Abstract
Background: There is increasing evidence that gut microbiota in offspring is derived in part from maternal environment such as diet. Thus, sweeteners intake including caloric or non-caloric during perinatal period can induce gut dysbiosis and program the offspring to develop cognitive problems later in life.Objective: To determine the effect of maternal high-sweeteners intake during gestation and lactation on gut microbiota shifts in adult male offspring rats and the impact on cognitive dysfunction.Methods: Thirty-four male pups from dams fed standard diet (Control-C, n = 10), high-sucrose diet (HS-C, n = 11), high-honey diet (Ho-C, n = 8), and high-stevia diet (HSt-C, n = 5) were fed standard diet after weaning, and body weight and food intake were recorded once a week for 26 weeks. Learning and memory tests were performed at week 23 of life using the Barnes maze. Fecal samples from the breastfeeding and adulthood periods were collected and analyzed by sequencing the 16S rRNA V3-V4 region of gut microbiota.Results: Maternal high-sucrose and stevia diets programmed the male offspring, and changes in microbial diversity by Shannon index were observed after weaning (p < 0.01). Furthermore, maternal high-stevia diet programming lasted into adulthood. The increase of Firmicutes abundance and the decrease in phylum Bacteroidetes were significant in HS-C and HSt-C groups. This led to an increase in the Firmicutes/Bacteroidetes index, although only in HS-C group was statistically significant (p < 0.05). Of note, the downstream gram-negative Bacteroidales and the upregulation of the gram-positive Clostridiales abundance contribute to cognitive dysfunction.Conclusion: These results suggest that dams fed a high-sucrose and stevia diets during gestation and lactation favor a deficient memory performance in adult male offspring rats through shifts gut microbiota diversity and relative abundance at several taxa.
Highlights
In recent years, the gut–brain axis has been highlighted as a key pathway in the development of mental illnesses such as anxiety and depression [1], as well as cognitive disorders, including memory flexibility [2]
Significant decrease in birth weight were found between HS-C (5.18 ± 0.27 g; p < 0.001) and Ho-C (5.46 ± 0.15; p < 0.01) groups compared with the Control-C group (6.41 ± 0.11 g) (Figure 3A)
We found a significant increase in the fasting glucose levels of male offspring rats in the HS-C (82.60 ± 3.40 mg/dl) and HSt-C (81.60 ± 2.63 mg/dl) groups when compared with the Control-C (67.20 ± 2.47 mg/dl; p < 0.01) (Figure 3D)
Summary
The gut–brain axis has been highlighted as a key pathway in the development of mental illnesses such as anxiety and depression [1], as well as cognitive disorders, including memory flexibility [2]. Recent studies indicate that bacteria colonization of the gastrointestinal tract through the microbial transmission of dams to offspring during early life modulates health in adult life [3]. Relatively minor changes occur, maintaining a stability of gut microbiota, with the possibility of reshaping by the environment, including diet [6]. This means that maternal nutritional exposures during pregnancy and breastfeeding could affect the microbial transmission to offspring modifying the microbiota ecosystem and setting health alterations associated with a dysbiotic microbiota [3]. Sweeteners intake including caloric or non-caloric during perinatal period can induce gut dysbiosis and program the offspring to develop cognitive problems later in life
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