A Short-Term High-Fat Diet Improved the Survival of Fat Grafts in Mice by Promoting Macrophage Infiltration and Angiogenesis

Abstract

Background: Adipose tissue is an ideal filler material that is widely used for soft tissue defects. But the low survival rate and complications associated with such grafts pose a serious challenge, which limits their clinical application. Adipose tissue is a metabolic diet-responsive tissue; however, the influence of diets on fat grafting remains ambiguous.Methods: We extracted inguinal fat pads from C57/BL6 male mice, and transplanted them into the dorsal region of recipient mice (0.3 ml). Post-fat-grafting, mice (n = 54) were randomized into three groups, namely normal diet (ND), high carbohydrate diet (HC), and high-fat diet (HF). Structural changes were assessed by histological staining. Lipolysis activity and vascular regeneration of grafts on day 30 were analyzed using real-time polymerase chain reaction, immunofluorescence, and western blotting.Results: The grafts of mice on HC and HF diets exhibited significantly fewer oil cysts and larger volume retention (0.18 ± 0.01, 0.21 ± 0.01, and 0.25 ± 0.01 ml, for ND, HC, and HF group, respectively, p < 0.05) on day 90. In comparison, grafts for the mice belonging to the HF groups exhibited higher expression of lipolysis-related genes, including adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), and carnitine palmitoyltransferase 1 (CPT1), on day 30. Furthermore, increased infiltration of macrophages (F4/80+) and the higher expression of angiogenesis genes were reported in the HF groups.Conclusion: Altogether, the administration of short-term HF diet remarkably enhanced angiogenesis and improved the quality of fat grafts, which was characterized by fewer oil cysts and higher long-term volume retention. The possible mechanisms may be due to the increased macrophage infiltration, and the promoted angiogenesis in HF grafts.

Lipolysis inhibition improves the survival of fat grafts through ameliorating lipotoxicity and inflammation

“…Adipose tissue inflammation is mostly caused by macrophages, 39 and the quantity and differentiation orientation of macrophages influence how well fat grafts regenerate. 20,40,41 In the early stage of fat grafting, the pro-inflammatory M1 type of macrophages dominated, and the timely conversion of M1 macrophages to the antiinflammatory M2 phenotype contributed positively to enhance vascularization and adipose tissue regeneration. 42 Long-term M1 macrophage infiltration and blockade of M2 macrophage polarization could lead to the elevated levels of inflammation in fat grafts, attract more fibroblasts and result in fibrosis and oil cyst formation.…”

“…Adipose tissue inflammation is mostly caused by macrophages, 39 and the quantity and differentiation orientation of macrophages influence how well fat grafts regenerate 20,40,41 . In the early stage of fat grafting, the pro‐inflammatory M1 type of macrophages dominated, and the timely conversion of M1 macrophages to the anti‐inflammatory M2 phenotype contributed positively to enhance vascularization and adipose tissue regeneration 42 .…”

“…Fat grafts were collected and stored in liquid nitrogen, and then the total proteins in grafts were extracted for Western blot assay. The detailed method is reported previously 20 . For detection of ATGL and GCI58 protein, anti‐ATGL (Proteintech, China) and anti‐GCI58 polyclonal antibodies were used at a dilution of 1:500.…”

“…The detailed method is reported previously. 20 For detection of ATGL and GCI58 protein, anti-ATGL (Proteintech, China) and anti-GCI58 polyclonal antibodies were used at a dilution of 1:500. To compare the protein expression levels, GAPDH was used as a standard internal reference protein.…”

Vocal Fold Augmentation: Current Review

“…17) 이식된 지방의 부피 변화를 일으키는 요인들은 아직 완전히 밝혀지지 않았으나, 이식된 지방에 신생혈관이 생성되지 못하는 것도 중요 원인들 중 하 나로 고려되고 있으며, 이를 극복하기 위한 연구도 진행되고 있다. [18][19][20]…”