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Human milk composition is variable. The identification of influencing factors and interdependencies of components may help to understand the physiology of lactation. In this study, we analyzed linear trends in human milk composition over time, the variation across different European countries and the influence of maternal celiac disease. Within a multicenter European study exploring potential prevention of celiac disease in a high-risk population (PreventCD), 569 human milk samples were donated by women from five European countries between 16 and 163 days postpartum. Some 202 mothers provided two samples at different time points. Protein, carbohydrates, fat and fatty acids, insulin, adiponectin, and insulin-like growth factor II (IGF-II) were analyzed. Milk protein and n-6 long chain polyunsaturated fatty acids decreased during the first three months of lactation. Fatty acid composition was significantly influenced by the country of residence. IGF-II and adiponectin concentrations correlated with protein content (r = 0.24 and r = 0.35), and IGF-II also correlated with fat content (r = 0.36), suggesting a possible regulatory role of IGF in milk macronutrient synthesis. Regarding the impact of celiac disease, only the level in palmitic acid was influenced by this disease, suggesting that breastfeeding by celiac disease mothers should not be discouraged.

Background Adiponectin is an adipokine that is elevated in kidney disease. Evidence suggests that adiponectin exerts a direct effect on the podocyte and may play a role in the pathogenesis of proteinuria. The objectives of this study were to characterize serum and urine adiponectin levels over time in patients with focal segmental glomerulosclerosis (FSGS) and to evaluate the role of baseline levels of adiponectin as a predictor of clinical remission. Methods This was a study of 60 individuals, ages 3–38 years, with steroid-resistant FSGS enrolled in the FSGS clinical trial. Serial measurements of serum and urine adiponectin were obtained at baseline and 26 and 52 weeks. Results Participants were of mean age 19.4 ± 10.2 years (50 % male, 33 % black). Serum adiponectin (baseline mean 14.3 ± 6.6 μg/ml) and urine adiponectin:creatinine (Uadp/cr) (baseline mean 126.8 ± 178.9 μg/ml) directly correlated with proteinuria at all time points ( r  = 0.37–0.81; all p  < 0.05). Proteinuria, hypoalbuminemia, and hyperlipidemia were significant independent predictors of greater serum adiponectin and Uadp/cr in multivariate analysis. Lower tertiles of baseline serum adiponectin were associated with greater response to treatment at 52 weeks when adjusted for age, sex, body mass index (BMI) z score, and estimated glomerular filtration rate (eGFR) [odds ratio (OR) 0.48; 95 % confidence interval (CI) 0.26–0.91, p  = 0.023). For log Uadp/cr, the OR for remission was 0.43 (95 % CI 0.21–0.89, p  = 0.02) at 52 weeks. However, when baseline urine protein:creatinine was added to the models, the relationships were no longer significant. Conclusions Serum and urine adiponectin levels were directly associated with proteinuria and paralleled changes in proteinuria over time in children and young adults with FSGS. Although baseline adiponectin was lower in responders, response to treatment in patients with FSGS was not associated with serum and urine adiponectin levels but, rather, was related to proteinuria.

Adiponectin is the most abundant peptide secreted by adipocytes, whose reduction plays a central role in obesity-related diseases, including insulin resistance/type 2 diabetes and cardiovascular disease. In addition to adipocytes, other cell types, such as skeletal and cardiac myocytes and endothelial cells, can also produce this adipocytokine. Adiponectin effects are mediated by adiponectin receptors, which occur as two isoforms (AdipoR1 and AdipoR2). Adiponectin has direct actions in liver, skeletal muscle, and the vasculature.Adiponectin exists in the circulation as varying molecular weight forms, produced by multimerization. Several endoplasmic reticulum ER-associated proteins, including ER oxidoreductase 1-α (Ero1-α), ER resident protein 44 (ERp44), disulfide-bond A oxidoreductase-like protein (DsbA-L), and glucose-regulated protein 94 (GPR94), have recently been found to be involved in the assembly and secretion of higher-order adiponectin complexes. Recent data indicate that the high-molecular weight (HMW) complexes have the predominant action in metabolic tissues. Studies have shown that adiponectin administration in humans and rodents has insulin-sensitizing, anti-atherogenic, and anti-inflammatory effects, and, in certain settings, also decreases body weight. Therefore, adiponectin replacement therapy in humans may suggest potential versatile therapeutic targets in the treatment of obesity, insulin resistance/type 2 diabetes, and atherosclerosis. The current knowledge on regulation and function of adiponectin in obesity, insulin resistance, and cardiovascular disease is summarized in this review.

