Adropin Concentrations Research Articles

Relationship between human cord blood adropin levels and fetal growth

Adropin is a recently identified peptide and participates in the regulation of energy homeostasis and vascular function. The aim of this study was to examine the relationships between human cord blood adropin levels and fetal growth. A total of 159 newborns [preterm delivery (PTD), n=72; term delivery, n=87] were recruited. Adropin levels in cord blood were determined using enzyme-linked immunosorbent assay kits. Clinical information on fetal growth was collected. Adropin levels in PTD babies (median, 2028; 25th–75th, 1413–2484pg/ml) were lower than those in term delivery babies (median, 2305; 25th–75th, 1960–2684pg/ml, P=0.01). Birth weight and length z score, Ponderal index, placental length, breadth, thickness, surface area, volume and density were not significantly correlated to adropin concentrations in term delivery group. However, we found adropin concentrations were significantly correlated to gestational age at birth (Spearman's correlation coefficient=0.35, P<0.01) and placental weight (Spearman's correlation coefficient=0.24, P=0.04) in PTD group. We also found that boys had lower adropin levels than girls in PTD group (P=0.01). When the analysis was extended to the whole group (PTD and term deliveries combined), the results were similar to those for PTD group alone. After adjusting for maternal age and newborn's sex, every 100pg/ml increase of adropin concentration was significantly associated with a decreased risk of PTD (odds ratio, 0.95; 95% confidence interval, 0.91–0.99). Our study showed that cord blood adropin levels were positively correlated with gestational age and placental weight but not with other fetal growth parameters.

Fasting plasma adropin concentrations correlate with fat consumption in human females

ObjectiveThis study investigated whether plasma adropin concentrations are influenced by sleep restriction and correlate with dietary preferences.Design and MethodsPlasma adropin concentrations were measured by ELISA using samples from a study that investigated feeding behavior in sleep deprived lean (body mass index 22–26 kg/m2) men and women aged 30–45 y. Sleep (habitual or restricted to 4h/night) and diet were controlled during a 4-day inpatient period. On day 5, food was self-selected (FS). Adropin was measured on day 4 in samples collected throughout the day, and then after an overnight fast at 0730 on days 5 (Pre-FS) and 6 (Post-FS).ResultsPlasma adropin concentrations were not affected by sleep restriction. However, circulating adropin concentrations correlated with food selection preferences in women, irrespective of sleep status. Pre-FS adropin correlated positively with fat intake (total fat, r=0.867, P<0.05; saturated fat, r=0.959, P<0.01) and negatively with carbohydrate intake (r=−0.894, P<0.05) as a percent total energy. Post-FS adropin correlated with total (r=0.797, P<0.05) and saturated fat intake (r=0.945, P<0.01), and negative with total carbohydrate intake (r=−0.929, P<0.01). Pre-FS adropin also correlated with fat intake in kcal adjusted for body size (total fat, r=0.852, P<0.05; saturated fat, r=0.927, P<0.01).ConclusionsPlasma adropin concentrations correlate with fat consumption in women.

Plasma adropin levels in children with obstructive sleep apnea

Adropin is a peptide hormone encoded by the Energy Homeostasis-Associated gene. Circulating adropin concentrations are regulated by energy intake and affect cardiovascular function, particularly in endothelial function. In this issue of The Journal, Gozal et al from the University of Chicago investigated the hypothesis that adropin levels would be lower in children with obstructive sleep apnea (OSA), especially in those with evidence of endothelial dysfunction because they might provide a reliable marker for endothelial dysfunction in pediatric obstructive sleep apnea. The results show that children with OSA and abnormal endothelial function had significantly lower adropin levels compared with match controls and with children with OSA and normal endothelial function. Adropin concentrations below 4.2 ng/mL reliably predicted abnormal endothelial function. It was interesting that adropin levels assessed after adenotonsillectomy in a subset of their patients showed a significant increase in adropin levels post-operatively if they had pre-existing endothelial dysfunction, but not if they did not. The authors conclude that plasma adropin levels are reduced and correlate with endothelial dysfunction in children with OSA and that they returned to normal values after adenotonsillectomy. They propose that assessment of plasma adropin concentrations may provide a reliable indicator of vascular injury in the context of OSA in children.Article page 1122▶ Adropin is a peptide hormone encoded by the Energy Homeostasis-Associated gene. Circulating adropin concentrations are regulated by energy intake and affect cardiovascular function, particularly in endothelial function. In this issue of The Journal, Gozal et al from the University of Chicago investigated the hypothesis that adropin levels would be lower in children with obstructive sleep apnea (OSA), especially in those with evidence of endothelial dysfunction because they might provide a reliable marker for endothelial dysfunction in pediatric obstructive sleep apnea. The results show that children with OSA and abnormal endothelial function had significantly lower adropin levels compared with match controls and with children with OSA and normal endothelial function. Adropin concentrations below 4.2 ng/mL reliably predicted abnormal endothelial function. It was interesting that adropin levels assessed after adenotonsillectomy in a subset of their patients showed a significant increase in adropin levels post-operatively if they had pre-existing endothelial dysfunction, but not if they did not. The authors conclude that plasma adropin levels are reduced and correlate with endothelial dysfunction in children with OSA and that they returned to normal values after adenotonsillectomy. They propose that assessment of plasma adropin concentrations may provide a reliable indicator of vascular injury in the context of OSA in children. Article page 1122▶ Circulating Adropin Concentrations in Pediatric Obstructive Sleep Apnea: Potential Relevance to Endothelial FunctionThe Journal of PediatricsVol. 163Issue 4PreviewTo test the hypothesis that concentrations of adropin, a recently discovered peptide that displays important metabolic and cardiovascular functions, are lower in obstructive sleep apnea (OSA), especially when associated with endothelial dysfunction. Full-Text PDF

