Unknown

Dataset Information

0

Adipocyte Dynamics and Reversible Metabolic Syndrome in Mice with an Inducible Adipocyte-Specific Deletion of the Insulin Receptor.


ABSTRACT: Insulin and IGF1 signaling are important for adipose tissue development and function; however, their role in mature adipocytes is unclear. Mice with a tamoxifen-inducible knockout of insulin and/or IGF1 receptors (IR/IGF1R) demonstrate a rapid loss of white and brown fat due to increased lipolysis and adipocyte apoptosis. This results in insulin resistance, glucose intolerance, hepatosteatosis, islet hyperplasia with hyperinsulinemia, and cold intolerance. This phenotype, however, resolves over 10-30 days due to a proliferation of preadipocytes and rapid regeneration of both brown and white adipocytes as identified by mTmG lineage tracing. This cycle can be repeated with a second round of receptor inactivation. Leptin administration prior to tamoxifen treatment blocks development of the metabolic syndrome without affecting adipocyte loss or regeneration. Thus, IR is critical in adipocyte maintenance, and this loss of adipose tissue stimulates regeneration of brown/white fat and reversal of metabolic syndrome associated with fat loss.

SUBMITTER: Sakaguchi M 

PROVIDER: S-EPMC5304432 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

altmetric image

Publications

Adipocyte Dynamics and Reversible Metabolic Syndrome in Mice with an Inducible Adipocyte-Specific Deletion of the Insulin Receptor.

Sakaguchi Masaji M   Fujisaka Shiho S   Cai Weikang W   Winnay Jonathon N JN   Konishi Masahiro M   O'Neill Brian T BT   Li Mengyao M   García-Martín Rubén R   Takahashi Hirokazu H   Hu Jiang J   Kulkarni Rohit N RN   Kahn C Ronald CR  

Cell metabolism 20170105 2


Insulin and IGF1 signaling are important for adipose tissue development and function; however, their role in mature adipocytes is unclear. Mice with a tamoxifen-inducible knockout of insulin and/or IGF1 receptors (IR/IGF1R) demonstrate a rapid loss of white and brown fat due to increased lipolysis and adipocyte apoptosis. This results in insulin resistance, glucose intolerance, hepatosteatosis, islet hyperplasia with hyperinsulinemia, and cold intolerance. This phenotype, however, resolves over  ...[more]

Similar Datasets

| S-EPMC5345851 | biostudies-literature
| S-EPMC7813145 | biostudies-literature
| S-EPMC7398165 | biostudies-literature
| S-EPMC3782286 | biostudies-literature
| S-EPMC5123203 | biostudies-literature
| S-EPMC9261351 | biostudies-literature
| S-EPMC8742433 | biostudies-literature
| S-EPMC4916414 | biostudies-literature
| S-EPMC7567653 | biostudies-literature
| S-EPMC3338749 | biostudies-literature