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Journal articles on the topic 'Hight fat Diet'

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Published: 10 March 2023
Last updated: 11 March 2023

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1

Dewi, Ervina, Fadliyani Fadliyani, and Ismiranda Ismiranda. "ANALISIS POTENSI ANTIHIPERKOLESTEROLEMIA EKSTRAK ETANOL BUAH ASAM JAWA (Tamarindus indica L) TERHADAP STRUKTUR MIKROSKOPIS HATI MENCIT (Mus musculus)." Jurnal Kedokteran Syiah Kuala 18, no. 2 (August 1, 2018): 86–92. http://dx.doi.org/10.24815/jks.v18i2.17998.

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Abstrak. Penelitian ini bertujuan untuk mengetahui potensi antihiperkolesterolemia ekstrak etanol buah asam jawa terhadap struktur mikroskopis hati mencit. Rancangan yang digunakan adalah Rancangan Acak Lengkap, terdiri atas 6 perlakuan dan 4 ulangan. Perlakuan terdiri atas Pemberian pakan standard dan akuades (P0), pakan aterogenik dan Aquades (P1), pakan aterogenik dan simvastatin 10 mg (P2), pakan aterogenik dan ekstrak asam jawa 5, 25 dan 50 mg/kg bb (P3, P4, P5). Volume simvastatin dan ekstrak etanol buah asam jawa adalah 0,5mL. Pembuatan sediaan histologis menggunakan metode parafin. Parameter yang diamati adalah kadar kolesterol total, infiltrasi lemak, degenerasi lemak dan nekrosa hepatosit. Data hasil penelitian dianalisis dengan analisis varian dan dilanjutkan dengan Uji Berjarak ganda Duncan. Hasil penelitian menunjukkan ekstrak etanol buah asam jawa berpengaruh nyata dalam menurunkan rerata infiltrasi lemak, degenerasi lemak dan nekrosa sel hati yan diindikasikan dengan penurunan kadar kolesterol secara bermakna. Kesimpulannya, ekstrak etanol buah asam jawa mampu menurunkan rerata infiltrasi lemak, degenerasi lemak dan nekrosa sel hati mencit akibat pakan aterogenikKata Kunci : Pakan Aterogenik, Hiperkolesterolemia, Hati, Ekstrak Etanol Buah Asam Jawa, SimvastatinAbstract. This research aimed to determine the potential antihypercholesterolemic of ethanol extract of tamarind at heart microscopic structure of mice induced with high cholesterol diet. A completely randomized-block design was used with 6 treatments and 4 repetitions of eachtreatment. The treatments were normal diet and aquadest (P0), hight-fat diet and aquadest (P1), hight-fat diet and Simvastatin 10 mg/Kg (P2), hight-fat diet and tamarind extract 5, 25 and 50 mg/Kg (P3, P4, P5). The volume of Simvastatin and tamarind extract given to each mice is 0,5 mL. Paraffin method was apllied of microscopic structure observation. The parameters observed were total cholesterol level, lipid infiltration, lipid degeneration and necrosis of hepatocyte of hepatocyte. A variance analysis followed by Duncan Multiple Range Test was tested to the data mice microscopic structure. The result showed that etnanol extract of tamarind could significant to decrease of lipid infiltration, lipid degeneration and necrosis of hepatocyte showed decrease total cholesterol level. Inconlusion, the that etnanol extract of tamarind could significant to decrease of lipid infiltration, lipid degeneration and necrosis of hepatocyte due to hight-fat diet.Key Word : Atherogenic Feed, Hypercholesterolemia, Liver, Ethanol Extract of Tamarind, Simvastatin
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2

Hadi, Novian Swasono, Arta Farmawati, and Ahmad Ghozali. "Pencegahan hipertensi dan penebalan dinding aorta dengan pemberian kecambah kacang hijau (Phaseolus radiatus (L)) pada tikus putih Sprague Dawley." Jurnal Gizi Klinik Indonesia 12, no. 3 (January 30, 2016): 116. http://dx.doi.org/10.22146/ijcn.22454.

