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Their profile and abundance can be significantly changed by altering microbial composition because certain bacteria preferentially produce specific SCFA.
Conversely, early life sub-therapeutic antibiotic therapy increased adiposity and altered metabolism in mice, which was associated with an increase in SCFA produced by antibiotic-disrupted gut microbiota.
Body weights did not differ significantly between the two groups, both at birth and PND 49 (Supplemental Fig. To examine the effect of antibiotic treatment on glucose homeostasis, responses to oral glucose tolerance test (OGTT) were measured at PND 49.
The OGTT was used as an indicator of insulin sensitivity and pancreatic β-cell function.
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.
Newborn piglets were treated for two weeks with 30 mg/kg/day of amoxicillin, which is equivalent to the dose often prescribed to human infants.
It has been shown that sub-therapeutic antibiotic treatment of C57BL/6 J mice prenatally or at weaning resulted in a changed gut microbiome, increased adiposity and subsequently altered hepatic metabolism of lipid and cholesterol.
These findings support the potential role of early-life antibiotic-disrupted microbiota in mediating the development of childhood overweight/obesity, which strongly predicts chronic metabolic diseases such as diabetes in adulthood.