Adiponectin has antidiabetic properties, and patients with obesity, diabetes, and insulin resistance have low plasma adiponectin levels. However, although kidney disease is associated with insulin resistance, adiponectin is elevated in end-stage renal disease. Here we determine whether adipose tissue production of adiponectin is increased in renal disease in a case–control study of 36 patients with end-stage renal disease and 23 kidney donors. Blood and tissue samples were obtained at kidney transplantation and donation. The mean plasma adiponectin level was significantly increased to 15.6mg/ml in cases compared with 8.4mg/ml in controls. Plasma levels of the inflammatory adipokines tumor necrosis factor α, interleukin 6, and high-sensitivity C-reactive protein were significantly higher in cases compared with controls. Adiponectin mRNA and protein expression in visceral and subcutaneous fat were significantly higher in cases than controls, while adiponectin receptor-1 mRNA expression was significantly increased in peripheral blood cells, muscle, and adipose tissue in cases compared with controls. Thus, our study suggests that adipose tissue production of adiponectin contributes to the high plasma levels seen in end-stage renal disease.

Background/Objectives:Breastfeeding may protect against excessive weight gain during infancy. However, the breast milk components responsible for this effect are unknown. We examined the variation of three breast milk hormones (adiponectin, leptin and insulin) according to maternal characteristics and determined their association with infant body composition.Subjects/Methods:We studied a representative subset of 430 breastfed infants in the CHILD birth cohort. Breast milk was collected at 4 months postpartum and hormone concentrations were measured using the MesoScale Discovery System. Weight-for-length (WFL) and body mass index (BMI) z-scores were calculated according to the World Health Organization reference standard from infant anthropometrics measured at 4 months and 1 year. Maternal BMI and demographics were self-reported.Results:Breast milk hormone concentrations varied widely between mothers. The geometric mean (range) was 19.4 (3.7-74.4) ngml-1 for adiponectin; 361 (31-3968) pgml-1 for leptin; and 589 (53-5557) pgml-1 for insulin. Maternal BMI was positively correlated with breast milk insulin (r=+0.40, P<0.0001) and leptin (r=+0.71, P<0.0001), but not adiponectin (r=-0.02, P=0.68). Breast milk hormone concentrations were also associated with maternal ethnicity, parity and breastfeeding exclusivity at sample collection. Independent of these factors and maternal diabetes, smoking and breastfeeding duration, higher breast milk leptin was associated with lower infant WFL z-score at 4 months (β -0.67, 95% confidence interval (CI): -1.17, -0.17 for highest vs lowest quintile) and 1 year (β -0.58, 95% CI: -1.02, -0.14). Insulin showed a U-shaped association, with intermediate concentrations predicting the lowest infant WFL z-score at 4 months (β -0.51, 95% CI: -0.87, -0.15 for third vs lowest quintile) and 1 year (β -0.35, 95% CI: -0.66, -0.04). Similar results were seen with infant BMI. Breast milk adiponectin was not significantly associated with infant body composition.Conclusions:Breast milk hormone concentrations were associated with several fixed and modifiable maternal characteristics. Higher concentrations of leptin and intermediate concentrations of insulin were associated with lower infant WFL in the first year of life.

The aim of this study was to evaluate whether soluble frizzled-related protein 4 (sFRP4) concentration in the first trimester of pregnancy is individually, or in combination with Leptin, Chemerin and/or Adiponectin, associated with the development of gestational diabetes (GDM). In a nested case-control study, 50 women with GDM who spontaneously conceived and delivered a live-born infant were matched with a total of 100 uncomplicated singleton control pregnancies based on body mass index (± 2 kg/m2), gestational age at sampling (exact day) and maternal age (± 2 years). In serum samples, obtained between 70-90 days gestational age, sFRP4, Chemerin, Leptin and Adiponectin concentrations were determined by ELISA. Statistical comparisons were performed using univariate and multi-variate logistic regression analysis after logarithmic transformation of the concentrations. Discrimination of the models was assessed by the area under the curve (AUC). First trimester sFRP4 concentrations were significantly increased in GDM cases (2.04 vs 1.93 ng/ml; p<0.05), just as Chemerin (3.19 vs 3.15 ng/ml; p<0.05) and Leptin (1.44 vs 1.32 ng/ml; p<0.01). Adiponectin concentrations were significantly decreased (2.83 vs 2.94 ng/ml; p<0.01) in GDM cases. Further analysis only showed a weak, though significant, correlation of sFRP4 with Chemerin (R2 = 0.124; p<0.001) and Leptin (R2 = 0.145; p<0.001), and Chemerin with Leptin (R2 = 0.282; p<0.001) in the control group. In a multivariate logistic regression model of these four markers, only Adiponectin showed to be significantly associated with GDM (odds ratio 0.12, 95%CI 0.02-0.68). The AUC of this model was 0.699 (95%CI 0.605-0.793). In the first trimester of pregnancy, a multi-marker model with sFRP4, Leptin, Chemerin and Adiponectin is associated with the development of GDM. Therefore, this panel seems to be an interesting candidate to further evaluate for prediction of GDM in a prospective study.

Background/Objectives: Appetite-regulating hormones are bioactive components of human milk. We tested the associations of leptin and adiponectin with infant growth and eating behaviors to age 6 months. Methods: In a cohort of 70 healthy, full-term infants and their mothers, human milk adiponectin and leptin were assayed at age 2 months (m). At infant ages 2, 4, and 6 m, infant anthropometry was obtained, mothers reported feeding frequency, duration, and breastfeeding intensity and completed the Baby Eating Behavior Questionnaire (Enjoyment of Food, Food Responsiveness, and General Appetite), and infant sucking vigor using an artificial nipple (burst duration and sucking frequency) was measured. Mothers reported demographics, gestational diabetes and pre-pregnancy body mass index (BMI), gestational age, and infant birthweight. Multivariate models evaluated predictors of leptin and adiponectin, and associations of leptin and adiponectin with infant growth and eating behaviors. Results: Human milk leptin was predicted by maternal BMI (β = 0.02) and breastfeeding intensity (β = −0.32). Regarding infant growth, infant weight-for-age and weight-for-length z-scores at 6 m were predicted by leptin (β = 0.91 and β = 1.22, respectively) and adiponectin (β = 0.01 and β = 0.01, respectively). Regarding infant eating behaviors, feeding duration at 2 m and feeding frequency at 4 m were predicted by adiponectin (β = 0.03 and β = −0.02, respectively). Conclusions: Human milk leptin and adiponectin may contribute to weight gain in early infancy, but the effect does not appear to be mediated substantially by infant eating behaviors. Further investigation into the metabolic programming of early infant weight gain is warranted.

Background/objectivesAdiponectin represents an important link between adipose tissue dysfunction and cardiometabolic risk in obesity; however, there is a lack of data on the effects of adiponectin-related genetic variations and gene-diet interactions on metabolic disorders in children. We aimed to investigate possible interactions between adiponectin-related genetic variants and habitual dietary patterns on metabolic health among children with normal weight versus overweight/obesity, and whether these effects in childhood longitudinally contribute to metabolic risk at follow-up.Subjects/methodsIn total, 3,317 Chinese children aged 6–18 at baseline and 339 participants at 10-year follow-up from the Beijing Child and Adolescent Metabolic Syndrome study cohort were included. Baseline lifestyle factors, plasma adiponectin levels, and six adiponectin-related genetic variants resulting from GWAS in East Asians (loci in/near ADIPOQ, CDH13, WDR11FGF, CMIP, and PEPD) were assessed for their associations with the metabolic disorders. Being metabolically unhealthy was defined by exhibiting any metabolic syndrome component.ResultsAmong the six loci, ADIPOQ rs6773957 (OR 1.26, 95% CI:1.07–1.47, P = 0.004) and adiponectin receptor CDH13 rs4783244 (0.82, 0.69–0.96, P = 0.017) were correlated with metabolic risks independent of lifestyle factors in normal-weight children, but the associations were less obvious in those with overweight/obesity. A significant interaction between rs6773957 and diet (Pinteraction = 0.004) for metabolic health was observed in normal-weight children. The adiponectin-decreasing allele of rs6773957 was associated with greater metabolic risks in individuals with unfavorable diet patterns (P < 0.001), but not in those with healthy patterns (P > 0.1). A similar interaction effect was observed using longitudinal data (Pinteraction = 0.029).ConclusionsThese findings highlight a novel gene-diet interaction on the susceptibility to cardiometabolic disorders, which has a long-term impact from childhood onward, particularly in those with normal weight. Personalized dietary advice in these individuals may be recommended as an early possible therapeutic measure to improve metabolic health.

