Late prematurity and adiposity in adolescents: Evidence from “Children of 1997” birth cohort

Hui, Lucas Chi Kwong; Lam, Hugh Simon; Leung, Gabriel M.; Schooling, CM

doi:10.1002/oby.21267

Cited by 20 publications

(21 citation statements)

References 43 publications

(58 reference statements)

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“…Specifically, we identified increased body mass, increased RV mass, and a decreased RV ejection fraction in rats 1 year after postnatal Hx, consistent with clinical studies of adults born prematurely (10,31). Our model was also characterized by chronic RV pressure overload due to hypertensive pulmonary vascular disease, as well as intrinsic RV dysfunction noted by the inability to maintain contractility in the setting of increased afterload.…”

Section: Discussionsupporting

confidence: 83%

Postnatal Hyperoxia Exposure Durably Impairs Right Ventricular Function and Mitochondrial Biogenesis

Goss

Kumari

Tetri³

et al. 2017

Am J Respir Cell Mol Biol

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Prematurity complicates 12% of births, and young adults with a history of prematurity are at risk to develop right ventricular (RV) hypertrophy and impairment. The long-term risk for pulmonary vascular disease, as well as mechanisms of RV dysfunction and ventricular-vascular uncoupling after prematurity, remain poorly defined. Using an established model of prematurity-related lung disease, pups from timed-pregnant Sprague Dawley rats were randomized to normoxia or hyperoxia (fraction of inspired oxygen, 0.85) exposure for the first 14 days of life. After aging to 1 year in standard conditions, rats underwent hemodynamic assessment followed by tissue harvest for biochemical and histological evaluation. Aged hyperoxia-exposed rats developed significantly greater RV hypertrophy, associated with a 40% increase in RV systolic pressures. Although cardiac index was similar, hyperoxia-exposed rats demonstrated a reduced RV ejection fraction and significant RV-pulmonary vascular uncoupling. Hyperoxia-exposed RV cardiomyocytes demonstrated evidence of mitochondrial dysregulation and mitochondrial DNA damage, suggesting potential mitochondrial dysfunction as a cause of RV dysfunction. Aged rats exposed to postnatal hyperoxia recapitulate many features of young adults born prematurely, including increased RV hypertrophy and decreased RV ejection fraction. Our data suggest that postnatal hyperoxia exposure results in mitochondrial dysregulation that persists into adulthood with eventual RV dysfunction. Further evaluation of long-term mitochondrial function is warranted in both animal models of premature lung disease and in human adults who were born preterm.Keywords: pulmonary hypertension; mitochondrial biogenesis; prematurity Clinical RelevanceThis study used a common rat model of chronic lung disease of prematurity aged to 1 year, similar to young adulthood in humans, to study the long-term effects on the right ventricle (RV) and pulmonary vasculature. These rats demonstrated significant RV hypertrophy and dysfunction, similar to human studies, and newly identified significant chronic pulmonary hypertension. In addition, there was evidence of mitochondrial dysregulation in the RV, which may provide new insight into the pathogenesis of RV dysfunction in human adults born prematurely.

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Section: Discussionsupporting

confidence: 83%

Postnatal Hyperoxia Exposure Durably Impairs Right Ventricular Function and Mitochondrial Biogenesis

Goss

Kumari

Tetri³

et al. 2017

Am J Respir Cell Mol Biol

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“…Huke 2013 and Willemsen 2008 found that preterm infants had a lower risk of central obesity than term infants in TAAT and trunk fat assessments. However, no significances were found in % IAAT and ratio of trunk fat/total fat [44,47] [48]. (Table 2).…”

Section: Plos Onementioning

confidence: 90%

Accelerated weight gain, prematurity, and the risk of childhood obesity: A meta-analysis and systematic review

Ou‐Yang¹,

Sun²,

Liebowitz³

et al. 2020

PLoS ONE

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The purpose of this systematic review and meta-analysis of the literature was to analyze and evaluate the impact of prematurity and accelerated weight gain on the risk of childhood and adolescent obesity. CINAHL, Embase, PubMed, and Web of Science databases were searched until December 2019 which yielded 19 studies with a total of 169,439 children enrolled were systematically reviewed. The results revealed that preterm infants had a greater likelihood of childhood obesity (defined as BMI �95 th percentile for age-sex), than term infants (OR = 1.19, 95% CI [1.13, 1.26]). However, no difference of childhood obesity was found between "small for gestational age"(SGA) and "appropriate for gestational age"(AGA) among preterms. Accelerated weight gain (defined as weight gain velocity during first two years after birth) significantly increased the likelihood of subsequent childhood obesity among preterms (aOR = 1.87, 95% CI [1.57, 2.231]). In conclusion, accelerated weight gain at infancy among preterm children may be a critical contributor to obesity in later life. Establishing optimal growth trajectories and timely referral to health care providers may be of clinical importance.

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“…The meta-analysis demonstrated that there was no difference in BMI between those born preterm and at term (MD, 0.13 kg/m 2 , 95% CI: −0.40 to 0.14 Supplementary Fig. 1) 16 could not be included in the meta-analysis 14,35,57,58 . Of these, one showed that obesity was more prevalent among those born preterm (Supplementary Table 1) 14 .…”

Section: Risk Factor Profile Between Those Born Preterm Compared To Termmentioning

confidence: 99%

Cardiovascular risk factors in those born preterm – systematic review and meta-analysis

Condon

Collett

Lassi

2020

J Dev Orig Health Dis

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Emerging evidence demonstrates a link between preterm birth (PTB) and later life cardiovascular disease (CVD). We conducted a systematic review and meta-analysis to compare conventional CVD risk factors between those born preterm and at term. PubMed, CINAHL, SCOPUS, and EMBASE databases were searched. The review protocol is registered in PROSPERO (CRD42018095005). CVD risk factors including systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index, lipid profile, blood glucose, and fasting insulin among those born preterm (<37 weeks’ gestation) were compared with those born at term (≥37 weeks’ gestation). Subgroup analyses based on gender, age, gestational at birth (<32 weeks’ gestation and <28 weeks’ gestation), and PTB associated with small for gestational age or average for gestational age were also performed. Fifty-six studies provided data on 308,987 individuals. Being born preterm was associated with 3.26 mmHg (95% confidence interval [CI] 2.08 to 4.44) higher mean SBP and 1.32 mmHg (95% CI: 0.61 to 2.04) higher mean DBP compared to being born at term. Subgroup analyses demonstrated that SBP was higher among (a) preterm compared to term groups from early adolescence until adulthood; (b) females born preterm but not among males born preterm compared to term controls; and (c) those born at <32 weeks or <28 weeks compared to term. Our meta-analyses demonstrate higher SBP and DBP among those born preterm compared to term. The difference in SBP is evident from early adolescence until adulthood.

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Late prematurity and adiposity in adolescents: Evidence from “Children of 1997” birth cohort

Abstract: Late prematurity was associated with higher BMI and waist ratios in adolescence, but only the association with BMI was mediated by infant weight gain, suggesting vulnerability to metabolic risk in late premature births may arise through multiple pathways.

Cited by 20 publications

References 43 publications

Postnatal Hyperoxia Exposure Durably Impairs Right Ventricular Function and Mitochondrial Biogenesis

Postnatal Hyperoxia Exposure Durably Impairs Right Ventricular Function and Mitochondrial Biogenesis

Accelerated weight gain, prematurity, and the risk of childhood obesity: A meta-analysis and systematic review

Cardiovascular risk factors in those born preterm – systematic review and meta-analysis

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