The Association Between Sleep Duration and Leptin, Ghrelin, and Adiponectin Among Children and Adolescents

Hagen, Erika W.; Starke, Samuel J.; Peppard, Paul E.

doi:10.1007/s40675-015-0025-9

Cited by 20 publications

(12 citation statements)

References 34 publications

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“…Importantly, future studies should be careful to control for potential nuisance or confounding variables (eg, time-of-day of blood draws, BMI, or adiposity) as hormone levels are highly sensitive to circadian effects and other difficult to control influences. See Hagan et al63 for a thorough discussion of these concerns and future directions.…”

Section: Proposed Mechanisms Impacting Energy Intakementioning

confidence: 99%

<p>Poor sleep and adolescent obesity risk: a narrative review of potential mechanisms</p>

Duraccio¹,

Krietsch²,

Chardon³

et al. 2019

AHMT

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Poor sleep is related to increased obesity risk in adolescents, though the mechanisms of this relationship are unclear. This paper presents a conceptual framework of the various pathways that have been proposed to drive this relationship. In this framework, increased food reward, emotional reactivity, decreased inhibitory control, metabolic disturbances, poorer dietary quality, and disrupted meal timings may increase the likelihood of increasing overall energy intake. This paper further notes how poor sleep increases sedentary behavior and screen time, which likely limits overall energy expenditure. The model posits that these mechanisms result in an imbalance of energy intake and expenditure following poor sleep, intensifying the overall risk for obesity. Increases in food reward processes, decreases in insulin sensitivity, disrupted meal timing, and increases in sedentary behavior seem to be the most compelling mechanisms linking poor sleep with increased obesity risk in adolescents. Future directions and clinical implications of this framework are discussed.

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Section: Proposed Mechanisms Impacting Energy Intakementioning

confidence: 99%

<p>Poor sleep and adolescent obesity risk: a narrative review of potential mechanisms</p>

Duraccio¹,

Krietsch²,

Chardon³

et al. 2019

AHMT

View full text Add to dashboard Cite

show abstract

“…Fourth, leptin has circadian variations in its secretion (Radić et al 2003) and is highly dependent on recent meal times and sleep (GarciaGarcia et al 2014;Hagen et al 2015). However, in our study, the information about recent sleep times and quality and food intake were not obtained.…”

Section: Discussionmentioning

confidence: 69%

Serum leptin level measured 48 h after delivery is associated with development of postpartum depressive symptoms: a 3-month follow-up study

Chen

Gao

Zhang

et al. 2016

Arch Womens Ment Health

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The aim of this study was to assess the possible relationship between leptin status and postpartum depressive symptoms using serum levels of leptin collected 24-48 h after delivery in a cohort Chinese sample. Women delivering a full-term, singleton, and live-born infant in the period from August 2013 to March 2014 were enrolled immediately postpartum. A blood sample was obtained 24-48 h after childbirth to test serum levels of leptin. Participation consisted of a visit in an obstetric unit at 3 months after delivery. The Edinburgh Postnatal Depression Scale (EPDS), completed at 3 months postpartum, was used to classify each woman's depression symptom severity. Demographic, obstetric, behavioral risk, mental health, and psychosocial factors were considered. Multiple logistic regression analyses were used to identify risk factors most predictive of postpartum depressive symptoms. During the study period, 407 individuals were included and completed follow-up. At 3 months, according to EPDS score, 53 women (13.0 %) were considered as postpartum depressive symptoms. Serum leptin levels in women with PPD were significantly greater than those in women without depressive symptoms (36.5 [IQR, 25.5-50.4] vs. 14.5 [IQR, 9.4-22.4] ng/ml, P < 0.0001). Based on the ROC curve, the optimal cutoff value of serum leptin levels as an indicator for predicting of depressive symptoms was projected to be 24.3 ng/mL, which yielded a sensitivity of 88.7 % and a specificity of 73.4 %, with the area under the curve at 0.867 (95 % CI, 0.817-0.916). In multivariate analysis, there was an increased risk of depressive symptoms associated with leptin levels ≥24.3 ng/ml (OR 8.234; 95 % CI, 3.572-15.876; P < 0.0001) after adjusting for possible confounders. Elevated serum leptin levels at delivery could eventually serve as a biological marker for the prediction of depressive symptoms. These associations were independent of other possible variables.

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“…Leptin resistance is associated with insulin resistance and abdominal obesity. Increased appetite is associated with altered levels of appetite regulatory hormones and thus, these hormones are identi ed as potential neuroendocrine markers and mediators in childhood obesity, as insisted by Hagen et al, (2015) [20].…”

Section: Discussionmentioning

confidence: 99%

Salivary Metabolic Hormones as Biomarkers of Childhood Obesity

Manohar¹,

Janardhanam²,

Ravichandran³

2021

Preprint

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PurposeObesity is a major threat to the health and development of children. While hormones in serum samples have been extensively investigated in childhood obesity research, our study attempts to explore salivary metabolic hormones as biomarkers of childhood obesity.MethodsObese (n=83) and non-obese (n=83) school children aged 6-11 years were recruited as cases and controls, respectively, for this case-control study. Salivary concentrations of the hormones, Ghrelin, Leptin, Adiponectin and Insulin were assessed and compared between obese and non-obese children to evaluate their role in childhood obesity.Results The mean ghrelin (1.69 ± 0.38) and adiponectin (95627.56 ± 64915.04) levels of the non-obese children were higher than the mean values of the obese, while the mean values of the hormones leptin (265.95 ± 83.16) and insulin (224.56 ± 184.86) were found to be higher among the obese. Higher levels of the hormones insulin (OR: 1.09; 95% CI: 1.05-1.12) and leptin (OR: 1.03; 95% CI: 1.02-1.04) posed higher risks for childhood obesity, followed by adiponectin, which was found to be lower among the cases (OR: 0.99; 95% CI: 0.99995-0.99998) which increased the risk of childhood obesity.ConclusionThis study demonstrates the efficacy of saliva as a promising non-invasive tool in childhood obesity research and highlights the significance of appetite regulatory hormones as biomarkers of childhood obesity.Level of evidenceLevel III, Case-control study.

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The Association Between Sleep Duration and Leptin, Ghrelin, and Adiponectin Among Children and Adolescents

Cited by 20 publications

References 34 publications

<p>Poor sleep and adolescent obesity risk: a narrative review of potential mechanisms</p>

<p>Poor sleep and adolescent obesity risk: a narrative review of potential mechanisms</p>

Serum leptin level measured 48 h after delivery is associated with development of postpartum depressive symptoms: a 3-month follow-up study

Salivary Metabolic Hormones as Biomarkers of Childhood Obesity

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