title: Both obesity-prone and obesity-resistant rats present delayed cutaneous wound healing.
abstract: Diet-induced overweight rats exhibit delayed cutaneous healing; however, when receiving an obesogenic diet, some rats are susceptible to developing the overweight phenotype, whereas others are resistant. We investigated cutaneous healing in diet-induced obesity (DIO)-prone and diet-resistant (DR) rats. Male rats were fed with a standard (control) or a high-saturated fat (30 % fat, w/w) diet for 20 weeks. Then, the experimental group was subdivided into DIO (n 17) and DR (n 16) groups. An excision lesion was made, and the animals were killed 7 or 14 d later. The average body weight was 29 and 25 % higher in the DIO group compared with the C and DR groups. Retroperitoneal fat was higher in the DIO group than in the control and DR groups (518 and 92 %) and was higher in the DR group than in the control group (223 %). The DIO group presented glucose intolerance, and both the DIO and DR groups presented delayed wound contraction (50 %) and re-epithelialisation (20 %). Compared with the DR group, the DIO group displayed higher amounts of inflammatory cells as well as higher levels of lipid peroxidation (P < 0·05). Myofibroblastic differentiation and vessel remodelling were delayed in both the DIO and DR groups. Nitrite levels were lower in the DIO group (340 % less) than in the DR group. TNF-α expression was increased in the DIO group (130 %) compared with the DR group. Our results showed that DIO as well as DR rats present delays in cutaneous wound healing, even though the DR group does not have an overweight phenotype.
authors.affiliation: Tissue Repair Laboratory, Histology and Embryology Department, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. amacosta@uerj.br
authors.forename: Adriana
authors.initials: A
authors.lastname: Paulino do Nascimento
authors.forename: Andréa
authors.initials: A
authors.lastname: Monte-Alto-Costa
mesh_terms: D050154:Adiposity; D000818:Animals; D004041:Dietary Fats / Q000009:adverse effects; D004198:Disease Susceptibility; D018149:Glucose Intolerance / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology; D050152:Intra-Abdominal Fat / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008407:Mast Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D058628:Myofibroblasts / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic; D009573:Nitrites / Q000378:metabolism; D009765:Obesity / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000098:blood supply / Q000293:injuries / Q000473:pathology / Q000503:physiopathology*; D040521:Subcutaneous Tissue / Q000098:blood supply / Q000293:injuries / Q000473:pathology / Q000503:physiopathology*; D044242:Trans Fatty Acids / Q000009:adverse effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015430:Weight Gain; D014945:Wound Healing
chemical_list: D004041:Dietary Fats; D009573:Nitrites; D044242:Trans Fatty Acids; D014409:Tumor Necrosis Factor-alpha