The Relationship between Cutaneous Wounds Made on Obese Mice or Those with Decreased Body Weight and Serum Leptin Level

Urai, Tamae; Haryanto, Haryanto; Mukai, Kanae; Matsushita, Tatsuhiko; Asano, Kazushi; Nakajima, Yukari; Okuwa, Mayumi; Sugama, Junko; Nakatani, Toshio

doi:10.4236/health.2016.811105

Cited by 7 publications

(12 citation statements)

References 27 publications

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“…However, at 15 weeks after feeding, the day before wounding, the leptin concentration in the obesity group (42.3 ± 3.5 ng/mL) was significantly higher than that in the control group (3.5 ± 1.1 ng/mL) [9]. In this study and our previous study, obese mice were fed the same diet for the same period.…”

Section: Discussionsupporting

confidence: 37%

“…In our previous study [9], circular wounds became oval after wounding, and, thus, wound distances in the minor axis became short without a splint. In the present study and our previous study [10], the use of a splint decreased tension T. Urai et al Health because it maintained the shape of the circular wound in obese mice.…”

Section: Discussionmentioning

confidence: 81%

“…We previously investigated circular (diameter of 6 mm) full-thickness skin wound healing in diet-induced obese mice, and found no significant differences in the progression of wound healing between obese and non-obese mice [9]. We identified two factors that contributed to wound healing in obese mice; wound tension and stress of wounding.…”

Section: Discussionmentioning

confidence: 89%

“…(the feeding period) (9). The high-fat diet had 1.4-fold the energy and 6.5-fold the fat of the commercial diet fed to the control group (Table 1).…”

Section: Animals and Dietsmentioning

confidence: 99%

“…Tissue oxygen tension in obese patients was previously shown to be low at and near incisions [8], and contributed to wound dehiscence [3] [5]. Circular wounds in the obese mice changed to oval wounds [9].…”

Section: Introductionmentioning

confidence: 98%

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Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Urai¹,

Nakajima²,

Mukai³

et al. 2017

Health

Self Cite

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It was unclear that wound healing was delayed in obesity without hyperglycemia. The purpose of this study was to compare the wound healing process between obese and non-obese mice without hyperglycemia by attaching a splint. Three-week-old male mice (C57BL/6N) were fed high-fat diets (60% of calories from fat) in the obesity group, and commercial diets in the control group for 15 weeks. Two circular (4 mm in diameter) full-thickness wounds were made on the dorsal skin. Body weights and serum leptin levels were significantly higher in the obesity group than in the control group until day 15 after wounding. Fasting blood glucose levels before wounding were lower in the obesity group than in a hyperglycemic rodent model. The macrophage infiltration into subcutaneous fat before wounding in the obesity group was negligible. The ratios of the wound area were not significantly different between the two groups. No significant differences were observed in the number of neutrophils or macrophages or new blood vessels and ratio of myofibroblasts or collagen fibers between the two groups. Our results demonstrated that cutaneous wound healing was not delayed in the obesity group without hyperglycemia and macrophage infiltration into the subcutaneous fat and with high serum leptin levels.

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Section: Discussionsupporting

confidence: 37%

Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 89%

“…(the feeding period) (9). The high-fat diet had 1.4-fold the energy and 6.5-fold the fat of the commercial diet fed to the control group (Table 1).…”

Section: Animals and Dietsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

See 3 more Smart Citations

Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Urai¹,

Nakajima²,

Mukai³

et al. 2017

Health

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Lactobacillus acidophilus LA5 improves saturated fat-induced obesity mouse model through the enhanced intestinal Akkermansia muciniphila