Copeptin, adropin and irisin concentrations in breast milk and plasma of healthy women and those with gestational diabetes mellitus

Copeptin, adropin and irisin are polypeptide hormones implicated in energy homostasis and diabetes. The purposes of this study were (1) to compare the copeptin, adropin and irisin concentrations between colostrum, transitional and mature milk and plasma in lactating women with and without GDM and (2) to compare these values with those from non-lactating women. Venous blood samples were obtained before suckling from 15 healthy lactating women aged 26–30 years, 15 lactating women with GDM aged 26–32 years, and 14 age-matched controls aged 25–31 years. Colostrum, transitional milk and mature milk samples were collected just before suckling. The concentration of copeptin was determined by EIA while the concentrations of adropin and irisin were determined by ELISA. The levels of copeptin, adropin and irisin in the colostrum were significantly higher than those in transitional and mature milk samples from healthy women; also, transitional milk had higher copeptin, adropin and irisin concentrations than mature milk. The amounts of copeptin in the colostrum and transitional milk were significantly higher than in mature milk samples from women with GDM, while the amounts of adropin and irisin were significantly lower. The relative concentrations of copeptin, adropin and irisin in the plasma samples from these groups of women were similar to those in the colostrum, transitional and mature milk samples, but the latter concentrations were higher than those in the plasma. These peptides could influence the regulation of metabolic pathways and the postnatal growth and development of different organs in the newborn.

Circulating adropin concentrations in pediatric obstructive sleep apnea: potential relevance to endothelial function.

To test the hypothesis that concentrations of adropin, a recently discovered peptide that displays important metabolic and cardiovascular functions, are lower in obstructive sleep apnea (OSA), especially when associated with endothelial dysfunction. Age-, sex-, and ethnicity-matched children (mean age, 7.2 ± 1.4 years) were included into 1 of 3 groups based on the presence of OSA in an overnight sleep study, and on the time to postocclusive maximal reperfusion (Tmax >45 seconds) with a modified hyperemic test. Plasma adropin concentrations were assayed using a commercial enzyme-linked immunosorbent assay kit. Among controls, the mean morning adropin concentration was 7.4 ng/mL (95% CI, 5.2-16.3 ng/mL). Children with OSA and abnormal endothelial function (EF) (OSA(+)/EF(+) group) had significantly lower adropin concentrations (2.7 ± 1.1 ng/mL; n = 35) compared with matched controls (7.6 ± 1.4 ng/mL; n = 35; P < .001) and children with OSA and normal EF (OSA(+)/EF(-) group; 5.8 ± 1.5 ng/mL; n = 47; P < .001). A plasma adropin concentration <4.2 ng/mL reliably predicted EF status, but individual adropin concentrations were not significantly correlated with age, body mass index z-score, obstructive apnea-hypopnea index, or nadir oxygen saturation. Mean adropin concentration measured after adenotonsillectomy in a subset of children with OSA (n = 22) showed an increase in the OSA(+)/EF(+) group (from 2.5 ± 1.4 to 6.4 ± 1.9 ng/mL; n = 14; P < .01), but essentially no change in the OSA(+)EF(-) group (from 5.7 ± 1.3 to 6.4 ± 1.1 ng/mL; n = 8; P > .05). Plasma adropin concentrations are reduced in pediatric OSA when endothelial dysfunction is present, and return to within normal values after adenotonsillectomy. Assessment of circulating adropin concentrations may provide a reliable indicator of vascular injury in the context of OSA in children.

