass-related anthropometric parameters such as the birth weight/birth length ratio were controlled, plasma adiponectin concentrations had a significant inverse correlation with insulin concentrations (r = -0.35, P = 0.01). There was no significant gender difference in adiponectin concentrations among newborns. The adiponectin concentrations in neonates (postnatal day 3-7) did not change significantly compared with those in cord blood. CONCLUSIONS: In contrast to the findings in adults, these results suggest that the adiponectin concentration increases with the mass of fetal fat.

Adiponectin↗
PubMed2004

Maternal soluble tumour necrosis factor receptor type 2 (sTNFR2) and adiponectin are both related to blood pressure during gestation and infant's birthweight.

OBJECTIVE: Tumour necrosis factor alpha (TNF-alpha) and adiponectin are strongly related to insulin sensitivity; insulin resistance of pregnancy is a major determinant of infant's birthweight. We aimed to study the contributions of maternal serum concentrations of soluble TNF-alpha receptors (sTNFR1 and sTNFR2) and adiponectin to infant's birthweight. DESIGN: Cross-sectional, hospital-based study of insulin sensitivity during gestation. PATIENTS: Fifty-one healthy women with uncomplicated pregnancy and delivery (except for elective Caesarian section) and their healthy newborn infants. measurements Maternal blood levels of glucose, insulin, glycosylated haemaglobin (HbA1c), sTNFR1, sTNFR2 and adiponectin at delivery; cord-blood levels of sTNFR1, sTNFR2 and adiponectin. RESULTS: At delivery, maternal sTNFR2 correlated with systolic blood pressure (SBP; r = 0.38, P = 0.005). In multiple regression analyses, SBP and HbA1c were independent predictors of sTNFR2, explaining 18 and 7% of its variance, respectively; insulin resistance index (HOMA-IR), body mass index at delivery and SBP were independent predictors of adiponectin, explaining 15, 8 and 7% of its variance, respectively. Both maternal sTNFR2 and SBP were negatively correlated with infant's birthweight (r = -0.28, P = 0.04 and r = -0.36, P = 0.01 respectively, adjusted for sex and gestational age). In multivariate regression analyses, infant's sex and either maternal sTNFR2 or adiponectin were independent predictors of infant's birthweight, each explaining between 6 and 9% of birthweight variance. Further addition of maternal SBP to these models revealed that this variable was the main predictor of infant's birthweight, explaining 13% of its variance. CONCLUSIONS: Maternal sTNFR2 and adiponectin are independently related to both maternal blood pressure and infant's birthweight in uncomplicated pregnancy. The contributions of the TNF-alpha system and adiponectin to hypertensive disorders of pregnancy and fetal growth merit further studies.

Adiponectin↗
PubMed2005

Distribution and determinants of adiponectin, resistin and ghrelin in a randomly selected healthy population.

OBJECTIVE: Adiponectin, resistin, ghrelin and the IGF-I system seem to play an important role in the regulation of body composition throughout life, but the mechanisms are not well understood. The aim of our study was to analyse the distribution among sexes and all decades of the adult life of adiponectin, resistin and ghrelin and their relationship with anthropometric, body composition parameters and the IGF-I system. SUBJECTS: One hundred and thirty-four men and 127 healthy women were included in the study. MEASUREMENTS: Plasma concentration of adiponectin, resistin, ghrelin, total IGF-I, free IGF-I and IGFBP-3 were determined in all subjects. Body composition was evaluated by bioelectrical impedance. RESULTS: Resistin and ghrelin were not affected by age. Plasma adiponectin correlated negatively with age, body mass index (BMI), waist-to-hip ratio (WHR), waist circumference (WC), fat mass (FM) and body fat (BF) in men. Adiponectin correlated negatively with WHR and positively with free IGF-I in women. Resistin correlated positively with BMI and WC only in men, and ghrelin correlated positively with WC, BMI and FM and negatively with free IGF-I in men. In multiple regression analysis adiponectin remained associated with WHR (beta=-0.19, P=0.01) in women. Resistin was positively associated with BMI (beta=0.30, P=0.003) in women and ghrelin was negatively related to free IGF-I (beta=-0.158, P=0.019) in men. CONCLUSIONS: Plasma adiponectin declines with age and is negatively associated with FM in men. Our data suggest the existence of a positive correlation of adiponectin and the IGF-I axis in women and of an inverse relationship between ghrelin and the IGF-I system in men.

Adiponectin↗
PubMed2006

Does birthweight predict adolescent adiponectin levels?