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Background: Lifestyle changes with high-fat food consumption is one of the factors the risks of cardiovascular diseases like of coronary heart disease and atherosclerosis. A healthy diet and a balanced diet and consume foods that contain lots of antioxidants is one of the effective ways to prevent hyperlipidemia. Mung bean sprouts have properties that neutralize free radicals cause Hyperlipidemia and cardiovascular diseases because it is an antioxidant compound.Objective: The aim of this study was to determinate the effect of mung bean sprouts (Phaseolus radiatus (L)) to blood pressure and histopathology aorta of Sprague-Dawley male rats.Method: The type of study was experimental research using pre-post test controlled group design for blood pressure variable and post test only controlled group design histopathology aorta. The thirty-five of Sprague-Dawley male rats was eight weeks divided into 5 groups. The first group was given standard diet, group 2 was given a hight fat diet, the third group was given a high-fat diet and mung bean sprout 0,67 gram, group 4 was given a high-fat diet and mung bean 1,34 gram, and group 5 was given a high-fat diet and vitamin E doses of 23 IU.Results: Result of this study showed that after 4 weeks of treatment, increased in blood pressure systole in the given of high fat diet higher than group who were given a high fat diet and mung bean sprout and also on group who were given high fat diet and vitamin E, but there is no difference effect a decrease in blood pressure between the provision of mung bean sprouts and vitamin E (p>0,05). Statistical analysis to thick the wall the aorta show the similarity meaningful in all the treatment group, it can be said that overall thick the wall the aorta in this research is not different.Conclusion: A dose of mung bean sprout 0,67 g is optimal doses in preventing a rise in blood pressure and prevent alterations histopathology Sprague-Dawley male rats.
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3

Samiilenko, Natalia, Vira Khorunzha, Hanna Bielokoz, Olga Bezugla, Karina Deineko, Marta Lisevych, Olha Aleksieieva, Diana Zubach, and Olena Alypova. "The Effect of Chronobiology and Variety of Macronutrients on BMI, Waist, Body Fat and HOMA-IR in Patients with Metabolic Syndrome." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1685. http://dx.doi.org/10.1093/cdn/nzaa063_083.

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Abstract Objectives The aim of this study was to assess the effect of both meal timing and diet composition on BMI, waist, body fat and HOMA-IR in patients with metabolic syndrome (MS). Methods We studied 77 patients with MS (32 men and 45 women). Detailed analysis of baseline food-diaries showed that 43 patients (56%) were mostly eating after 3 p.m., generally skipping breakfast, and had more frequent carbohydrate snacks. We divided patients into two groups. The first group consisted of patients with most caloric intake after 3 PM, and the second group included patients who were evenly consuming their food throughout the day. Following diet were offered: 3-fold meal (food intake was at 7–9a.m., 1–2p.m. and 6–7p.m.) with very low-carbohydrate (LC) breakfast and dinner, lunch consisted of LC, proteins (P), polyunsaturated fatty acids (PUFAs) and non-starchy vegetables(V); there were absolutely no snacks during the day. Daily calorie intake was reduced by 20% from baseline. Diet intervention lasted 12 weeks. No medication were used during this period. Results 60 patients completed the trial (32 and 28 patients in first and second groups respectively). BMI was reduced from 33,1 ± 5,0 kg/m2 to 29,8 ± 4,6 kg/m2, the effect was similar in both groups (Cohen's d = 0,7, P = 0003). Mean body fat decreased from 40,7 ± 7,0% to 35,8 ± 7,5% in 12 weeks and treatment effect was more pronounced in second group (Cohen's d = 0,76, P = 0007). The most significant changes were observed in HOMA-IR, which decreased from 4,0 ± 1,1 to 2,1 ± 1,1, treatment effect was also more pronounced in second group (Cohen's d = 1,22, P = 0001). Waist circumference statistically decreased too (from 100,9 ± 16,8сm to 92,0 ± 14,6сm), although with more modest effect - Cohen's d = 0,58, P = 0003. Maximum effect size was in HOMA-IR changes. whereas minimum in waist circumference. Conclusions Our findings demonstrate that this diet (low carb, hight fat, 3-fold meal diet with lunch before 3 p.m.) is associated with statistically different changes in BMI, waist, body fat and HOMA-IR and the intervention was more effective among patients in second group. Funding Sources Not funded.
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4

