Kendig, M. D. | Search bioRxiv

bioRxiv2024

Impact of maternal obesogenic diet on maternal and offspring microbiome development

Pregnancy can alter gut microbiota composition, but how an obesogenic diet impacts maternal gut microbiota, and the extent to which this influences offspring microbiome can be obscured by confounding factors. This study examined changes in gut microbiota composition across pre-pregnancy, gestation and lactation in rat dams fed either a high-fat, high-sugar Cafeteria (Caf) diet or Chow. Microbiome development was assessed in their offspring weaned onto chow. Caf diet consumption during pregnancy increased weight gain and adiposity, and compromised subsequent maternal nursing behaviour. - and {beta} diversity measures in Caf-fed dams showed a different trajectory across the progression of pregnancy, with no change in Bacteroidetes and Firmicutes abundance compared with Chow dams. Offspring born to Caf dams exhibited greater adiposity and plasma leptin at weaning and 14 weeks of age than those born to Chow dams. Maternal Caf diet induced clear differences in {beta} diversity in weanlings but not diversity. SourceTracker analysis revealed similarities in the gut microbiota of Chow weanlings and maternal gut microbiota in lactation, whereas the microbiota of Caf weanlings was similar to the maternal gut microbiota during gestation. Maternal Caf diet exerted only marginal effects on gut microbiota composition in 14-week-old offspring.

developmental biology↗

bioRxiv2023

High fat diet allows food-predictive stimuli to energize action performance in the absence of hunger, without distorting insulin signaling on accumbal cholinergic interneurons.

Obesity can disrupt how food-predictive stimuli control action performance and selection. These two forms of control recruit cholinergic interneurons (CIN) located in the nucleus accumbens core (NAcC) and shell (NAcS), respectively. Given that obesity is associated with insulin resistance in this region, we examined whether interfering with CIN insulin signaling disrupts how food-predictive stimuli control actions. To interfere with insulin signaling we used a high-fat diet (HFD) or genetic excision of insulin receptor (InsR) from cholinergic cells. HFD left intact the capacity of food-predictive stimuli to energize performance of an action earning food when mice were tested hungry. However, it allowed this energizing effect to persist when the mice were tested sated. This persistence was linked to NAcC CIN activity but was not associated with distorted CIN insulin signaling. Accordingly, InsR excision had no effect on how food-predicting stimuli control action performance. Next, we found that neither HFD nor InsR excision altered the capacity of food-predictive stimuli to guide action selection. Yet, this capacity was associated with changes in NAcS CIN activity. These results indicate that insulin signaling on accumbal CIN does not modulate how food-predictive stimuli control action performance and selection. However, they show that HFD allows food-predictive stimuli to energize performance of an action earning food in the absence of hunger.

neuroscience↗