This 2016 California rodent study found:
“HF [high fat] diet leads to persistent alterations of chromatin accessibility that are partially mediated by transcription factors and histone post-translational modifications. These chromatin alterations are furthermore strain specific, indicating a genetic component to the response.
These results suggest that persistent epigenetic modifications induced by HF diet have the potential to impact the long-term risk for metabolic diseases.”
The experimental procedure was that 7-8 week old subjects of two mice strains “were placed on three diet regimens:
- control diet for sixteen weeks,
- HF diet for sixteen weeks, or
- HF diet for an initial eight weeks followed by control diet for eight weeks (diet reversal).”
On diet regimen 3, one of the mouse strains wasn’t able to reverse the epigenetic changes caused by eight weeks of a high-fat diet. The symptoms included:
- Elevated lipid accumulation and triglyceride levels
- 15% of chromatin sites were more accessible, with the HNF4α transcription factor implicated
- 6% of chromatin sites were less accessible due to H3K9 methylation
- Persistently up-regulated genes were more likely to be in the vicinity of a persistently accessible site
- A set of persistently up-regulated genes enriched for mitochondrial genes was present only with diet regimen 3 subjects.
A second mouse strain “known to display differences in metabolic dysfunction under HF diet” compared to the first strain didn’t experience the same symptoms on diet regimen 3:
- Lipid accumulation and triglyceride levels weren’t elevated
- The majority of diet-induced chromatin remodeling [was] reversible
- Little overlap with the first strain in the set of genes that changed expression.
The study didn’t suggest any specific human applicability.
http://www.jbc.org/content/early/2016/03/22/jbc.M115.711028.long (pdf) “Persistent chromatin modifications induced by high fat diet”