Baz, Lina, Salha Algarni, Mona Al-thepyani, Abdullah Aldairi, and Hana Gashlan. "Lycopene Improves Metabolic Disorders and Liver Injury Induced by a Hight-Fat Diet in Obese Rats." Molecules 27, no. 22 (November 10, 2022): 7736. http://dx.doi.org/10.3390/molecules27227736.

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Epidemiological studies have shown that the consumption of a high-fat diet (HFD) is positively related to the development of obesity. Lycopene (LYC) can potentially combat HFD-induced obesity and metabolic disorders in rats. This study aimed to investigate the effect of LYC on metabolic syndrome and assess its anti-inflammatory and antioxidant effects on the liver and adipose tissue in rats fed an HFD. Thirty-six male Wistar albino rats were divided into three groups. Group Ι (the control group) was fed a normal diet, group ΙΙ (HFD) received an HFD for 16 weeks, and group ΙΙΙ (HFD + LYC) received an HFD for 12 weeks and then LYC (25 mg/kg b.wt) was administered for four weeks. Lipid peroxidation, antioxidants, lipid profile, liver function biomarkers, and inflammatory markers were determined. The results showed that long-term consumption of an HFD significantly increased weight gain, liver weight, and cholesterol and triglyceride levels. Rats on an HFD displayed higher levels of lipid peroxidation and inflammatory markers. Moreover, liver and white adipose tissue histopathological investigations showed that LYC treatment mended the damaged tissue. Overall, LYC supplementation successfully reversed HFD-induced changes and shifts through its antioxidant and anti-inflammatory activity. Therefore, LYC displayed a therapeutic potential to manage obesity and its associated pathologies.
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5

Sokolova, I. B. "Effects of Metabolic Disorders and Streptozotocin-Induced Diabetes on Cerebral Circulation in Rats on a Hight-Fat Diet." Journal of Evolutionary Biochemistry and Physiology 58, no. 3 (May 2022): 915–21. http://dx.doi.org/10.1134/s0022093022030255.

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6

Chen, D., J. Kang, L. Li, and H. Ma. "Long-term administration of DHEA prevents fat deposition in rats fed a high-fat diet." Czech Journal of Animal Science 61, No. 4 (July 15, 2016): 177–85. http://dx.doi.org/10.17221/8849-cjas.

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7

P. Angelova, P. Angelova, N. Boyadjiev N. Boyadjiev, and K. Georgieva K. Georgieva. "Aerobic Capacity of Rats Subjected to a Combined High-Fat-Carbohydrate Diet." Indian Journal of Applied Research 3, no. 10 (October 1, 2011): 1–3. http://dx.doi.org/10.15373/2249555x/oct2013/8.

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8

Leitch, Harry G., and Petra Hajkova. "Eggs sense high-fat diet." Nature Genetics 50, no. 3 (March 2018): 318–19. http://dx.doi.org/10.1038/s41588-018-0068-1.

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9

Mukai, Rieko. "High-fat diet and constipation." Free Radical Biology and Medicine 120 (May 2018): S134—S135. http://dx.doi.org/10.1016/j.freeradbiomed.2018.04.443.

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10

Hao, Yilin, Toshihiro Tsuruda, Yoko Sekita-Hatakeyama, Sumiharu Sakamoto, and Kazuo Kitamura. "A high-fat diet is deleterious to mice under glycolysis restriction." Applied Physiology, Nutrition, and Metabolism 43, no. 4 (April 2018): 419–22. http://dx.doi.org/10.1139/apnm-2017-0506.

