Short-Term Administration of a High-Fat Diet Impairs Wound Repair in Mice

Lipids. 2020 Jan;55(1):23-33. doi: 10.1002/lipd.12189. Epub 2019 Sep 11.

Abstract

High intake of dietary fat plays an important role in obesity development in animals and humans, and prolonged intake of high-fat diet might lead to low-grade chronic inflammation. Previous study showed that diet-induced overweight delays cutaneous wound healing in both obesity-prone and obesity-resistant animals, highlighting the importance of diet composition in the wound healing process. This study evaluated the hypothesis that a short-term administration of high-fat diet could affect cutaneous wound healing. Male mice (C57/bl6) were randomly divided into standard (10% energy from fat) or high-fat (60% energy from fat) chow groups. After 10 days of diet administration, an excisional lesion was performed and the animals were sacrificed 6 or 10 days later. There was no difference in the fasting blood glucose between groups. Ten days after wounding, high-fat chow group presented increased inflammatory infiltrate, levels of inducible nitric oxide synthase and cyclo-oxygenase-2 proteins, and lipid peroxidation. The high-fat chow group presented delayed wound closure, increased amount of myofibroblasts and vessels, and decreased deposition of type I collagen. These findings support the hypothesis that short-term administration of high-fat diet exerts negative effects on mice cutaneous wound healing, due to the interference in the inflammatory phase.

Keywords: High-fat diet; Mouse; Short-term; Skin; Wound healing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cyclooxygenase 2 / metabolism*
  • Diet, High-Fat / adverse effects*
  • Disease Models, Animal
  • Gene Expression Regulation / drug effects
  • Lipid Peroxidation / drug effects
  • Male
  • Mice
  • Nitric Oxide Synthase / metabolism*
  • Random Allocation
  • Wound Healing / drug effects*

Substances

  • Nitric Oxide Synthase
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2