scholarly journals High-Fat Diet and Alcohol Intake Promotes Inflammation and Impairs Skin Wound Healing in Wistar Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Daiane Figueiredo Rosa ◽  
Mariáurea Matias Sarandy ◽  
Rômulo Dias Novaes ◽  
Mariella Bontempo Freitas ◽  
Maria do Carmo Gouveia Pelúzio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Alcohol Intake ◽  
Skin Wound ◽  
Chow Diet ◽  
High Fat ◽  
Skin Wound Healing ◽  
Standard Chow Diet

The wound-healing process is complex and remains a challenging process under the influence of several factors, including eating habits. As improper diets may lead to disorders such as dyslipidemia, insulin resistance, and chronic inflammation, potentially affecting the tissue ability to heal, we decided to investigate the effect of a high-fat diet and alcohol intake on the inflammatory process and skin wound healing in Wistar rats. Male rats (n=30) were individually housed in cages with food and water ad libitum (registration number 213/2014). After anesthesia, at day 40, three circular wounds (12 mm diameter) were made on the back of each animal, which were then randomly assorted into five treatment groups: C1 (control 1)—water via gavage and standard chow diet; C2 (control 2)—water (no gavage) and standard chow diet; AL (alcohol)—water (no gavage) and alcohol (40%) via gavage and standard chow diet; HF (high fat)—water (no gavage) and high-fat diet (50%); and HF + AL (alcohol/high fat)—water (no gavage), alcohol (40%) via gavage, and high-fat diet. Animals were treated for 61 days. Every seven days, the area and the rate of wound contraction were evaluated. Tissue samples were removed for histopathological analysis and biochemical analyses. Our results showed that wound contraction was not complete in the HF + AL rats. Two specific indices of wound-healing impairment (total cell number and levels of the inflammatory cytokine TGF-β) were increased in the HF + AL rats. We also observed decreased type I and III collagen fibers in the HF, AL, and HF + AL groups and increased oxidative stress markers in the same groups. We suggest that a high-fat diet combined with alcohol intake contributed to delayed skin wound healing through increase of the inflammatory phase and promoting oxidative stress, which may have led to morphological alterations and impaired matrix remodeling.

scholarly journals Wound Healing in Mice with High-Fat Diet- orobGene-Induced Diabetes-Obesity Syndromes: A Comparative Study

2010 ◽  
Vol 2010 ◽  
pp. 1-15 ◽  
Author(s):  
Oliver Seitz ◽  
Christoph Schürmann ◽  
Nadine Hermes ◽  
Elke Müller ◽  
Josef Pfeilschifter ◽  
...  
Keyword(s):  
Wound Healing ◽  
High Fat Diet ◽  
Chronic Wounds ◽  
Mouse Strains ◽  
Chow Diet ◽  
High Fat ◽  
Impaired Wound Healing ◽  
Standard Chow Diet ◽  
Inflammatory State ◽  
Endothelial Growth Factor

In the past, the genetically diabetic-obesediabetes/diabetes(db/db) andobese/obese(ob/ob) mouse strains were used to investigate mechanisms of diabetes-impaired wound healing. Here we determined patterns of skin repair in genetically normal C57Bl/6J mice that were fed using a high fat diet (HFD) to induce a diabetes-obesity syndrome. Wound closure was markedly delayed in HFD-fed mice compared to mice which had received a standard chow diet (CD). Impaired wound tissue of HFD mice showed a marked prolongation of wound inflammation. Expression of vascular endothelial growth factor (VEGF) was delayed and associated with the disturbed formation of wound margin epithelia and an impaired angiogenesis in the reduced granulation tissue. Normal wound contraction was retarded and disordered. Wound disorders in obese C57Bl/6J mice were paralleled by a prominent degradation of the inhibitor of NFκB (IκB-α) in the absence of an Akt activation. By contrast to impaired wound conditions inob/obmice, late wounds of HFD mice did not develop a chronic inflammatory state and were epithelialized after 11 days of repair. Thus, only genetically obese and diabeticob/obmice finally developed chronic wounds and therefore represent a better suited experimental model to investigate diabetes-induced wound healing disorders.

scholarly journals Imaging Fibrogenesis in a Diet-Induced Model of Nonalcoholic Steatohepatitis (NASH)