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It is debated whether carbohydrate restriction has metabolic advantage for its variable weight loss. Five-week-old male mice fed a high-fat diet and receiving a glycolytic inhibitor, 2-deoxyglucose, died within 9 days. They exhibited greater decreases in rectal temperature, appetite, and decline in body weight accompanied by increasing total cholesterol level than the other groups. This study suggests that carbohydrate is necessary for adequate physical and metabolic performance when lipid-rich diet is loaded.
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11

Asqari, Qazaleh, Farhad Gholami, Jabbar Bashiri, and Adel Donyaei. "High-intensity interval training ameliorates high-fat diet-induced elevation of aminotransferases in male Wistar rats." Journal of Shahrekord University of Medical Sciences 23, no. 3 (September 29, 2021): 111–15. http://dx.doi.org/10.34172/jsums.2021.19.

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Background and aims: A high-fat diet increases triglyceride (TG) accumulations in hepatocytes and results in non-alcoholic fatty liver diseases (NAFLDs). In this regard, this study investigated the effect of high-intensity interval training (HIIT), along with a high-fat diet on the serum levels of aminotransferases in male Wistar rats. Methods: Forty male Wistar rats were randomly assigned to the standard diet, high-fat diet, exercise + standard diet, and exercise + high-fat diet groups (each containing 10 animals). HIIT program consisted of 6-12 repetitions of 2-minute highs-intensity exercise (85-90% of the maximum speed) interspersed with 1-minute low-intensity exercise (45-50% peak speed) with the frequency of 5 sessions a week over 12 weeks. High-fat diet groups received a diet regimen including 58% fat, 25% protein, and 17% carbohydrate, ad libitum. The blood samples were taken from the left ventricle 48 hours following the last intervention to assess TG, alanine aminotransferase (ALT), and aspartate amino-transferase (AST) concentrations. Data were analyzed using one-way ANOVA and Tukey’s post-hoc tests. Results: The findings showed the mean of ALT, AST, and TG in the high-fat diet group was significantly greater compared to the standard diet group (P=0.001). Furthermore, the mean of ALT, AST, and TG in the exercise + high-fat diet group was significantly lower in comparison with the high-fat diet group (P=0.01, P=0.017, and P=0.012, respectively). Conclusion: Although HIIT ameliorated high-fat diet-induced elevations in the serum levels of TG, ALT, and AST, they did not reach the baseline levels. Thus, it may indicate that a diet as the underlying cause of NAFLDs is more important than any other interventions such as exercise.
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12

NAKASHIMA, Yoko. "Zinc's Role in Rat Preference for a Low-Fat Diet in a Two-Choice Diet Program of Low- and High-Fat Diets." Journal of Nutritional Science and Vitaminology 57, no. 1 (2011): 42–47. http://dx.doi.org/10.3177/jnsv.57.42.

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13

Hohos, Natalie M., and Malgorzata E. Skaznik-Wikiel. "High-Fat Diet and Female Fertility." Endocrinology 158, no. 8 (June 6, 2017): 2407–19. http://dx.doi.org/10.1210/en.2017-00371.

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14

Chang, Richard Cheng-An, Liheng Shi, Cathy Chia-Yu Huang, Andy Jeesu Kim, Michael L. Ko, Beiyan Zhou, and Gladys Y. P. Ko. "High-Fat Diet–Induced Retinal Dysfunction." Investigative Opthalmology & Visual Science 56, no. 4 (April 22, 2015): 2367. http://dx.doi.org/10.1167/iovs.14-16143.

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15

Stenholm, C. W. "The high-priority/low-fat diet." Academic Medicine 68, no. 3 (March 1993): 198–200. http://dx.doi.org/10.1097/00001888-199303000-00005.

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16

Dirkx, Ellen, Robert W. Schwenk, Jan F. C. Glatz, Joost J. F. P. Luiken, and Guillaume J. J. M. van Eys. "High fat diet induced diabetic cardiomyopathy." Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) 85, no. 5 (November 2011): 219–25. http://dx.doi.org/10.1016/j.plefa.2011.04.018.

