Absence of a gestational diabetes phenotype in the LepRdb/+ mouse is independent of control strain, diet, misty allele, or parity
| Autor: | Chao Tong, Joanna L. Stanley, Mark H. Vickers, Philip N. Baker, Hongbo Qi, Xinyang Yu, Hua Zhang, Jasmine F. Plows, Ric Broadhurst |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty endocrine system diseases 030209 endocrinology & metabolism Biology Article 03 medical and health sciences Mice 0302 clinical medicine Insulin resistance Pregnancy Internal medicine Diabetes mellitus medicine Animals Allele Alleles Multidisciplinary nutritional and metabolic diseases medicine.disease Phenotype Diet Gestational diabetes Mice Inbred C57BL Diabetes Gestational Parity 030104 developmental biology Endocrinology Immunology Receptors Leptin Female medicine.symptom Parity (mathematics) Weight gain |
| Zdroj: | Scientific Reports |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/srep45130 |
| Popis: | Treatment options for gestational diabetes (GDM) are limited. In order to better understand mechanisms and improve treatments, appropriate animal models of GDM are crucial. Heterozygous db mice (db/+) present with glucose intolerance, insulin resistance, and increased weight gain during, but not prior to, pregnancy. This makes them an ideal model for GDM. However, several recent studies have reported an absence of GDM phenotype in their colony. We investigated several hypotheses for why the phenotype may be absent, with the aim of re-establishing it and preventing further resources being wasted on an ineffective model. Experiments were carried out across two laboratories in two countries (New Zealand and China), and were designed to assess type of control strain, diet, presence of the misty allele, and parity as potential contributors to the lost phenotype. While hyperleptinemia and pre-pregnancy weight gain were present in all db/+mice across the four studies, we found no consistent evidence of glucose intolerance or insulin resistance during pregnancy. In conclusion, we were unable to acquire the GDM phenotype in any of our experiments, and we recommend researchers do not use the db/+ mouse as a model of GDM unless they are certain the phenotype remains in their colony. |
| Databáze: | OpenAIRE |
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