PUBLICATION
Leptin system loss of function in the absence of obesity in zebrafish
- Authors
- Bagivalu Lakshminarasimha, A., Page McCaw, P., Möckel, D., Gremse, F., Michel, M.
- ID
- ZDB-PUB-210716-17
- Date
- 2021
- Source
- The Journal of endocrinology 251(1): 41-52 (Journal)
- Registered Authors
- Michel, Max
- Keywords
- none
- MeSH Terms
-
- Adiposity
- Animals
- Female
- Leptin/physiology*
- Loss of Function Mutation
- Male
- Obesity/genetics*
- Receptors, Leptin/physiology*
- Weight Gain
- Zebrafish/genetics*
- PubMed
- 34265742 Full text @ J. Endocrinol.
Citation
Bagivalu Lakshminarasimha, A., Page McCaw, P., Möckel, D., Gremse, F., Michel, M. (2021) Leptin system loss of function in the absence of obesity in zebrafish. The Journal of endocrinology. 251(1):41-52.
Abstract
The leptin system plays a crucial role in the regulation of appetite and energy homeostasis in vertebrates. While the phenotype of morbid obesity due to leptin or leptin receptor (lepr) loss of function is well established in mammals, evidence in fish is controversial, questioning the role of leptin as the vertebrate adipostat. Here we report on 3 lepr loss of function (lof) and one leptin loss of function allele in zebrafish. In order to demonstrate that the lepr lof alleles cannot transduce a leptin signal, we measured socs3a transcription after intraperitoneal leptin which is abolished by lepr lof. None of the lepr/lepa lof alleles lead to obesity / a body growth phenotype. We explore possible reasons leading to the difference in published results and find that even slight changes in background genetics such as inbreeding siblings and cousins can lead to significant variance in growth.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping