Establishing a model for childhood obesity in adolescent pigs

• Published in: Obesity science & practice 2018-08, Vol.4 (4), p.396-406
• Main Authors: Fouhse, J., Yang, K., Li, J., Mills, E., Ju, T., Alvarado, C. S., Chan, C. B., Willing, B. P.
• Format: Article
• Language: English
• Subjects: Animal euthanasia; Body weight gain; Childhood obesity; Children; Cholesterol; Chromatography; Colon; Deoxyribonucleic acid; Diabetes; Diet; Disease; DNA; dyslipidaemia; Dyslipidemia; Fatty acids; Feeding; Gene expression; Glucose; Glucose tolerance; High fat diet; Hogs; Ileum; impaired glucose tolerance; Inflammation; Insulin resistance; Intestine; Intolerance; Lipid metabolism; Lipopolysaccharides; Low fat diet; Metabolic disorders; Metabolism; Metabolites; microbiome; Microbiota; Nutrient deficiency; Obesity; Original; Phosphatase; Plasma; Polymerase chain reaction; Tumor necrosis factor; Tumors
• ISSN: 2055-2238; 2055-2238
• DOI: 10.1002/osp4.273

Summary Objective Rising worldwide prevalence of obesity and metabolic diseases in children has accentuated the importance of developing prevention and management strategies. The objective of this study was to establish a model for childhood obesity using high‐fat feeding of adolescent pigs, as pigs have a longer developmental period and are physiologically more similar to humans than rodents. Methods Crossbred pigs were fed a high‐fat diet (HFD) or low‐fat diet (n = 6/treatment) from postnatal day 49 to 84. On postnatal day 84, an oral glucose tolerance test was performed, jugular blood sampled to determine lipopolysaccharide levels and plasma lipids, intestinal digesta collected to characterize microbial and metabolite composition and back fat and intestinal tissue assayed for gene expression. Results Five‐week HFD increased weight gain and back fat thickness, caused dyslipidaemia and impaired glucose tolerance and increased expression of genes in back fat suggesting inflammation. HFD pigs had distinct proximal colon microbiota with 48% reduction (P