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Metabolic Decisions in Development and Disease | EK27


Combination of Maternal High Fat Diet and β3-adrenergic Activation in Offspring Alters the Structure and Functional Potential of the Gut Bacterial Community


Mar 27, 2021 12:00am ‐ Mar 27, 2021 12:00am

Description

Combination of Maternal High Fat Diet and β3-adrenergic Activation in Offspring Alters the Structure and Functional Potential of the Gut Bacterial Community Henry A. Paz1,2, Ying Zhong1,2, Ping Kang1,2, Sree V. Chintapalli1,2, Kartik Shankar3, Umesh D. Wankhade1,2* 1Department of Pediatrics, College of Medicine, University of Arkansas, Little Rock, Arkansas, USA; 2Arkansas Children’s Nutrition Center, Little Rock, Arkansas, USA; 3Department of Pediatrics, Section of Nutrition, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado, USA The gut microbiota plays a critical role in energy homeostasis and an imbalance in the bacterial community has been associated with obesity. Recent studies have indicated that housing temperature impacts the adipose tissue phenotype and microbiota composition in mice. Decreasing the housing temperature is associated with improvements in adipose tissue thermogenic capacity and energy expenditure of the host. We previously demonstrated that maternal HFD alters the gut microbiota composition of the offspring. However, integrative regulation of microbiome and adipose tissue function is not clear. In this study, we evaluated the changes in the microbiota composition in response to combination of maternal HFD and thermogenic challenge in the offspring. Five-week-old female C57BL6/J mice were fed either control (17% fat) or HFD (45% fat) and bred with lean male mice at 17 weeks of age. Following weaning, offspring were fed the control diet for 13 weeks. During the 14th week, offspring received a daily intraperitoneal injection of vehicle or β3-adrenergic receptor agonist CL-316,243 (1 mg/kg BW). Mice were euthanized and cecal contents were collected for bacterial community analysis through 16S rRNA gene sequencing of the V4 region. No differences were observed in a-diversity metrics for richness (observed OTUs) and diversity (Shannon index) across treatments. However, b-diversity as indicated by Bray-Curtis dissimilarities was affected by both maternal HFD and thermogenic challenge. At the phylum level, lower abundance of Bacteroidetes and greater abundance of Firmicutes in offspring from maternal HFD increased the Firmicutes/Bacteroidetes ratio. The abundance of the genera Bifidobacterium and Mucispirillum increased in offspring from maternal HFD compared to control diet, while the abundance of the genera Akkermansia and Dehalobacterium decreased and the genera Allobaculum, Lactococcus, and Mucispirillum increased in offspring receiving the CL-316,243 challenge compared to vehicle. Dissimilarities in the bacterial community structure resulted in distinct functional profiles by maternal HFD and thermogenic challenge. Predicted bacterial functions including an increase in lipid metabolism and a decrease in bile acid biosynthesis were observed in offspring with a maternal HFD background and receiving the thermogenic challenge. In conclusion, these results indicate that maternal HFD promotes marked differences in the offspring’s gut bacterial community which in turn could be responsible for differential response to thermogenic challenge in offspring. (Funding source-USDA-ARS Project 6026-51000-012-06S)

Speaker(s):

  • Henry Paz, PhD, Arkansas Children's Nutrition Center

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