OBJECTIVE: Low birthweight is associated with insulin resistance later in life, and adiponectin is known to play an important role in insulin resistance. We have investigated whether birthweight has a relationship with adiponectin levels in adolescence. PATIENTS: An at-home questionnaire survey was completed by 660 middle-school students (aged 12-15 years) in Seoul, Korea, and 152 participants were selected randomly based on their birthweight. MEASUREMENTS Subjects were separated into three groups according to birthweight. We recorded the birthweight and measured anthropometric factors including blood pressure, lipid profile, homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-beta), and adiponectin levels of the subjects. These parameters were compared among the groups. The relationship between birthweight and physiological characteristics in adolescence was examined. RESULTS: Systolic blood pressure, lipid profiles and fasting plasma glucose were not significantly different among the groups, but diastolic blood pressure was lower in the third tertile. Insulin, C-peptide and HOMA-IR were higher in the low birthweight tertile. After adjustment for confounding factors, birthweight was inversely related to diastolic blood pressure, insulin, C-peptide and HOMA-IR. Adiponectin level had a significant relationship with current body mass index (BMI) (r=-0.291; P< 0.001) but not with birthweight (r = 0.117; P = 0.166). CONCLUSIONSP: Although birthweight is closely related to insulin resistance during adolescence, adiponectin levels during adolescence had no significant relationship with birthweight. This result implies that low birthweight may not permanently affect adiponectin levels, but current body size is more closely associated with a decreased adiponectin level. However, the limited importance of birthweight as a determining factor on the adiponectin level later in life needs to be further evaluated.

Adiponectin↗
PubMed2005

Adiponectin--journey from an adipocyte secretory protein to biomarker of the metabolic syndrome.

Adiponectin is an adipocyte-derived hormone that was discovered in 1995. Unlike leptin, which was identified around the same time, the clinical relevance of adiponectin remained obscure for a number of years. However, starting in 2001, several studies were published from different laboratories that highlighted the potential antidiabetic, antiatherosclerotic and anti-inflammatory properties of this protein complex. Methods to measure the protein with high throughput assays in clinical samples were developed shortly thereafter, and as a result hundreds of clinical studies have been published over the past 3 years describing the role of adiponectin in endocrine and metabolic dysfunction. Furthermore, adiponectin research has expanded to include a role for adiponectin in cancer and other disease areas. Although it is an impossible task to summarize the findings from all these studies in a single review, we aim to demonstrate the utility of circulating adiponectin as a biomarker of the metabolic syndrome. Evidence for this relationship will include how decreased levels of plasma adiponectin ('hypoadiponectinaemia') are associated with increased body mass index (BMI), decreased insulin sensitivity, less favourable plasma lipid profiles, increased levels of inflammatory markers and increased risk for the development of cardiovascular disease. Therefore, adiponectin levels hold great promise for use in clinical application serving as a potent indicator of underlying metabolic complications.

Adipocytes↗
PubMed2006

Regulation of adiponectin in adipocytes upon exposure to HIV-1.

OBJECTIVES: Adipose dysregulation, dyslipidemia, and insulin resistance are hallmarks of HIV-related lipodystrophy. The precise mechanisms behind these disturbances are unknown. In HIV-infected patients, we previously demonstrated a strong relationship between lipodystrophy and levels of adiponectin, an adipose peptide implicated in regulation of glucose and lipid metabolisms. In this study we investigated the effect of HIV on adipocytes, to determine whether HIV can directly infect adipocytes and/or alter the regulation and secretion of the adipocyte-derived hormone adiponectin. METHODS: Human subcutaneous preadipocytes and adipocytes were exposed to HIV-1 under various conditions. Adiponectin was measured in supernatants and cell lysates. RESULTS: Although adipocytes expressed CD4, the major HIV receptor, they could not be infected in vitro. However, exposure to HIV dramatically increased the secretion of adiponectin from human adipocytes, in the absence of infection. This was exacerbated with sustained exposure to HIV in a transwell assay. Further, human peripheral mononuclear cells also produced adiponectin, but this was largely dependent upon T-cell activation. CONCLUSIONS: We propose that the stimulation of adiponectin production by HIV can perturb adiponectin regulation, leading to substantially decreased levels upon viral suppression by antiretroviral therapy. These data suggest a potential molecular mechanism of adiponectin regulation in HIV-infected patients.

Adipocytes↗
PubMed2006

Adiponectin and insulin resistance in early- and late-onset pre-eclampsia.

OBJECTIVE: To evaluate the importance of adiponectin and insulin resistance in early- and late-onset pre-eclampsia. DESIGN: A nested case-control study in 72 pregnant women who participated in the first-trimester Down-syndrome-screening programme and who delivered at our hospital. SETTING: University Hospital, Department of Obstetrics and Gynecology. POPULATION: Pregnant women: 36 women with pre-eclampsia of which 20 late onset and 16 early onset were compared with 36 uncomplicated pregnancies who delivered at term. METHODS: In all the women, insulin resistance was calculated by the homeostasis model assessment ratio (HOMA-IR) and plasma adiponectin was determined using an enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURES: Insulin resistance and adiponectin concentration. RESULTS: First-trimester plasma adiponectin mean levels in the whole pre-eclampsia group were significantly lower than that in the control group (8.4 +/- 3.3 versus 14.8 +/- 4.6 microgram/ml; P < 0.001), whereas first-trimester mean HOMA-IR values were significantly higher in the pre-eclampsia group than that in the control group (2.0 +/- 1.1 versus 1.0 +/- 0.4; P= 0.01). Plasma adiponectin concentrations at delivery in the pre-eclampsia group were significantly higher than that in the control group (9.2 +/- 3.7 versus 7.8 +/- 2.6 microgram/ml; P= 0.04). First-trimester plasma adiponectin mean concentrations in the late-onset subgroup were significantly lower compared with the concentrations in early-onset subgroup (6.2 +/- 1.4 microgram/ml versus 11.1 +/- 3.2 microgram/ml; P < 0.001), and there was a significant difference in adiponectin plasma values only between women in the late-onset pre-eclampsia group versus those in the control group (P < 0.001). First-trimester mean HOMA-IR values were significantly higher in the late-onset subgroup compared with that of the early-onset subgroup (2.5 +/- 1.3 versus 1.3 +/- 0.3; P= 0.02), and there was a significant difference only between the control group versus the late-onset subgroup (P= 0.001). CONCLUSIONS: First-trimester adiponectin and HOMA-IR values seem to select two completely different populations: early- and late-onset pre-eclampsia, which might suggest a different pathogenesis.

