Chronic cold stress promotes inflammation and ER stress via inhibiting GLP-1R signaling, and exacerbates the risk of ferroptosis in the liver and pancreas.
Level 5 - mechanism / opinion, no new human data
Animal model study (Yorkshire pigs) without human clinical data
PubMed 39089475 · doi:10.1016/j.envpol.2024.124647
What was done
Yorkshire pigs were assigned to a control group or a chronic cold stress (CCS) group to examine the effects of prolonged cold exposure on the liver and pancreas. Investigators assessed GLP-1R expression, oxidative stress (Nrf2 pathway), TLR4-mediated inflammatory markers (IL-1β, TNF-α), endoplasmic reticulum (ER) stress markers (PERK, IRE1, XBP1, eIF2α), and ferroptosis markers (PTGS2, FtH).
What was found
The abstract reports statistical significance without specific numerical values or baseline measurements: - CCS significantly inhibited GLP-1R expression and activated the Nrf2 pathway in liver and pancreas (P < 0.05). - TLR4 pathway activation occurred alongside increased IL-1β and TNF-α in both organs (P < 0.05). - ER stress markers (PERK, IRE1, XBP1, eIF2α) were significantly upregulated in liver and pancreas (P < 0.05). - Hepatic PTGS2 expression increased while ferritin H (FtH) expression decreased under CCS.
Why it matters
This study provides an animal model mechanism linking sustained cold exposure to down-regulated GLP-1R signaling, inflammatory cascade activation, and heightened markers of ER stress and ferroptosis in metabolic organs.
Limits
The study was conducted in swine, and direct applicability to human physiology or cold exposure is unverified. The abstract does not state the sample size (n), the exact temperature, the duration of cold exposure, or quantitative effect sizes and confidence intervals.
Cited by
- contradicts Cold exposure has been shown to decrease the Nrf2 pathway in animal studies.