Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse.
Obesity in many current pre-clinical animal models of obesity and diabetes is mediated by monogenic mutations; these are rarely associated with the development of human obesity. A new mouse model, the FATZO mouse, has been developed to provide polygenic obesity and a metabolic pattern of hyperglycem...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2017-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0179808&type=printable |
| _version_ | 1826579455695388672 |
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| author | Brian A Droz Bria L Sneed Charles V Jackson Karen M Zimmerman M Dodson Michael Paul J Emmerson Tamer Coskun Richard G Peterson |
| author_facet | Brian A Droz Bria L Sneed Charles V Jackson Karen M Zimmerman M Dodson Michael Paul J Emmerson Tamer Coskun Richard G Peterson |
| author_sort | Brian A Droz |
| collection | DOAJ |
| description | Obesity in many current pre-clinical animal models of obesity and diabetes is mediated by monogenic mutations; these are rarely associated with the development of human obesity. A new mouse model, the FATZO mouse, has been developed to provide polygenic obesity and a metabolic pattern of hyperglycemia and hyperinsulinemia, that support the presence of insulin resistance similar to metabolic disease in patients with insulin resistance/type 2 diabetes. The FATZO mouse resulted from a cross of C57BL/6J and AKR/J mice followed by selective inbreeding for obesity, increased insulin and hyperglycemia. Since many clinical studies have established a close link between higher body weight and the development of type 2 diabetes, we investigated whether time to progression to type 2 diabetes or disease severity in FATZO mice was dependent on weight gain in young animals. Our results indicate that lighter animals developed metabolic disturbances much slower and to a lesser magnitude than their heavier counterparts. Consumption of a diet containing high fat, accelerated weight gain in parallel with disease progression. A naturally occurring and significant variation in the body weight of FATZO offspring enables these mice to be identified as low, mid and high body weight groups at a young age. These weight groups remain into adulthood and correspond to slow, medium and accelerated development of type 2 diabetes. Thus, body weight inclusion criteria can optimize the FATZO model for studies of prevention, stabilization or treatment of type 2 diabetes. |
| first_indexed | 2024-12-16T08:57:08Z |
| format | Article |
| id | doaj.art-bb9f14c1cae741f99f99a57996878039 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2025-03-14T14:18:33Z |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
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| spelling | doaj.art-bb9f14c1cae741f99f99a579968780392025-02-27T05:32:41ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01126e017980810.1371/journal.pone.0179808Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse.Brian A DrozBria L SneedCharles V JacksonKaren M ZimmermanM Dodson MichaelPaul J EmmersonTamer CoskunRichard G PetersonObesity in many current pre-clinical animal models of obesity and diabetes is mediated by monogenic mutations; these are rarely associated with the development of human obesity. A new mouse model, the FATZO mouse, has been developed to provide polygenic obesity and a metabolic pattern of hyperglycemia and hyperinsulinemia, that support the presence of insulin resistance similar to metabolic disease in patients with insulin resistance/type 2 diabetes. The FATZO mouse resulted from a cross of C57BL/6J and AKR/J mice followed by selective inbreeding for obesity, increased insulin and hyperglycemia. Since many clinical studies have established a close link between higher body weight and the development of type 2 diabetes, we investigated whether time to progression to type 2 diabetes or disease severity in FATZO mice was dependent on weight gain in young animals. Our results indicate that lighter animals developed metabolic disturbances much slower and to a lesser magnitude than their heavier counterparts. Consumption of a diet containing high fat, accelerated weight gain in parallel with disease progression. A naturally occurring and significant variation in the body weight of FATZO offspring enables these mice to be identified as low, mid and high body weight groups at a young age. These weight groups remain into adulthood and correspond to slow, medium and accelerated development of type 2 diabetes. Thus, body weight inclusion criteria can optimize the FATZO model for studies of prevention, stabilization or treatment of type 2 diabetes.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0179808&type=printable |
| spellingShingle | Brian A Droz Bria L Sneed Charles V Jackson Karen M Zimmerman M Dodson Michael Paul J Emmerson Tamer Coskun Richard G Peterson Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse. PLoS ONE |
| title | Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse. |
| title_full | Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse. |
| title_fullStr | Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse. |
| title_full_unstemmed | Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse. |
| title_short | Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse. |
| title_sort | correlation of disease severity with body weight and high fat diet in the fatzo pco mouse |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0179808&type=printable |
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