High-Fat Diet Induces Inflammation of Meibomian Gland

PURPOSE. To determine if a high-fat diet (HFD) induces meibomian gland (MG) inflammation in mice. METHODS. Male C57BL/6J mice were fed a standard diet (SD), HFD, or HFD supplemented with the peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist rosiglitazone for various durations. Body weight, blood lipid levels, and eyelid changes were monitored at regular intervals. MG sections were subjected to hematoxylin and eosin staining, LipidTox staining, TUNEL assay, and immunostaining. Quantitative RT-PCR and western blot analyses were performed to detect relative gene expression and signaling pathway activation in MGs. RESULTS. MG acinus accumulated more lipids in the mice fed the HFD. Periglandular CD45-positive and F4/80-positive cell infiltration were more evident in the HFD mice, and they were accompanied by upregulation of inflammation-related cytokines. PPAR-gamma downregulation accompanied activation of the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-kappa B) signaling pathways in the HFD mice. There was increased acini cell apoptosis and mitochondria damage in mice fed the HFD. MG inflammation was ameliorated following a shift to the standard diet and rosiglitazone treatment in the mice fed the HFD. CONCLUSIONS. HFD-induced declines in PPAR-gamma expression and MAPK and NF-kappa B signaling pathway activation resulted in MG inflammation and dysfunction in mice.

Automated summary

High-fat diet-induced declines in PPAR-gamma expression and activation of MAPK and NF-kappa B signaling pathways may lead to meibomian gland inflammation and dysfunction in mice, characterized by lipid accumulation, inflammatory cell infiltration, apoptosis, and mitochondria damage. Treatment involving dietary shifts and medication administration can alleviate this inflammation.