Phenotype of the taurine transporter knockout mouse.
Level 5 - mechanism / opinion, no new human data
Narrative review of animal genetic knockout studies with no human data
PubMed 17875433 · doi:10.1016/S0076-6879(07)28025-5
What was done
This chapter summarizes experimental findings from studies characterizing mice with targeted disruption of the sodium-dependent taurine transporter gene (taut-/- mice), comparing tissue taurine concentrations, physical performance, and multi-organ morphology and function against heterozygous (taut+/-) and wild-type controls.
What was found
Compared with wild-type controls, taut-/- mice exhibited profound reductions in tissue taurine concentrations: skeletal and cardiac muscle decreased by ~98%; brain, kidney, plasma, and retina decreased by 80% to 90%; and liver decreased by ~70%. Taut-/- mice also showed lower body mass, strongly reduced exercise capacity, subtle renal osmoregulation derangements, altered neuroreceptor expression, loss of striatal long-term potentiation, and age-dependent sensory (visual, auditory, olfactory) dysfunctions, unspecific hepatitis, and liver fibrosis.
Why it matters
Characterizing the taurine transporter knockout phenotype establishes that active transport is essential for systemic taurine homeostasis and illustrates the multi-organ pathology resulting from chronic, severe intracellular taurine deficiency.
Limits
The findings are derived entirely from murine genetic knockout models and narrative review of animal literature, which may not directly translate to human physiology or dietary deficiency states. The abstract reports no sample sizes or statistical variance measures.
Cited by
- supports Taurine is concentrated in the brain, retina, kidneys, and immune cells.