Dataset Information

Leptin Levels are Associated with Subclinical Cardiac Dysfunction in Obese Adolescents.

ABSTRACT: Purpose:The purposes of this study were to use speckle tracking echocardiography to confirm the influence of obesity on cardiac functions and to assess their relationships with leptin and uric acid levels in obese adolescents. Methods:Eighty-one participants aged 16-19 years were recruited and classified as either non-obese (n = 30) or obese (n = 51). Global longitudinal strain (GLS), leptin and uric acid levels for each group were assessed and compared. The data from obese participants were then compared based on their leptin levels and analyzed for correlation using regression analysis. Results:The obese group had significantly lower absolute GLS compared to the non-obese group (19.10 ± 0.30 versus 21.10 ± 0.30%, p < 0.001). In obese group, subclinical cardiac dysfunction was worse in the hyperleptinemic group than that of the normoleptinemic group (p = 0.03). Multivariate regression analysis showed that leptin and triglyceride levels were negatively associated with absolute GLS. Leptin could predict the absolute GLS with ? = -0.35 (p = 0.02). Conclusion:Subclinical left ventricular systolic dysfunction was found in obese adolescents, while GLS was worse in the hyperleptinemic subjects. Leptin, but not uric acid, levels were associated with a worsening of GLS.

SUBMITTER: Imerbtham T

PROVIDER: S-EPMC7108875 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Leptin Levels are Associated with Subclinical Cardiac Dysfunction in Obese Adolescents.

Imerbtham Thamonwan T Thitiwuthikiat Piyanuch P Jongjitwimol Jirapas J Nuamchit Teonchit T Yingchoncharoen Teerapat T Siriwittayawan Duangduan D

Diabetes, metabolic syndrome and obesity : targets and therapy 20200327

<h4>Purpose</h4>The purposes of this study were to use speckle tracking echocardiography to confirm the influence of obesity on cardiac functions and to assess their relationships with leptin and uric acid levels in obese adolescents.<h4>Methods</h4>Eighty-one participants aged 16-19 years were recruited and classified as either non-obese (n = 30) or obese (n = 51). Global longitudinal strain (GLS), leptin and uric acid levels for each group were assessed and compared. The data from obese partic ...[more]

PMID: 32273744

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Project description:Background/objectivesAdiponectin concentrations are low in obese pregnant women. Restoring normal adiponectin concentrations by infusion in obese pregnant mice prevents placental dysfunction, foetal overgrowth and metabolic syndrome in the offspring. We hypothesised that normalising maternal adiponectin in obese late pregnant dams prevents cardiac dysfunction in the adult offspring.Subjects/methodsPregnant female mice with diet-induced obesity were infused with adiponectin (0.62 μg g-1 day-1, n = 24) or saline (n = 22) over days 14.5-18.5 of pregnancy (term = day 19.5). Control dams ate standard chow and received saline (n = 22). Offspring were studied at 3 and 6 months of age.ResultsMaternal obesity impaired ventricular diastolic function, increased cardiomyocyte cross-sectional area and upregulated cardiac brain natriuretic peptide (Nppb) and α-skeletal actin (Acta1) gene expression in adult male offspring, compared to control offspring. In adult female offspring, maternal obesity increased Nppb expression, decreased end-diastolic volume and caused age-dependent diastolic dysfunction but not cardiomyocyte hypertrophy. Maternal obesity also activated cardiac Akt and mechanistic target of rapamycin (mTOR) signalling in male, but not in female, offspring and inhibited cardiac extracellular signal-regulated kinase 1/2 (ERK1/2) in both sexes. Normalising maternal circulating adiponectin concentrations by infusing obese dams with adiponectin prevented offspring diastolic dysfunction and ventricular dilation and normalised cardiac Akt-mTOR signalling irrespective of sex. Maternal adiponectin infusion also reduced cardiac Nppb expression and increased ERK1/2 signalling in offspring of obese dams. Adiponectin infusion did not prevent cardiomyocyte hypertrophy but reduced ventricular wall thickness in male offspring and increased collagen content in female offspring of obese dams, compared to controls.ConclusionsLow maternal adiponectin levels in obese mice in late pregnancy are mechanistically linked to in utero programming of cardiac dysfunction in their offspring. Interventions enhancing endogenous adiponectin secretion or signalling in obese pregnant women could prevent the development of cardiac dysfunction in their children.

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Dataset Information

Leptin Levels are Associated with Subclinical Cardiac Dysfunction in Obese Adolescents.

Publications

Leptin Levels are Associated with Subclinical Cardiac Dysfunction in Obese Adolescents.

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