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
S. V. Hartimath ◽  
R. Boominathan ◽  
V. Soh ◽  
P. Cheng ◽  
X. Deng ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Liver Fibrosis ◽  
Early Detection ◽  
Pet Imaging ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Detection Sensitivity ◽  
Chow Diet ◽  
High Fat ◽  
Standard Chow Diet

Purpose. Liver fibrosis is the hallmark of chronic nonalcoholic steatohepatitis (NASH) and is characterised by the excessive deposition of extracellular matrix proteins. Early detection and accurate staging of liver fibrosis is critically important for patient management. One of the earliest pathological markers in NASH is the activation of hepatic stellate cells (HSCs) which may be exploited as a marker of fibrogenesis. Activated HSCs secreting factors such as integrin αvβ3 propagate fibrosis. The purpose of the current study was to assess the utility of the integrin αvβ3 imaging agent [18F]FtRGD for the early detection of fibrosis in a diet-induced model of NASH longitudinally using PET imaging. Procedures. Mice were fed with either standard chow diet (SD), high-fat diet (HFD), or a choline-deficient, L-amino acid-defined high-fat fibrogenic diet (CDAHFD) to mimic the clinical pathology of liver disease and followed longitudinally for 10 weeks to assess the development of liver fibrosis using [18F]FtRGD positron emission tomography (PET) imaging. Standard blood biochemistry, histological measures, and qPCR were used to quantify integrin αvβ3, smooth muscle actin, and collagen types 1 and 6 to assess the extent of NASH pathology and accurately stage liver fibrosis. Results. The CDAHFD fibrogenic diet predictably developed hepatic inflammation and steatosis over the 10 weeks studied with little NASH pathology detected in high fat diet-treated animals. Stage 1 fibrosis was detected early by histology at day 21 and progressed to stage 2 by day 35 and stage 3 by day 56 in mice fed with CDAHFD diet only. Noninvasive imaging with [18F]FtRGD correlated well with integrin αvβ3 and was able to distinguish early mild stage 2 fibrosis in CDAHFD animals compared with standard chow diet-fed animals at day 35. When compared with high fat diet-fed animals, [18F]FtRGD was only able to distinguish later moderate stage 2 fibrosis in CDAHFD animals at day 49. Conclusions. The diet-induced progression of liver fibrosis was confirmed using histology and correlated well with the mRNA of integrin αvβ3 and extracellular matrix protein expression. [18F]FtRGD showed very good correlation between liver uptake and integrin αvβ3 expression and similar detection sensitivity to the current clinical gold standard modalities for staging of liver fibrosis.

Effects of chia (Salvia hispanica L.) on oxidative stress and inflammation in ovariectomized adult female Wistar rats

2019 ◽  
Vol 10 (7) ◽  
pp. 4036-4045 ◽  
Author(s):  
Bárbara Pereira da Silva ◽  
Renata Celi Lopes Toledo ◽  
Marcella Duarte Villas Mishima ◽  
Maria Eliza de Castro Moreira ◽  
Christiane Mileib Vasconcelos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adult Female ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Lipid Profiles ◽  
Ovariectomized Rats ◽  
High Fat ◽  
Salvia Hispanica ◽  
Female Wistar Rats ◽  
Salvia Hispanica L

The study investigated the influence of chia consumption on inflammation, oxidative stress, and lipid profiles in female ovariectomized rats fed a high-fat diet.

scholarly journals SIRT3 deficiency delays diabetic skin wound healing via oxidative stress and necroptosis enhancement

2020 ◽  
Vol 24 (8) ◽  
pp. 4415-4427
Author(s):  
Shengju Yang ◽  
Mengting Xu ◽  
Guoliang Meng ◽  
Yan Lu
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Skin Wound ◽  
Skin Wound Healing

scholarly journals Ameliorative Effects of Oral Glucosamine on Insulin Resistance and Pancreatic Tissue Damage in Experimental Wistar rats on a High-fat Diet

2021 ◽  
Author(s):  
Cornelio Barrientos ◽  
Angélica Pérez ◽  
Jorge Vázquez
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Fatty Infiltration ◽  
Pancreatic Tissue ◽  
Protein Glycosylation ◽  
Control Group ◽  
Chow Diet ◽  
High Fat ◽  
Nuclear Pyknosis

