Abstract
Obesity is a major public health problem that continues to be one of the leading risk factors for premature death. Early life is a critical period of time when the gut microbiota and host metabolism are developing in tandem and significantly contribute to long-term health outcomes. Dysbiosis of the gut microbiota, particularly in early life, can have detrimental effects on host health and increase the susceptibility of developing obesity later in life. Antibiotics are an essential lifesaving treatment; however, their use in early life may not be without risk. Antibiotics are a leading cause of intestinal dysbiosis, and early life administration is associated with obesity risk. The following review explores the relevant literature that simultaneously examines antibiotic-induced dysbiosis and obesity risk. Current evidence suggests that disruptions to the composition and maturation of the gut microbiota caused by antibiotic use in early life are a key mechanism linking the association between antibiotics and obesity. Without compromising clinical practice, increased consideration of the long-term adverse effects of antibiotic treatment on host health, particularly when used in early life is warranted. Novel adjunct interventions should be investigated (e.g., prebiotics) to help mitigate metabolic risk when antibiotic treatment is clinically necessary.
Highlights
Obesity is a major public health problem that continues to be one of the leading risk factors for premature death
Metabolic changes occurred in the Subtherapeutic antibiotic therapy (STAT) microbiota with upregulation of genes involved in the metabolism of carbohydrates that were associated with increased fecal short-chain fatty acids (SCFA) concentrations, potentially indicating increased energy extraction
Chen et al reported that any antibiotic use during the first year of life was associated with increased obesity risk at 15–60 months of age, but that relationship was strongest in boys who received ≥3 courses [122]
Summary
The etiology of obesity encompasses complex interactions between environmental and genetic factors that result in an energy imbalance, leading to the deposition of excess. Individuals may be exposed to a similar obesogenic environment, large variations in weight still occur, demonstrating the potential role genetics play in the development of obesity. Obesity-linked genes influence weight through alterations in key metabolic pathways, including, for example, appetite regulation [8]. While several genes linked to the regulation of body weight have been identified, genetic susceptibility accounts for only a small percentage of the variance in body weight, suggesting that other environmental factors play a large role [9]. Other important risk factors in early life include birth size, rapid and/or excessive weight gain during infancy, early onset of the adiposity rebound, and breast-feeding exposure [6,10,12]. Together with genetic and environmental factors, there is growing evidence that the gut microbiota plays an important role in the development of obesity. An imbalance or disrupted microbial environment termed gut microbiota dysbiosis, influences obesity pathogenesis by impacting energy harvest, nutrient metabolism, inflammatory pathways and the gut-brain axis [5,8,14]
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