SGA-born adults with postnatal catch-up have a persistently unfavourable metabolic health profile and increased adiposity at age 32 years

Abstract

Abstract Background Catch-up in weight-for-length in the first year of life results in more insulin resistance, an adverse lipid profile and more fat mass (FM) in 21-year-old adults born small for gestational age (SGA-CU) compared to peers born SGA without catch-up and those born appropriate for gestational age (AGA). The aim of present study was to investigate if the adverse metabolic health profile in the SGA-CU group would worsen or remain stable over the years and to determine the cardiometabolic health at 32 years between the SGA and AGA groups. Methods We longitudinally investigated 287 adults, 170 SGA with catch-up growth (SGA-CU) or persistent short stature (SGA-S) and 117 AGA at ages 21 and 32 years. Insulin sensitivity (Si) and β-cell function were measured by frequently sampled i.v. glucose tolerance test, body composition by dual-energy X-ray absorptiometry (DXA) scan, and abdominal adipose tissue and liver fat fraction by MRI scan. Also, fasting serum lipid levels and blood pressure were measured. Results At age 32 years, SGA-CU had lower Si than AGA (P  = 0.030), while SGA-S had similar Si than AGA. FM and trunk fat were higher in SGA-CU than AGA (P  = 0.033, P  = 0.024, respectively), while SGA-S had lower lean body mass than SGA-CU and AGA (P  = 0.001 and P  < 0.001, respectively). SGA-CU had significantly higher levels of adverse lipids than AGA. Beta-cell function, visceral fat, liver fat fraction and blood pressure were similar in all groups. Metabolic health parameters in SGA-CU and SGA-S did not worsen compared to AGA during 11 years of follow-up. Gain in weight SDS from birth to age 32 years was associated with a higher risk of developing metabolic syndrome at age 32 years. Conclusion At age 32 years, SGA-CU adults had insulin resistance, higher FM with central adiposity and an adverse lipid profile. Postnatal catch-up growth increases the cardiometabolic risk; therefore, accelerated gain in weight should be prevented in SGA-born children.