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17

Leong, Ivone. "Metabolic adaptations to high-fat diet." Nature Reviews Endocrinology 14, no. 12 (October 1, 2018): 689. http://dx.doi.org/10.1038/s41574-018-0108-z.

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18

Bheda, Poonam, and Cynthia Wolberger. "Sirtuin on a high-fat diet." Nature 496, no. 7443 (April 2013): 41–42. http://dx.doi.org/10.1038/496041a.

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19

STORLIEN, L. H., D. A. PAN, A. D. KRIKETOS, and L. A. BAUR. "High Fat Diet-Induced Insulin Resistance." Annals of the New York Academy of Sciences 683, no. 1 Dietary Lipid (June 1993): 82–90. http://dx.doi.org/10.1111/j.1749-6632.1993.tb35694.x.

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20

Hwang, S., LK Sarna, YL Siow, and K O. "High Fat Diet Disrupts Homocysteine Metabolism." Canadian Journal of Cardiology 29, no. 10 (October 2013): S168—S169. http://dx.doi.org/10.1016/j.cjca.2013.07.256.

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21

Galvao, Tatiana F., Bethany H. Brown, Kelly O'Connell, Peter Hecker, and William C. Stanley. "TREATMENT WITH A HIGH UNSATURATED FAT DIET, COMPARED WITH HIGH SATURATED FAT DIET OR LOW FAT DIET, INCREASES FAT PAD MASS, FREE FAT ACIDS LEVELS, AND MORTALITY IN CARDIOMYOPATHIC HAMSTERS." Journal of the American College of Cardiology 57, no. 14 (April 2011): E284. http://dx.doi.org/10.1016/s0735-1097(11)60284-2.

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22

Han, Kyu-Ho, Chang-Hyun Lee, Mikio Kinoshita, Chan-Ho Oh, Ken-ichiro Shimada, and Michihiro Fukushima. "Spent turmeric reduces fat mass in rats fed a high-fat diet." Food & Function 7, no. 4 (2016): 1814–24. http://dx.doi.org/10.1039/c5fo00764j.

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The industrial waste product spent turmeric remarkably reduced obesity in rats fed a high-fat diet. The mesentery adipocyte' size in rats fed a STP diet was smaller than that in rats fed a control diet with or without antibiotic cocktail.
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23

Licholai, Julia A., Katrina P. Nguyen, Wambura C. Fobbs, Corbin J. Schuster, Mohamed A. Ali, and Alexxai V. Kravitz. "Why Do Mice Overeat High-Fat Diets? How High-Fat Diet Alters the Regulation of Daily Caloric Intake in Mice." Obesity 26, no. 6 (April 29, 2018): 1026–33. http://dx.doi.org/10.1002/oby.22195.

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24

Erickson, Robert P., Achyut Bhattacharyya, Robert J. Hunter, Randall A. Heidenreich, and Nathan J. Cherrington. "Liver disease with altered bile acid transport in Niemann-Pick C mice on a high-fat, 1% cholesterol diet." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 2 (August 2005): G300—G307. http://dx.doi.org/10.1152/ajpgi.00568.2004.

