Differential adaptive responses to 1- or 2-day fasting in various mouse tissues revealed by quantitative PCR analysis.
Level 5 - mechanism / opinion, no new human data
Animal research with no human data.
PubMed 25973363 · doi:10.1016/j.fob.2015.04.012
What was done
Mice were subjected to 1- or 2-day fasting, and cellular adaptive responses were assessed across 13 tissues: thymus, liver, spleen, small intestine, stomach, kidney, colon, brain, eye, lung, heart, skeletal muscle, and testis. Expression of 15 gene markers was measured using quantitative PCR to evaluate the ubiquitin-proteasome system (Atrogin-1, MuRF1), autophagy-lysosome pathway (LC3b, p62, Lamp2), amino acid response (Asns, Trib3, Herpud1, xCT, Chop), Nrf2-mediated antioxidant system (HO-1, Gsta1), and amino acid transport (Slc38a2, Slc7a5, Slc7a1).
What was found
The authors report differential activation profiles among seven highly or mildly atrophied tissues (thymus, liver, spleen, small intestine, stomach, kidney, colon) compared to six non-atrophied tissues (brain, eye, lung, heart, skeletal muscle, testis). The abstract reports no numerical values, fold-changes, or statistical test results.
Why it matters
Short-term fasting is widely used in preclinical protocols, and these findings indicate that acute fasting causes widespread, tissue-dependent transcriptional remodeling that may alter baseline biology in mouse experiments.
Limits
This is an animal study, so findings cannot be directly translated to human fasting physiology. The abstract does not provide the sample size (n), mouse strain, sex, age, or any quantitative data or p-values. Only mRNA marker levels were evaluated, without measurements of protein abundance or functional metabolic flux.
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- supports Tissues like the liver, brain, and muscle are sensitive to fasting-induced autophagy, whereas blood cells have a restricted autophagy response to fasting.