Large birth size, infancy growth pattern, insulin resistance and β-cell function.

Area of Science:

• Pediatric endocrinology
• Metabolic health
• Developmental origins of health and disease (DOHaD)

Background:

• Large birth size is a known risk factor for adult type 2 diabetes.
• The impact of large birth size on infant glucose metabolism and beta-cell function remains understudied.
• Understanding early-life metabolic programming is crucial for preventing future chronic diseases.

Purpose of the Study:

• To investigate the association between large-for-gestational-age (LGA) birth size and insulin resistance and beta-cell function in infancy.
• To identify determinants of insulin resistance and beta-cell function in infancy, focusing on growth patterns.

Main Methods:

• A nested matched case-control study within the Canadian 3D birth cohort.
• Comparison of 70 LGA infants with 140 optimal-for-gestational-age (OGA) control infants.
• Assessment of homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-β) at 2 years of age.

Main Results:

• No significant differences in HOMA-IR or HOMA-β were observed between LGA and OGA infants.
• Decelerated length growth in early infancy was linked to decreased HOMA-β.
• Accelerated weight and length growth in mid-infancy were associated with increased HOMA-IR and HOMA-β.
• Decelerated length growth in late infancy was associated with decreased HOMA-IR and HOMA-β.

Conclusions:

• Large birth size itself is not associated with altered insulin resistance or beta-cell function in infancy.
• Infant growth trajectories, particularly decelerated length growth, play a significant role in modulating beta-cell function.
• Infancy growth patterns may be more critical than birth size in programming long-term metabolic health.