AI Article Synopsis

  • - The rise in obesity and type 2 diabetes is notably affecting pregnant women, leading to increased use of low-calorie sweeteners (LCSs) to reduce calorie intake while still providing sweetness.
  • - Research using a mouse model showed that male offspring from mothers consuming LCSs developed high body fat and glucose intolerance, with significant changes in brain circuits and pancreatic function.
  • - A metabolite called phenylacetylglycine (PAG) was found to be elevated in the milk of LCS-fed mothers and their offspring, suggesting it may play a role in the negative metabolic and neurodevelopmental effects observed from maternal LCS consumption.

Article Abstract

The prevalence of obesity and type 2 diabetes is growing at an alarming rate, including among pregnant women. Low-calorie sweeteners (LCSs) have increasingly been used as an alternative to sugar to deliver a sweet taste without the excessive caloric load. However, there is little evidence regarding their biological effects, particularly during development. Here, we used a mouse model of maternal LCS consumption to explore the impact of perinatal LCS exposure on the development of neural systems involved in metabolic regulation. We report that adult male, but not female, offspring from both aspartame- and rebaudioside A-exposed dams displayed increased adiposity and developed glucose intolerance. Moreover, maternal LCS consumption reorganized hypothalamic melanocortin circuits and disrupted parasympathetic innervation of pancreatic islets in male offspring. We then identified phenylacetylglycine (PAG) as a unique metabolite that was upregulated in the milk of LCS-fed dams and the serum of their pups. Furthermore, maternal PAG treatment recapitulated some of the key metabolic and neurodevelopmental abnormalities associated with maternal LCS consumption. Together, our data indicate that maternal LCS consumption has enduring consequences on the offspring's metabolism and neural development and that these effects are likely to be mediated through the gut microbial co-metabolite PAG.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10322686PMC
http://dx.doi.org/10.1172/jci.insight.156397DOI Listing

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