The expression signatures in liver and adipose tissue from obese Göttingen Minipigs reveal a predisposition for healthy fat accumulation.
Adipose Tissue
/ metabolism
Animals
Cholesterol
/ administration & dosage
Diabetes Mellitus, Experimental
/ metabolism
Diet, High-Fat
Disease Models, Animal
Dyslipidemias
/ metabolism
Fructose
/ administration & dosage
Humans
Insulin
/ metabolism
Intra-Abdominal Fat
/ metabolism
Liver
/ metabolism
Male
Obesity
/ genetics
Obesity, Morbid
/ genetics
Phenotype
Subcutaneous Fat
/ metabolism
Swine
Swine, Miniature
/ genetics
Journal
Nutrition & diabetes
ISSN: 2044-4052
Titre abrégé: Nutr Diabetes
Pays: England
ID NLM: 101566341
Informations de publication
Date de publication:
23 03 2020
23 03 2020
Historique:
received:
15
07
2019
accepted:
20
01
2020
revised:
14
01
2020
entrez:
25
3
2020
pubmed:
25
3
2020
medline:
23
1
2021
Statut:
epublish
Résumé
Model animals are valuable resources for dissecting basic aspects of the regulation of obesity and metabolism. The translatability of results relies on understanding comparative aspects of molecular pathophysiology. Several studies have shown that despite the presence of overt obesity and dyslipidemia in the pig key human pathological hepatic findings such as hepatocellular ballooning and abundant steatosis are lacking in the model. The aim of this study was to elucidate why these histopathological characteristics did not occur in a high fat, fructose and cholesterol (FFC) diet-induced obese Göttingen Minipig model. High-throughput expression profiling of more than 90 metabolically relevant genes was performed in liver, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) of male minipigs diet fed: standard chow (SD, n = 7); FFC diet (n = 14); FFC diet in streptozotocin-induced diabetic pigs (FFC 12, 4 and 1 genes were highly significantly differentially expressed in liver, SAT and VAT when comparing the FFC and SD groups whereas the corresponding numbers were 15, 2, and 1 when comparing the FFC The study shows that morbidly obese Göttingen Minipigs are protected against many of the metabolic and hepatic abnormalities associated with obesity due to a remarkable ability to expand the adipose compartments to accommodate excess calories.
Sections du résumé
BACKGROUND
Model animals are valuable resources for dissecting basic aspects of the regulation of obesity and metabolism. The translatability of results relies on understanding comparative aspects of molecular pathophysiology. Several studies have shown that despite the presence of overt obesity and dyslipidemia in the pig key human pathological hepatic findings such as hepatocellular ballooning and abundant steatosis are lacking in the model.
OBJECTIVES
The aim of this study was to elucidate why these histopathological characteristics did not occur in a high fat, fructose and cholesterol (FFC) diet-induced obese Göttingen Minipig model.
METHODS
High-throughput expression profiling of more than 90 metabolically relevant genes was performed in liver, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) of male minipigs diet fed: standard chow (SD, n = 7); FFC diet (n = 14); FFC diet in streptozotocin-induced diabetic pigs (FFC
RESULTS
12, 4 and 1 genes were highly significantly differentially expressed in liver, SAT and VAT when comparing the FFC and SD groups whereas the corresponding numbers were 15, 2, and 1 when comparing the FFC
CONCLUSION
The study shows that morbidly obese Göttingen Minipigs are protected against many of the metabolic and hepatic abnormalities associated with obesity due to a remarkable ability to expand the adipose compartments to accommodate excess calories.
Identifiants
pubmed: 32205840
doi: 10.1038/s41387-020-0112-y
pii: 10.1038/s41387-020-0112-y
pmc: PMC7090036
doi:
Substances chimiques
Insulin
0
Fructose
30237-26-4
Cholesterol
97C5T2UQ7J
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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