Dietary Conjugated Linoleic Acid Reduces Body Weight and Fat in Snord116m+/p− and Snord116m−/p− Mouse Models of Prader–Willi Syndrome

Prader–Willi Syndrome (PWS) is a human genetic condition that affects up to 1 in 10,000 live births. Affected infants present with hypotonia and developmental delay. Hyperphagia and increasing body weight follow unless drastic calorie restriction is initiated. Recently, our laboratory showed that on...

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Bibliographic Details
Published in:Nutrients 2022-02, Vol.14 (4), p.860
Main Authors: Knott, Brittney, Kocher, Matthew A., Paz, Henry A., Hamm, Shelby E., Fink, William, Mason, Jordan, Grange, Robert W., Wankhade, Umesh D., Good, Deborah J.
Format: Article
Language:English
Subjects:
Animal models
Anxiety
Body weight
Body weight loss
Chromosomes
Diet
dietary intervention
exercise
Food
Food additives
Food intake
Genetic disorders
Genetic engineering
Genotypes
Glucose
Growth hormones
High fat diet
Hyperphagia
Hypothalamus
Hypotonia
Linoleic acid
Metabolic rate
microbiome
Microbiomes
muscle function
Nutrient deficiency
Obesity
Prader-Willi syndrome
Rodents
Snord116
Weight control
Weight reduction
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Summary:Prader–Willi Syndrome (PWS) is a human genetic condition that affects up to 1 in 10,000 live births. Affected infants present with hypotonia and developmental delay. Hyperphagia and increasing body weight follow unless drastic calorie restriction is initiated. Recently, our laboratory showed that one of the genes in the deleted locus causative for PWS, Snord116, maintains increased expression of hypothalamic Nhlh2, a basic helix–loop–helix transcription factor. We have previously also shown that obese mice with a deletion of Nhlh2 respond to a conjugated linoleic acid (CLA) diet with weight and fat loss. In this study, we investigated whether mice with a paternal deletion of Snord116 (Snord116m+/p−) would respond similarly. We found that while Snord116m+/p− mice and mice with a deletion of both Snord116 alleles were not significantly obese on a high-fat diet, they did lose body weight and fat on a high-fat/CLA diet, suggesting that the genotype did not interfere with CLA actions. There were no changes in food intake or metabolic rate, and only moderate differences in exercise performance. RNA-seq and microbiome analyses identified hypothalamic mRNAs, and differentially populated gut bacteria, that support future mechanistic analyses. CLA may be useful as a food additive to reduce obesity in humans with PWS.
ISSN:2072-6643
2072-6643
DOI:10.3390/nu14040860