Hyperlipidemia due to a high-fat diet (HFD) is a risk factor for inducing insulin resistance (IR) and adverse effects onpancreatic β-cells in obesity and type 2 diabetes mellitus. This relationship may be due to activation of the hexosaminebiosynthesis pathway. Administration of exogenous glucosamine (GlcN) can increase the end product of this pathway(uridine-5′-diphosphate-N-acetyl-glucosamine), which can mediate IR and protein glycosylation. The objective of this study was to evaluate the effects of oral GlcN and HFD on IR and pancreatic histologic damage in a 22 wk study of 4 groups of male Wistar rats: control group with normal chow diet, HFD group (24%. g/g lard), GlcN group (500 mg/kg−1 per day of glucosamine hydrochloride in drinking water) and HFD plus oral GlcN. Metabolic variables related to IR that were measured included triglycerides (TG), free fatty acids (FFAs) and malondialdehyde (MDA). Histopathologic evaluation of the pancreas was also performed. The results showed IR in the HFD group, which had increased pancreatic nuclear pyknosis and vacuolization, with fatty infiltration and structural alteration of the islets of Langerhans. TG, FFAs and MDA were higher in serum and pancreatic tissue as compared with the control group. The GlcN group did not develop IR and had only mild nuclear pyknosis with no significant change in the pancreatic content of TG, FFAs and MDA. However, the combined administration of GlcN and HFD attenuated IR and improved TG, FFAs and MDA levels in serum and pancreatic tissue and the pancreatic histopathologic changes, with no significant differences as compared with the control group. These findings suggest that the oral GlcN at a dose of 500 mg/kg−1 is protective against IR and the pancreatic histologic damage caused by HFD.

scholarly journals The Role of Allium subhirsutum L. in the Attenuation of Dermal Wounds by Modulating Oxidative Stress and Inflammation in Wistar Albino Rats

Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 4875
Author(s):  
Mongi Saoudi ◽  
Riadh Badraoui ◽  
Ahlem Chira ◽  
Mohd Saeed ◽  
Nouha Bouali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Antioxidant Properties ◽  
Skin Wound ◽  
Bioactive Molecules ◽  
Albino Rats ◽  
Organosulfur Compounds ◽  
Skin Wound Healing ◽  
Reference Drug ◽  
Group I

In our study, Allium subhirsutum L. (AS) was investigated to assess its phenolic profile and bioactive molecules including flavonoids and organosulfur compounds. The antioxidant potential of AS and wound healing activity were addressed using skin wound healing and oxidative stress and inflammation marker estimation in rat models. Phytochemical and antiradical activities of AS extract (ASE) and oil (ASO) were studied. The rats were randomly assigned to four groups: group I served as a control and was treated with simple ointment base, group II was treated with ASE ointment, group III was treated with ASO ointment and group IV (reference group; Ref) was treated with a reference drug “Cytolcentella® cream”. Phytochemical screening showed that total phenols (215 ± 3.5 mg GAE/g) and flavonoids (172.4 ± 3.1 mg QE/g) were higher in the ASO than the ASE group. The results of the antioxidant properties showed that ASO exhibited the highest DPPH free radical scavenging potential (IC50 = 0.136 ± 0.07 mg/mL), FRAP test (IC50 = 0.013 ± 0.006 mg/mL), ABTS test (IC50 = 0.52 ± 0.03 mg/mL) and total antioxidant capacity (IC50 = 0.34 ± 0.06 mg/mL). In the wound healing study, topical application of ASO performed the fastest wound-repairing process estimated by a chromatic study, percentage wound closure, fibrinogen level and oxidative damage status, as compared to ASE, the Cytolcentella reference drug and the untreated rats. The use of AS extract and oil were also associated with the attenuation of oxidative stress damage in the wound-healing treated rats. Overall, the results provided that AS, particularly ASO, has a potential medicinal value to act as effective skin wound healing agent.

scholarly journals Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260546
Author(s):  
Mary J. Obayemi ◽  
Christopher O. Akintayo ◽  
Adesola A. Oniyide ◽  
Ayodeji Aturamu ◽  
Olabimpe C. Badejogbin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Food Intake ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Liver Lipid ◽  
Control Group ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Male Wistar Rats

Background Adipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats. Materials and methods Twenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks. Results HFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin. Conclusion Taken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.

