This 2015 Pennsylvania rodent study found:
Mitochondrial dysfunctions altered the
- hypothalamic–pituitary–adrenal [HPA] axis, sympathetic adrenal–medullary activation and catecholamine levels,
- the inflammatory cytokine IL-6,
- circulating metabolites, and
- hippocampal gene expression
responses to stress.
- metabolic, and
- transcriptional responses
coalesced into unique signatures that distinguish groups based on their mitochondrial genotype.”
The study’s design was comprehensive for the subject of mitochondrial function and stress response categories. It interrelated elements that had a common cause of stress, such as:
- Increased lipids
- Corticosterone sensitivity
- Epigenetic changes within the brain
The study’s Figure 6E was a hierarchical “heat map” of the correlations among the 77 stress-induced changes that were measured. Figure 6G presented these variables per the five mitochondrial genotypes (a control wild-type and four genetic dysfunctions). Many of the lines forming the hierarchy needed careful reading of the study’s interpretations.
I downgraded the study’s rating because the authors inappropriately forced the “allostatic load” buzzword into the Significance statement and otherwise informative Discussion section. The term refers to a hypothetical long-term situation, but the study’s experiments lasted 2 hours at most before the subjects were killed.
www.pnas.org/content/112/48/E6614.full “Mitochondrial functions modulate neuroendocrine, metabolic, inflammatory, and transcriptional responses to acute psychological stress”