Expression of adropin in rat brain, cerebellum, kidneys, heart, liver, and pancreas in streptozotocin-induced diabetes

We have investigated how diabetes affects the expression of adropin (ADR) in rat brain, cerebellum, kidneys, heart, liver, and pancreas tissues. The rats in the diabetic group were administered an intraperitoneal (i.p.) injection of a single dose of 60 mg/kg streptozotocin (STZ) dissolved in a 0.1 M phosphate-citrate buffer (pH 4.5). The rats were maintained in standard laboratory conditions in a temperature between 21 and 23 °C and a relative humidity of 70 %, under a 12-h light/dark cycle. The animals were fed a standard commercial pellet diet. After 10 weeks, the animals were sacrified. ADR concentrations in the serum and tissue supernatants were measured by ELISA, and immunohistochemical staining was used to follow the expression of the hormones in the brain, cerebellum, kidneys, heart, liver, and pancreas tissues. The quantities were then compared. Increased ADR immunoreaction was seen in the brain, cerebellum, kidneys, heart, liver, and pancreas in the diabetes-induced rats compared to control subjects. ADR was detected in the brain (vascular area, pia mater, neuroglial cell, and neurons), cerebellum (neuroglial cells, Purkinje cells, vascular areas, and granular layer), kidneys (glomerulus, peritubular interstitial cells, and peritubular capillary endothelial cells), heart (endocardium, myocardium, and epicardium), liver (sinusoidal cells), and pancreas (serous acini). Its concentrations (based on mg/wet weight tissues) in these tissues were measured by using ELISA showed that the levels of ADR were higher in the diabetic rats compared to the control rats. Tissue ADR levels based on mg/wet weight tissues were as follows: Pancreas > liver > kidney > heart > brain > cerebellar tissues. Evidence is presented that shows ADR is expressed in various tissues in the rats and its levels increased in STZ-induced diabetes; however, this effect on the pathophysiology of the disorder remains to be understood.

Maternal and fetal adropin levels in gestational diabetes mellitus

To evaluate maternal and cord blood serum adropin concentrations in pregnant women with gestational diabetes mellitus (GDM). Twenty pregnant women with GDM and 20 gestational age-matched healthy pregnant women participated in the study. Maternal serum and cord blood adropin levels were assessed using an enzyme immunosorbent assay, at the time of birth. The relation of maternal serum and cord blood adropin levels with metabolic parameters were also assessed. The mean maternal and cord serum adropin in the GDM group were significantly lower than those of the control women (P=0.01 and P<0.001, respectively). Maternal serum adropin levels did not correlate with either fetal serum adropin levels or maternal metabolic values. The data suggest that low adropin levels may contribute to the underlying pathogenesis of GDM.

Low Circulating Adropin Concentrations with Obesity and Aging Correlate with Risk Factors for Metabolic Disease and Increase after Gastric Bypass Surgery in Humans

Mouse studies suggest that adropin, a peptide hormone, is required for metabolic homeostasis and prevention of obesity-associated insulin resistance. Whether obesity and insulin resistance are associated with low plasma adropin levels in humans is not known. Our objective was to investigate the hypothesis that obesity and indicators of insulin resistance are associated with low adropin levels and determine whether weight loss regulates adropin levels. Plasma was obtained from 85 female [age 21-67 yr, body mass index (BMI) 19.4-71.5 kg/m2] and 45 male (age 18-70 yr, BMI 19.1-62.6 kg/m2) volunteers for other clinical studies. The impact of Roux-en-Y gastric bypass was investigated in 19 obese females (BMI 37-65 kg/m2) using samples collected at baseline and 1-12 months after surgery. Adropin levels correlate negatively with BMI (r=-0.335, P<0.001) and age (r=-0.263, P=0.003). Age-adjusted adropin levels are higher in males [4.1 ng/ml; 95% confidence interval (CI)=3.6-4.6 ng/ml] than females (3.0 ng/ml; 95% CI=2.6-3.4 ng/ml) (P=0.001). In all subjects, lower age-adjusted adropin levels were observed in overweight (3.3 ng/ml; 95% CI=2.8-3.8 ng/ml, P=0.033) and obese (2.7 ng/ml; 95% CI=2.1-3.3 ng/ml, P=0.001) compared with healthy-weight subjects (4.1 ng/ml; 95% CI=3.6-4.5 ng/ml). This effect was gender specific (weight category×gender, P<0.001) and was observed in males only. Aging and diagnosis with two or more metabolic syndrome risk factors was associated with low adropin levels, irrespective of sex. Adropin concentrations increased after Roux-en-Y gastric bypass, peaking 3 months after surgery (P<0.01). Although males exhibit higher adropin levels that are reduced by obesity, aging and markers of insulin resistance are associated with low plasma adropin irrespective of sex.