Ondee

Pongpirul

Visitchanakun

et al. 2021

Sci Rep

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Obesity, a major healthcare problem worldwide, induces metabolic endotoxemia through the gut translocation of lipopolysaccharides (LPS), a major cell wall component of Gram-negative bacteria, causing a chronic inflammatory state. A combination of several probiotics including Lactobacillus acidophilus 5 (LA5), a potent lactic acid-producing bacterium, has previously been shown to attenuate obesity. However, data on the correlation between a single administration of LA5 versus microbiota alteration might be helpful for the probiotic adjustment. LA5 was administered daily together with a high-fat diet (HFD) for 8 weeks in mice. Furthermore, the condition media of LA5 was also tested in a hepatocyte cell-line (HepG2 cells). Accordingly, LA5 attenuated obesity in mice as demonstrated by weight reduction, regional fat accumulation, lipidemia, liver injury (liver weight, lipid compositions, and liver enzyme), gut permeability defect, endotoxemia, and serum cytokines. Unsurprisingly, LA5 improved these parameters and acidified fecal pH leads to the attenuation of fecal dysbiosis. The fecal microbiome analysis in obese mice with or without LA5 indicated; (i) decreased Bacteroidetes (Gram-negative anaerobes that predominate in non-healthy conditions), (ii) reduced total fecal Gram-negative bacterial burdens (the sources of gut LPS), (iii) enhanced Firmicutes (Gram-positive bacteria with potential benefits) and (iv) increased Verrucomycobia, especially Akkermansia muciniphila, a bacterium with the anti-obesity property. With LA5 administration, A. muciniphila in the colon were more than 2,000 folds higher than the regular diet mice as determined by 16S rRNA. Besides, LA5 produced anti-inflammatory molecules with a similar molecular weight to LPS that reduced cytokine production in LPS-activated HepG2 cells. In conclusion, LA5 attenuated obesity through (i) gut dysbiosis attenuation, partly through the promotion of A. muciniphila (probiotics with the difficulty in preparation processes), (ii) reduced endotoxemia, and (iii) possibly decreased liver injury by producing the anti-inflammatory molecules.

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Obesity Exacerbates Lupus Activity in Fc Gamma Receptor IIb Deficient Lupus Mice Partly through Saturated Fatty Acid-Induced Gut Barrier Defect and Systemic Inflammation

Udompornpitak¹,

Charoensappakit²,

Sae-khow³

et al. 2022

J Innate Immun

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The prevalence of obesity is increasing, and the coexistence of obesity and systemic lupus erythematosus (lupus) is possible. A high-fat diet (HFD) was orally administered for 6 months in female 8-week-old Fc gamma receptor IIb deficient (FcgRIIb−/−) lupus or age and gender-matched wild-type (WT) mice. Lupus nephritis (anti-dsDNA, proteinuria, and increased creatinine), gut barrier defect (fluorescein isothiocyanate dextran), serum lipopolysaccharide (LPS), serum interleukin (IL)-6, liver injury (alanine transaminase), organ fibrosis (liver and kidney pathology), spleen apoptosis (activated caspase 3), and aorta thickness (but not weight gain and lipid profiles) were more prominent in HFD-administered FcgRIIb−/− mice than the obese WT, without injury in regular diet-administered mice (both FcgRIIb−/− and WT). In parallel, combined palmitic acid (PA; a saturated fatty acid) with LPS (PA + LPS) induced higher tumor necrotic factor-α, IL-6, and IL-10 in the supernatant, inflammatory genes (inducible nitric oxide synthase and IL-1β), reactive oxygen species (dihydroethidium), and glycolysis with reduced mitochondrial activity (extracellular flux analysis) when compared with the activation by each molecule alone in both FcgRIIb−/− and WT macrophages. However, the alterations of these parameters were more prominent in PA + LPS-administered FcgRIIb−/− than in the WT cells. In conclusion, obesity accelerated inflammation in FcgRIIb−/− mice, partly due to the more potent responses from the loss of inhibitory FcgRIIb against PA + LPS with obesity-induced gut barrier defect.

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The Relationship between Cutaneous Wounds Made on Obese Mice or Those with Decreased Body Weight and Serum Leptin Level

Cited by 7 publications

References 27 publications

Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Lactobacillus acidophilus LA5 improves saturated fat-induced obesity mouse model through the enhanced intestinal Akkermansia muciniphila

Obesity Exacerbates Lupus Activity in Fc Gamma Receptor IIb Deficient Lupus Mice Partly through Saturated Fatty Acid-Induced Gut Barrier Defect and Systemic Inflammation

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