Stimulation of NPY Y2 receptors by PYY3-36 reveals divergent cardiovascular effects of endogenous NPY in rats on different dietary regimens

2004 ◽  
Vol 286 (1) ◽  
pp. R138-R142 ◽  
Author(s):  
Ulrich Nordheim ◽  
Karl G. Hofbauer
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Chow Diet ◽  
High Fat ◽  
Standard Chow Diet ◽  
Ad Libitum

In the present experiments the gut hormone peptide YY3-36 (PYY3-36), which inhibits neuropeptide Y (NPY) release, was used as a tool to study the cardiovascular effects of endogenous NPY under different dietary regimens in rats instrumented with a telemetry transmitter. In a first experiment, rats were placed on a standard chow diet ad libitum and in a second experiment on a high-fat diet ad libitum. After 6 wk, PYY3-36 (300 μg/kg) or vehicle was injected intraperitoneally. In a third experiment, PYY3-36 or vehicle was administered after 14 days of 50% restriction of a standard chow diet. In food-restricted rats, PYY3-36 increased mean arterial pressure (7 ± 1 mmHg, mean ± SE, P < 0.001 vs. saline, 1-way repeated-measures ANOVA with Bonferroni t-test) and heart rate (22 ± 4 beats/min, P < 0.001) during 3 h after administration. Conversely, PYY3-36 did not influence mean arterial pressure (0 ± 1 mmHg) and heart rate (-8 ± 5 beats/min) significantly in rats on a high-fat diet. Rats fed standard chow diet ad libitum showed an intermediate response (mean arterial pressure 4 ± 1 mmHg, P < 0.05, and heart rate 5 ± 2 beats/min, not significant). Thus, in our studies, divergent cardiovascular responses to PYY3-36 were observed in rats on different dietary regimens. These findings suggest that the cardiovascular effects of PYY3-36 depend on the hypothalamic NPY release, which is increased after chronic food restriction and decreased during a high-fat diet.

scholarly journals Effects of High-Fat Diet and Exercise Intervention on the Metabolism Regulation of Infant Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Xiaofeng Zhu ◽  
Yun Ma ◽  
Qun Ye ◽  
Yue Shi
Keyword(s):  
High Fat Diet ◽  
Exercise Intervention ◽  
Exercise Group ◽  
Diet Group ◽  
Chow Diet ◽  
High Fat ◽  
Standard Chow Diet ◽  
Diet And Exercise ◽  
Maternal Exercise

Maternal exercise is crucial for promoting the health of the offspring. Previous studies showed that long-term maternal exercise improves energy metabolism during pregnancy. Whether swimming exercise can reverse the metabolic disorders caused by high-fat exposure in the early life of the offspring is yet to be elucidated. Three-week-old C57BL/6 female mice were randomly assigned to the standard chow diet group (SC), standard chow diet and exercise group (SC-Ex), high-fat diet group (HFD), and high-fat diet and exercise group (HFD-Ex). After swimming intervention for 13 weeks, male and female mice were caged, and the exercise intervention lasted until delivery. Then, the mothers were fed standard chow diet. A total of 8 offsprings/group were randomly selected after 4 weeks of lactation for GTT and ITT. After body composition analysis, the mice were sacrificed to obtain specimens. The levels of metabolism factors and IL-6 were measured by suspension microarray. Subsequently, 15 min after starting the GTT and ITT, the curve detected significant difference between the HFD and other groups. The body fat percentage of the HFD-Ex offspring was significantly lower than that of HFD offspring (p<0.05) irrespective of the gender. The levels of IL-6 and TG in the male offspring in the HFD-Ex group were improved significantly (p<0.05). Compared to the HFD offspring, serum glucose and GIP in the female offspring in the HFD-Ex group was significantly reduced (p<0.05). Long-term exercise of the mother effectively improved the metabolic disorder caused by high-fat exposure in the infant offspring. Thus, the metabolic inheritance of the offspring is gender-dependent; the maternal metabolism can make male offspring genetically susceptible.

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