The effect of low-calorie sweetener exposure during pregnancy on the development of neural systems engaged in metabolic regulation

According to a study published in the Journal of Clinical Investigation Insight, consuming low-calorie sweeteners during pregnancy can impact the offspring’s metabolism and neural development. A gut microbial-host co-metabolite is identified as a possible causative factor mediating these changes in the research.

Obesity and diabetes are becoming increasingly common around the globe. This could be attributed to a rise in refined sugar consumption, specifically in sugar-sweetened beverages.

People are opting for low-calorie sweeteners that provide a sweet taste without consuming too many calories as a healthier option. However, there is proof that low-calorie sweeteners can cause weight gain and glucose intolerance.

Exposure to low-calorie sweeteners during pregnancy is known to cause adversities in infants, including body weight gain, insulin resistance, the formation of a sweet taste preference, and changes in gut microbiota makeup.

The current research looked into how exposure to low-calorie sweeteners during pregnancy might affect the offspring’s metabolism and neural development.

They have concentrated on developing hypothalamic melanocortin and autonomic circuits, which are associated with regulating energy expenditure and glucose homeostasis, in addition to studying potential metabolic abnormalities.

Study layout
The research used adult female mice that were exposed to two popular low-calorie sweeteners, aspartame, and rebaudioside A, during pregnancy and lactation.

Both sweeteners’ doses were maintained well within the daily permissible intake limit in humans.

Significant remarks
Adult female mice were exposed to low-calorie sweeteners during pregnancy and lactation, which caused certain alterations. The mice exposed to rebaudioside A experienced a change in body makeup, including a decrease in fat mass and an increase in lean mass. Aspartame-exposed rodents had higher insulin levels in their blood.

In adult female mice, however, there were no impacts of low-calorie sweetener exposure on body weight, food intake, glucose tolerance, leptin level, and size and proportion of pancreatic beta cell mass.

The effect of low-calorie sweetener intake in children
In utero low-calorie sweetener exposure had an impact on adult male offspring (14-week-old), but not on female offspring.

When compared to non-exposed control progeny, the male offspring had increased fat mass, decreased lean mass, and glucose intolerance.

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The adult offspring showed a long-term effect of in-utero low-calorie sweetener exposure on gut microbiota composition and diversity. The offspring gut microbiota contained a higher abundance of the Enterobacteriaceae genus. In exposed dams, however, no significant changes in gut microbiota were detected.

In terms of neural development, in-utero exposure to low-calorie sweeteners resulted in the rewiring of hypothalamic melanocortin circuits in the paraventricular region of the hypothalamus and disruption of pancreatic islet parasympathetic innervation in male progeny.

The researchers performed an untargeted metabolomic investigation on samples of maternal milk and offspring blood. Significant changes in metabolite profiles were found in both samples as a result of low-calorie sweetener exposure.

Rebaudioside A and aspartame exposure produced differential regulation of 151 and 92 metabolites in maternal milk samples, respectively. Similarly, rebaudioside A and aspartame exposure induced differential regulation of 9 and 35 metabolites in offspring blood samples, respectively.

The only metabolite that varied frequently across all samples was phenylacetylglycine, a co-metabolite of gut microbiota and host. This metabolite may also be a marker for cardiovascular illness. This metabolite’s transcript was found to be increased in low-calorie sweetener-exposed milk and blood samples.

These findings were verified by giving the mice phenylacetylglycine during pregnancy and lactation. The results show that phenylacetylglycine treatment produces similar metabolic and neurodevelopmental changes in offspring as low-calorie sweetener exposure in utero.

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The importance of the research
The research found that exposing offspring to low-calorie sweeteners in utero can cause significant metabolic and neurodevelopmental changes. Furthermore, the research identifies phenylacetylglycine, a gut microbial-host co-metabolite, as a potential mediator of low-calorie sweetener-related changes.

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