Adiponectin↗
PubMed2005

Adiponectin levels among patients with chronic hepatitis B and C infections and in response to IFN-alpha therapy.

AIMS: The study was designed to survey the change of adiponectin levels before and after interferon-alpha (IFN-alpha) therapy in patients with chronic hepatitis B and C infections. METHODS: Twenty-one biopsy-proved patients with chronic hepatitis B (10 cases) and hepatitis C (11 cases) were given IFN-alpha for a total of 24 weeks. Fasting plasma glucose, insulin and adiponectin levels were obtained before and 12 weeks after completion of IFN-alpha therapy. Insulin suppression test was conducted before and within 1 week after IFN-alpha therapy. RESULTS: The change of adiponectin levels differed significantly between responders (eight cases) and non-responders (13 cases) to IFN-alpha treatment (-4.8+/-2.2 vs. 0.5+/-1.0 microg/ml, P=0.03). After adjusting for age, gender and change in body mass index, the study found the change of adiponectin levels still significantly related to the response to IFN-alpha (P=0.04). When hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected patients were separately analyzed, the adiponectin levels reported a trend to decrease in HCV responders (11.9+/-3.2 vs. 10.8+/-3.0 microg/ml, P=0.02, n=4) and HBV responders (17.7+/-4.1 vs. 9.2+/-1.0 microg/ml, P=0.10, n=4). In addition, a significant decrease of steady-state plasma glucose in insulin suppression test was noted in responders (13.6+/-1.8-11.7+/-1.2 mmol/l, P=0.03), but not in non-responders (12.3+/-1.1-11.0+/-1.0 mmol/l, P=0.20), after IFN-alpha therapy. CONCLUSIONS: IFN-alpha resulted in a decrease of serum adiponectin levels but an improvement of insulin resistance in responders to the treatment. The result contradicts previous concept of the relationship between insulin resistance and adiponectin levels. Whether and how the augmented immune response, which was supposed to result from the disappearance or the profound down-regulation of the virus or viral antigens in responders to IFN-alpha treatment, contributes to the lowering of adiponectin levels needs to be further investigated.

Adiponectin↗
PubMed2006

Circulating levels of adiponectin in preterm infants.

OBJECTIVE: To determine circulating levels of adiponectin in preterm infants and examine possible associations with anthropometric measurements, weight gain, and leptin and insulin levels. DESIGN: Prospective study. SETTING: A university hospital neonatal care unit. STUDY POPULATION: 62 preterm (mean (SD) gestational age 32.0 (2.1) weeks) and 15 full-term infants (reference group). INTERVENTIONS: Blood samples taken at discharge (40.9 (14.8) days of life) from the preterm infants and at a comparable postnatal age in full-term infants. All infants were fed the same commercial formula, but in nine preterms the formula contained long-chain polyunsaturated fatty acids (LCPUFAs). MAIN OUTCOME MEASURES: Serum levels of adiponectin, leptin and insulin. Associations of adiponectin levels were tested only in the preterm group. RESULTS: Serum levels of adiponectin were lower in preterm (40.9 (14.8) microg/ml) than full-term infants (53.1 (16.0) microg/ml, p<0.01). However, after adjustment for body weight, the influence of prematurity on adiponectin levels was no longer significant. In preterm infants, adiponectin levels independently correlated with being born small for gestational age (SGA) (beta=-0.35, p=0.01), weight gain (beta=0.28, p=0.03) and LCPUFA-supplemented formula (beta=0.34, p=0.009). Serum adiponectin levels did not correlate with insulin or leptin levels. However, insulin levels were higher in preterm than in full-term infants after adjustment for body weight. CONCLUSIONS: Adiponectin levels are lower in preterm infants at discharge than full-term infants probably due to decreased adiposity. The levels are influenced by being born SGA, weight gain and, possibly, by dietary LCPUFAs. The importance of these findings in the development of insulin or leptin resistance in children born prematurely needs to be further studied.

Adiponectin↗