Leptin trajectories from birth to mid-childhood and cardio-metabolic health in early adolescence

Li, Lingjun; Rifas‐Shiman, Sheryl L.; Aris, Izzuddin M.; Mantzoros, Christos S.; Hivert, Marie‐France; Oken, Emily

doi:10.1016/j.metabol.2018.11.003

Cited by 27 publications

(23 citation statements)

References 50 publications

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“…Interestingly, it was previously reported that neonatal leptin levels might be associated with growth trajectories and childhood BMI [48,49], but other studies showed that both lower and higher leptin levels are associated with weight gain [50][51][52][53][54][55][56][57]. Nevertheless, although the association between neonatal leptinemia and childhood growth and adiposity (e.g., weight gain, BMI, and/or obesity) has been previously reported [48][49][50][51][52][53][54][55][56][57][58], the impacts of altered neonatal leptin levels on fat distribution during childhood still need to be clearly defined.…”

Section: Discussionmentioning

confidence: 96%

Mediation Analysis Supports a Causal Relationship between Maternal Hyperglycemia and Placental DNA Methylation Variations at the Leptin Gene Locus and Cord Blood Leptin Levels

Gagné-Ouellet

Breton

Thibeault

et al. 2020

IJMS

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Changes in fetal DNA methylation (DNAm) of the leptin (LEP) gene have been associated with exposure to maternal hyperglycemia, but their links with childhood obesity risk are still unclear. We investigated the association between maternal hyperglycemia, placental LEP DNAm (25 5′-C-phosphate-G-3′ (CpG) sites), neonatal leptinemia, and adiposity (i.e., BMI and skinfold thickness (ST) (subscapular (SS) + triceps (TR) skinfold measures, and the ratio of SS:TR) at 3-years-old, in 259 mother–child dyads, from Gen3G birth cohort. We conducted multivariate linear analyses adjusted for gestational age at birth, sex of the child, age at follow-up, and cellular heterogeneity. We assessed the causal role of DNAm in the association between maternal glycemia and childhood outcomes, using mediation analysis. We found three CpGs associated with neonatal leptinemia (p ≤ 0.002). Of these, cg05136031 and cg15758240 were also associated with BMI (β = −2.69, p = 0.05) and fat distribution (β = −0.581, p = 0.05) at 3-years-old, respectively. Maternal glycemia was associated with DNAm at cg15758240 (β = −0.01, p = 0.04) and neonatal leptinemia (β = 0.19, p = 0.004). DNAm levels at cg15758240 mediates 0.8% of the association between maternal glycemia and neonatal leptinemia (p < 0.001). Our results support that DNAm regulation of the leptin pathway in response to maternal glycemia might be involved in programming adiposity in childhood.

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Section: Discussionmentioning

confidence: 96%

Mediation Analysis Supports a Causal Relationship between Maternal Hyperglycemia and Placental DNA Methylation Variations at the Leptin Gene Locus and Cord Blood Leptin Levels

Gagné-Ouellet

Breton

Thibeault

et al. 2020

IJMS

Self Cite

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“…There is a high degree of tracking for BMD [53] and it was therefore reasonable to assume that this was the case for the bone-active substances and BTMs, which was also found. To our knowledge there are only a few reports on tracking of individual bone related substances [54, 55], but none where these substances and the BTMs are evaluated together. This high degree of tracking makes it likely that our cross-sectional results are valid for bone metabolism over time and not only represent findings from a single measurement.…”

Section: Discussionmentioning

confidence: 99%

Smoking and other determinants of bone turnover

et al. 2019

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The balance between bone resorption and formation may be assessed by measurement of bone turnover markers (BTMs), like carboxyl-terminal cross-linked telopeptide of type 1 collagen (CTX-1) and procollagen type 1 amino-terminal propeptide (P1NP). Smoking has been shown to influence bone turnover and to reduce bone mass density (BMD), the exact mechanism for this is, however, not settled. In this post-hoc study including 406 subjects (mean age 51.9 years), we aimed to study the impact of smoking on bone turnover. Moreover, we wanted to assess the inter-correlation between substances regulating bone metabolism and BTMs, as well as tracking over time. BMD measurements and serum analyses of CTX-1, P1NP, osteoprotegerin (OPG), receptor activator of nuclear factor ĸB ligand (RANKL), Dickkopf-1 (DKK1), sclerostin, tumor necrosis factor-α (TNF-α), and leptin were performed. Repeated serum measurements were made in 195 subjects after four months. Adjustments were made for sex, age, body mass index (BMI), smoking status, insulin resistance, serum calcium, parathyroid hormone, 25-hydroxyvitamin D and creatinine. Smokers had higher levels of DKK1 and OPG, and lower levels of RANKL, as reflected in lower BTMs and BMD compared to non-smokers. There were strong and predominantly positive inter-correlations between BTMs and the other substances, and there was a high degree of tracking with Spearman’s rho from 0.72 to 0.92 (P < 0.001) between measurements four months apart. In conclusion, smokers exhibited higher levels of DKK1 and OPG and a lower bone turnover than did non-smokers. The strong inter-correlations between the serum parameters illustrate the coupling between bone resorption and formation and crosstalk between cells.

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“…On the other hand, leptin can impel the hepatic stellate cell activation and liver fibrosis, control the energy balance, and suppress appetite [91]. Increased levels of leptin were found in subjects with increased body fat and cardiometabolic disorders [92]. Authors noted in a cross-sectional study that NAFLD patients have lower adiponectin levels, higher serum leptin levels, and higher leptin-to-adiponectin (L/A) ratio [93].…”

Section: Adipokinesmentioning

confidence: 99%

The Intricate Relationship between Type 2 Diabetes Mellitus (T2DM), Insulin Resistance (IR), and Nonalcoholic Fatty Liver Disease (NAFLD)

Tănase

Gosav

Costea

et al. 2020

Journal of Diabetes Research

320

180

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Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) remain as one of the most global problematic metabolic diseases with rapidly increasing prevalence and incidence. Epidemiological studies noted that T2DM patients have by two-fold increase to develop NAFLD, and vice versa. This complex and intricate association is supported and mediated by insulin resistance (IR). In this review, we discuss the NAFLD immunopathogenesis, connection with IR and T2DM, the role of screening and noninvasive tools, and mostly the impact of the current antidiabetic drugs on steatosis liver and new potential therapeutic targets.

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Leptin trajectories from birth to mid-childhood and cardio-metabolic health in early adolescence

Cited by 27 publications

References 50 publications

Mediation Analysis Supports a Causal Relationship between Maternal Hyperglycemia and Placental DNA Methylation Variations at the Leptin Gene Locus and Cord Blood Leptin Levels

Mediation Analysis Supports a Causal Relationship between Maternal Hyperglycemia and Placental DNA Methylation Variations at the Leptin Gene Locus and Cord Blood Leptin Levels

Smoking and other determinants of bone turnover

The Intricate Relationship between Type 2 Diabetes Mellitus (T2DM), Insulin Resistance (IR), and Nonalcoholic Fatty Liver Disease (NAFLD)

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