Childhood obesity and dental caries are among the most prevalent chronic conditions, but their biological interplay remains poorly understood. This study aimed to investigate the associations between childhood obesity, salivary adiponectin levels, and dental caries. In this comparative cross-sectional study, 120 children aged 7–12 years were recruited and classified into two groups: Group 1 (body mass index (BMI) percentile < 85; underweight or normal-weight, n  = 60) and Group 2 (BMI percentile ≥ 85; overweight or obese, n  = 60). The dental caries experience was recorded using WHO criteria for primary (dmft) and permanent (DMFT) scores. Unstimulated whole saliva samples were collected, processed, and analyzed for adiponectin concentrations using an ELISA assay. Dietary behaviors (sugar intake, consumption of acidic or pickled foods, and dairy intake) and oral hygiene practices were assessed. Student t-test, Mann-Whitney test, Spearman’s correlations, and multivariable linear regression were conducted. Overweight/obese children exhibited significantly lower salivary adiponectin levels (2.49 ± 0.39 vs. 2.84 ± 0.43 ng/mL; P  < 0.001) compared to their normal-weight peers and significantly lower total dental caries scores compared with normal-weight peers (5.05 ± 2.46 vs. 7.37 ± 3.25; P  < 0.001). Salivary adiponectin was inversely correlated with BMI (Spearman’s correlation coefficient (ρ) = −0.39) and dental caries (ρ = 0.14). Obese children showed lower salivary adiponectin levels but unexpectedly had lower dental caries scores than their normal-weight peers. These findings reinforce the multifactorial nature of pediatric oral health and highlight the need to integrate metabolic, behavioral, and environmental factors into preventive strategies.

Periodontitis is an inflammatory disease caused by pathogenic microorganisms, such as Porphyromonas gingivalis, and characterized by the destruction of the periodontium. Obese individuals have an increased risk for periodontitis and show decreased serum levels of adiponectin. This in-vitro study was established to examine whether adiponectin modulates critical effects of lipopolysaccharide (LPS) from P. gingivalis on oral epithelial cells (OECs). The presence of adiponectin and its receptors in human gingival tissue samples and OECs was analyzed by immunohistochemistry and PCR. Furthermore, OECs were treated with LPS and/or adiponectin for up to 72 h, and the gene expression and protein synthesis of pro- and anti-inflammatory mediators, matrix metalloproteinases (MMPs) and growth factors were analyzed by real-time PCR and ELISA. Additionally, cell proliferation, differentiation and in-vitro wound healing were studied. The nuclear translocation of NFκB was investigated by immunofluorescence. Gingival tissue sections showed a strong synthesis of adiponectin and its receptors in the epithelial layer. In cell cultures, LPS induced a significant up-regulation of interleukin (IL) 1β, IL6, IL8, MMP1 and MMP3. Adiponectin abrogated significantly the stimulatory effects of LPS on these molecules. Similarly, adiponectin inhibited significantly the LPS-induced decrease in cell viability and increase in cell proliferation and differentiation. Adiponectin led to a time-dependent induction of the anti-inflammatory mediators IL10 and heme oxygenase 1, and blocked the LPS-stimulated NFκB nuclear translocation. Adiponectin may counteract critical actions of P. gingivalis on oral epithelial cells. Low levels of adiponectin, as observed in obese individuals, may increase the risk for periodontal inflammation and destruction.