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Cholestatic hepatitis is frequently found in Niemann-Pick C (NPC) disease. We studied the influence of diet and the low density lipoprotein receptor (LDLR, Ldlr in mice, known to be the source of most of the stored cholesterol) on liver disease in the mouse model of NPC. Npc1−/− mice of both sexes, with or without the Ldlr knockout, were fed a 18% fat, 1% cholesterol (“high-fat”) diet and were evaluated by chemical and histological methods. Bile acid transporters [multidrug resistance protein (Mrps) 1–5; Ntcp, Bsep, and OatP1, 2, and 4] were quantitated by real-time RT-PCR. Many mice died prematurely (within 6 wk) with hepatomegaly. Histopathology showed an increase in macrophage and hepatocyte lipids independent of Ldlr genotype. Non-zone-dependent diffuse fibrosis was found in the surviving mice. Serum alanine aminotransferase was elevated in Npc1−/− mice on the regular diet and frequently became markedly elevated with the high-fat diet. Serum cholesterol was increased in the controls but not the Npc1−/− mice on the high-fat diet; it was massively increased in the Ldlr−/− mice. Esterified cholesterol was greatly increased by the high-fat diet, independent of Ldlr genotype. γ-Glutamyltransferase was also elevated in Npc1−/− mice, more so on the high-fat diet. Mrps 1–5 were elevated in Npc1−/− liver and became more elevated with the high-fat diet; Ntcp, Bsep, and OatP2 were elevated in Npc1−/− liver and were suppressed by the high-fat diet. In conclusion, Npc1−/− mice on a high-fat diet provide an animal model of NPC cholestatic hepatitis and indicate a role for altered bile acid transport in its pathogenesis.
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Hsu, Mei-Hsin, Jiunn-Ming Sheen, I.-Chun Lin, Hong-Ren Yu, Mao-Meng Tiao, You-Lin Tain, and Li-Tung Huang. "Effects of Maternal Resveratrol on Maternal High-Fat Diet/Obesity with or without Postnatal High-Fat Diet." International Journal of Molecular Sciences 21, no. 10 (May 12, 2020): 3428. http://dx.doi.org/10.3390/ijms21103428.

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To examine the effects of maternal resveratrol in rats borne to dams with gestational high-fat diet (HFD)/obesity with or without postnatal high-fat diet. We first tested the effects of maternal resveratrol intake on placenta and male fetus brain in rats borne to dams with gestational HFD/obesity. Then, we assessed the possible priming effect of a subsequent insult, male offspring were weaned onto either a rat chow or a HFD. Spatial learning and memory were assessed by Morris water maze test. Blood pressure and peripheral insulin resistance were examined. Maternal HFD/obesity decreased adiponectin, phosphorylation alpha serine/threonine-protein kinase (pAKT), sirtuin 1 (SIRT1), and brain-derived neurotrophic factor (BDNF) in rat placenta, male fetal brain, and adult male offspring dorsal hippocampus. Maternal resveratrol treatment restored adiponectin, pAKT, and BDNF in fetal brain. It also reduced body weight, peripheral insulin resistance, increased blood pressure, and alleviated cognitive impairment in adult male offspring with combined maternal HFD and postnatal HFD. Maternal resveratrol treatment restored hippocampal pAKT and BDNF in rats with combined maternal HFD and postnatal HFD in adult male offspring dorsal hippocampus. Maternal resveratrol intake protects the fetal brain in the context of maternal HFD/obesity. It effectively reduced the synergistic effects of maternal HFD/obesity and postnatal HFD on metabolic disturbances and cognitive impairment in adult male offspring. Our data suggest that maternal resveratrol intake may serve as an effective therapeutic strategy in the context of maternal HFD/obesity.
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Lee, Ji Min, Tahmarah Otoo, Marisol Brito, Amanda Jaimes, Arlene Martinez, and Jennifer Trevitt. "Effects of High-Sucrose and High-Saturated Fat Diets on Learning Abilities in Old Sprague-Dawley Rats." Californian Journal of Health Promotion 19, no. 1 (September 8, 2021): 84–94. http://dx.doi.org/10.32398/cjhp.v19i1.2653.

