Establishing a model for childhood obesity in adolescent pigs

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...

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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
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Yang, K.
Li, J.
Mills, E.
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Chan, C. B.
Willing, B. P.
description 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 
doi_str_mv 10.1002/osp4.273
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S. ; Chan, C. B. ; Willing, B. P.</creator><creatorcontrib>Fouhse, J. ; Yang, K. ; Li, J. ; Mills, E. ; Ju, T. ; Alvarado, C. S. ; Chan, C. B. ; Willing, B. P.</creatorcontrib><description>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 &lt; 0.05) in Bacteroidetes and increased expression of pro‐inflammatory genes interleukin‐18 and tumour necrosis factor in ileum (P &lt; 0.05). Conclusions These findings indicate that adolescent pigs should be considered a suitable model for childhood obesity, because short‐term HFD feeding is sufficient to induce obesity and glucose intolerance, recapitulating disease characteristics in adolescent pigs.</description><identifier>ISSN: 2055-2238</identifier><identifier>EISSN: 2055-2238</identifier><identifier>DOI: 10.1002/osp4.273</identifier><identifier>PMID: 30151234</identifier><language>eng</language><publisher>United States: John Wiley &amp; Sons, Inc</publisher><subject>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</subject><ispartof>Obesity science &amp; practice, 2018-08, Vol.4 (4), p.396-406</ispartof><rights>2018 The Authors. 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S.</creatorcontrib><creatorcontrib>Chan, C. B.</creatorcontrib><creatorcontrib>Willing, B. P.</creatorcontrib><title>Establishing a model for childhood obesity in adolescent pigs</title><title>Obesity science &amp; practice</title><addtitle>Obes Sci Pract</addtitle><description>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 &lt; 0.05) in Bacteroidetes and increased expression of pro‐inflammatory genes interleukin‐18 and tumour necrosis factor in ileum (P &lt; 0.05). Conclusions These findings indicate that adolescent pigs should be considered a suitable model for childhood obesity, because short‐term HFD feeding is sufficient to induce obesity and glucose intolerance, recapitulating disease characteristics in adolescent pigs.</description><subject>Animal euthanasia</subject><subject>Body weight gain</subject><subject>Childhood obesity</subject><subject>Children</subject><subject>Cholesterol</subject><subject>Chromatography</subject><subject>Colon</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>Diet</subject><subject>Disease</subject><subject>DNA</subject><subject>dyslipidaemia</subject><subject>Dyslipidemia</subject><subject>Fatty acids</subject><subject>Feeding</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>High fat diet</subject><subject>Hogs</subject><subject>Ileum</subject><subject>impaired glucose tolerance</subject><subject>Inflammation</subject><subject>Insulin resistance</subject><subject>Intestine</subject><subject>Intolerance</subject><subject>Lipid metabolism</subject><subject>Lipopolysaccharides</subject><subject>Low fat diet</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>microbiome</subject><subject>Microbiota</subject><subject>Nutrient deficiency</subject><subject>Obesity</subject><subject>Original</subject><subject>Phosphatase</subject><subject>Plasma</subject><subject>Polymerase chain reaction</subject><subject>Tumor necrosis factor</subject><subject>Tumors</subject><issn>2055-2238</issn><issn>2055-2238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><recordid>eNp1kV1LwzAUhoMobsyBv0AK3njTme-uFwoy5gcMJqjXIW3TNSNtatMq-_embM4peJUDeXnOc3gBOEdwgiDE19bVdIIjcgSGGDIWYkymxwfzAIydW0MIEYs5wugUDIifESZ0CG7mrpWJ0a7Q1SqQQWkzZYLcNkFaaJMV1maBTZTT7SbQVSAza5RLVdUGtV65M3CSS-PUePeOwNv9_HX2GC6WD0-zu0WYUs5JmGZUKsZgzBIK417a28SRlAQlmFICpeQqjSKWJ7GUiTeLFI8IJ5xKjlVGRuB2y627pFRZv7-RRtSNLmWzEVZq8fun0oVY2Q_BEWQRJB5wtQM09r1TrhWl9mcYIytlOyewd2OEIb91BC7_RNe2ayp_nsCEIIpwTKc_wLSxzjUq38sgKPoLRV-L8LX46MWh_D74XYIPhNvApzZq8y9ILF-eaQ_8AuvklOw</recordid><startdate>201808</startdate><enddate>201808</enddate><creator>Fouhse, J.</creator><creator>Yang, K.</creator><creator>Li, J.</creator><creator>Mills, E.</creator><creator>Ju, T.</creator><creator>Alvarado, C. 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S.</au><au>Chan, C. B.</au><au>Willing, B. P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Establishing a model for childhood obesity in adolescent pigs</atitle><jtitle>Obesity science &amp; practice</jtitle><addtitle>Obes Sci Pract</addtitle><date>2018-08</date><risdate>2018</risdate><volume>4</volume><issue>4</issue><spage>396</spage><epage>406</epage><pages>396-406</pages><issn>2055-2238</issn><eissn>2055-2238</eissn><abstract>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 &lt; 0.05) in Bacteroidetes and increased expression of pro‐inflammatory genes interleukin‐18 and tumour necrosis factor in ileum (P &lt; 0.05). 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source Wiley Online Library Open Access; Publicly Available Content Database; PubMed Central
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
title Establishing a model for childhood obesity in adolescent pigs
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