Abstract

Premature birth in conjunction with extremely low birth weight (<1 kg, ELBW) is associated with insulin resistance and increased cardiometabolic health risk compared to birth at full term with normal birth weight (NBW). However, little is known regarding the biologic mediators of these effects. Abdominal and ectopic lipid accumulation is linked to insulin resistance and metabolic dysfunction, yet whether ELBW survivors are predisposed to aberrant lipid deposition in adulthood is unknown. We used magnetic resonance imaging in a cohort of 16 NBW and 29 ELBW participants to determine if ELBW survivors have differences in pancreatic, hepatic, subcutaneous and visceral fat distribution compared to NBW participants. ELBW individuals had a higher proportion of liver and pancreatic fat compared to NBW subjects (P < 0.05). Abdominal subcutaneous fat, but not visceral fat, area was higher in ELBW survivors compared to NBW individuals. In multivariate analyses, tissue fat measures were most highly related to BMI and sex, but not preterm birth. This work highlights that fat deposition is enhanced in adults born preterm and suggests that ectopic fat accretion driven by their relatively greater adiposity may contribute to the higher rates of metabolic dysfunction seen in ELBW survivors.

Highlights

  • Birth weight and is thought to underlie observations that low birth weight individuals have more abdominal[11,12] or truncal[13,14] adipose tissue and increased metabolic health risk[15,16,17] as adults

  • As pancreatic tissue is sensitive to oxidative stress[28,29], and given that retinopathy of prematurity (ROP) was associated with 2 hour blood glucose in our full cohort[24], we were interested in further examining the potential relationship of ROP to pancreatic fat content and volume

  • While there was a tendency for ELBW survivors to have a greater body mass index (BMI) and to be classified as obese (BMI > 30 kg/m2), these did not reach statistical significance

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Summary

Introduction

Birth weight and is thought to underlie observations that low birth weight individuals have more abdominal[11,12] or truncal[13,14] adipose tissue and increased metabolic health risk[15,16,17] as adults. In adults, accumulated abdominal fat, within the visceral compartment, is associated with dysglycemia, dyslipidemia and insulin resistance[18,19] and is a major cardiovascular risk factor[20]. Whether extremely low birth weight and preterm birth are associated with alterations in abdominal, hepatic and pancreatic fat accumulation is not clear. As ELBW birth has been connected with higher adiposity and a greater prevalence of dysglycemia[24] and prematurity has been linked to type 2 diabetes[25,26], the characterization of different abdominal adipose depots may provide insight into the pathophysiological consequences of premature birth. We hypothesized that adults born extremely premature (ELBW) would have higher hepatic and pancreatic fat fractions and a greater area of subcutaneous and visceral fat and that those with ROP would have higher pancreatic fat and lower pancreatic volume

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