Abstract
Childhood antibiotic exposure has been recently linked with increased risk of metabolic disease later in life. A better understanding of this association would potentially provide strategies to reduce the childhood chronic disease epidemic. Therefore, we explored the underlying mechanisms using a swine model that better mimics human infants than rodents, and demonstrated that early life antibiotic exposure affects glucose metabolism 5 weeks after antibiotic withdrawal, which was associated with changes in pancreatic development. Antibiotics exerted a transient impact on postnatal gut microbiota colonization and microbial metabolite production, yet changes in the expression of key genes involved in short-chain fatty acid signaling and pancreatic development were detected in later life. These findings suggest a programming effect of early life antibiotic exposure that merits further investigation.
Highlights
(GPR) 41 and GPR43 have been reported to be expressed in various organs and implicated as mediators of host energy metabolism using knockout mouse models[31,32]
In response to glucose challenge, the ANTI group had higher glucose excursion during oral glucose tolerance test (OGTT) compared to control groups (CON) with no effect of litter (Fig. 1A, P < 0.05)
As antibiotics will continue to be a key tool required to support infant health, it is crucial to understand how early life antibiotics contribute to chronic diseases
Summary
(GPR) 41 and GPR43 have been reported to be expressed in various organs and implicated as mediators of host energy metabolism using knockout mouse models[31,32] They exert direct effects on pancreatic β-cells by modulating insulin secretion and cell proliferation[33,34,35,36]. Amoxicillin, a broad-spectrum antibiotic commonly prescribed to infants, was administered from birth to postnatal day (PND) 14 at a therapeutic dose By adopting this well-controlled animal model that resembles traits of human infants, we aimed to 1) investigate the effects of antibiotic exposure before weaning (day 0 to 14) on metabolic outcomes later in life, 2) examine the impact of antibiotic exposure on pancreatic development, and 3) determine antibiotic-induced changes in microbial composition and metabolism in order to explore the possible mechanisms of early-life antibiotic exposure and metabolic outcomes later in life
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