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The structural alteration of gut microbiota in low-birth-weight mice undergoing accelerated postnatal growth

Jingjing Wang1,2, Huang Tang2, Xiaoxin Wang2

  • 1Ministry of Education Key Laboratory for Systems Biomedicine, Shanghai Centre for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, PR China.

Scientific Reports
|June 10, 2016
PubMed

Insights

Infant gut microbiome disruption from antibiotics increases adult obesity risk, especially in low birth-weight mice. Early life gut dysbiosis in low birth-weight mice leads to metabolic syndrome, unlike normal birth-weight mice.

Area of Science:

  • Microbiology
  • Metabolic Syndrome Research
  • Developmental Biology

Background:

  • Accelerated postnatal growth increases metabolic syndrome risk in low birth-weight humans, but mechanisms are unclear.
  • Antibiotic-induced disruption of the infant gut microbiota can lead to adult adiposity in mice.
  • Low birth-weight and accelerated growth interact to influence metabolic health outcomes.

Purpose of the Study:

  • To investigate the impact of low birth-weight and accelerated postnatal growth on gut microbiota and metabolic health in mice.
  • To elucidate the mechanisms linking early-life factors to adult metabolic syndrome.
  • To compare the gut microbiome composition and function in low birth-weight mice with accelerated growth versus normal birth-weight mice.

Main Methods:

  • Establishment of three mouse groups: low birth-weight with accelerated growth (LB+A), normal birth-weight with accelerated growth (NB+A), and normal birth-weight controls (NB).
  • Analysis of gut microbiota composition and fermentation activity in infancy and adulthood (24 weeks).
  • Assessment of body fat content and glucose tolerance in adulthood.

Main Results:

  • Low birth-weight mice with accelerated growth (LB+A) exhibited excessive adiposity and glucose intolerance in adulthood.
  • LB+A mice showed increased levels of obesity-associated bacteria (e.g., Desulfovibrionaceae) and disrupted fermentation activity in infancy.
  • Normal birth-weight mice with accelerated growth (NB+A) maintained normal body fat and glucose tolerance, with distinct gut microbiota profiles compared to LB+A mice.

Conclusions:

  • Early-life gut dysbiosis in low birth-weight mice with accelerated growth is a key factor contributing to adult metabolic syndrome.
  • The composition and function of the infant gut microbiome play a critical role in long-term metabolic health.
  • Interventions targeting the infant gut microbiome may be crucial for preventing metabolic disorders in at-risk populations.

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