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With an increase in longevity, many studies have explored the influences of different lifestyle factors on successful aging. This study hypothesizes that older rats fed with a nutritionally balanced standard diet would perform better on learning tasks than rats fed with either a high-sucrose or a high-saturated fat. It also hypothesizes that older rats fed with a high-sucrose diet would perform better than those fed with a high-saturated fat. The learning abilities of the 15-month-old rats (N = 36) were assessed by conducting forward and reverse learning tasks using a T-maze apparatus. The results showed that rats on a nutritionally balanced diet performed significantly better on both learning tasks than those on either the high-sucrose or the high-saturated fat (p’s < .05). This may be due to the fact that the high-sucrose and high-saturated fat diets exacerbated a cognitive decline in geriatric rats. There was no significant difference between the learning abilities of the rats on a high-sucrose or high-saturated fat diet (p’s > .05). This finding suggests that, at an older age, both high-sucrose and high-saturated fat diets have a similarly detrimental influence on cognitive health.
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Ramadan, Mohamed F., R. Zayed, M. Abozid, and M. M. S. Asker. "Apricot and pumpkin oils reduce plasma cholesterol and triacylglycerol concentrations in rats fed a high-fat diet." Grasas y Aceites 62, no. 4 (September 28, 2011): 443–52. http://dx.doi.org/10.3989/gya.032911.

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28

Tain, You-Lin, and Chien-Ning Hsu. "Maternal High-Fat Diet and Offspring Hypertension." International Journal of Molecular Sciences 23, no. 15 (July 25, 2022): 8179. http://dx.doi.org/10.3390/ijms23158179.

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The incidence of hypertension has increased to epidemic levels in the past decades. Increasing evidence reveals that maternal dietary habits play a crucial role in the development of hypertension in adult offspring. In humans, increased fat consumption has been considered responsible for obesity and associated diseases. Maternal diets rich in saturated fats have been widely employed in animal models to study various adverse offspring outcomes. In this review, we discussed current evidence linking maternal high-fat diet to offspring hypertension. We also provided an in-depth overview of the potential mechanisms underlying hypertension of developmental origins that are programmed by maternal high-fat intake from animal studies. Furthermore, this review also presented an overview of how reprogramming interventions can prevent maternal high-fat-diet-induced hypertension in adult offspring. Overall, recent advances in understanding mechanisms behind programming and reprogramming of maternal high-fat diet on hypertension of developmental origins might provide the answers to curtail this epidemic. Still, more research is needed to translate research findings into practice.
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Sim, Young-Je. "A Low-carbohydrate and High-fat Diet." Korean Journal of Obesity 25, no. 4 (December 30, 2016): 188–89. http://dx.doi.org/10.7570/kjo.2016.25.4.188.

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30

Brown, R. C. "EXERCISE ENDURANCE ON A HIGH FAT DIET." Medicine & Science in Sports & Exercise 27, Supplement (May 1995): S12. http://dx.doi.org/10.1249/00005768-199505001-00069.

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31

McNay, David E. G., and John R. Speakman. "High fat diet causes rebound weight gain." Molecular Metabolism 2, no. 2 (April 2013): 103–8. http://dx.doi.org/10.1016/j.molmet.2012.10.003.

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32

Mykoniatis, Andreas, Joseph Pierre, Candace Cham, Dengping Yin, John Alverdy, and Eugene Chang. "Enterohormones Down-Regulated in High-Fat Diet." American Journal of Gastroenterology 109 (October 2014): S113. http://dx.doi.org/10.14309/00000434-201410002-00373.

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33

Leitch, Harry G., and Petra Hajkova. "Publisher Correction: Eggs sense high-fat diet." Nature Genetics 50, no. 8 (June 21, 2018): 1196. http://dx.doi.org/10.1038/s41588-018-0137-5.

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34

van den Heijkant, A. C., M. D. P. Luyer, and W. A. Buurman. "High Fat Diet and Gut Barrier Function." Current Nutrition & Food Science 9, no. 2 (April 1, 2013): 108–12. http://dx.doi.org/10.2174/1573401311309020005.

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35

Lapachet, R. A., W. C. Miller, and D. A. Arnall. "Body fat and exercise endurance in trained rats adapted to a high-fat and/or high-carbohydrate diet." Journal of Applied Physiology 80, no. 4 (April 1, 1996): 1173–79. http://dx.doi.org/10.1152/jappl.1996.80.4.1173.

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To study how diet composition affects exercise endurance and body composition, 48 male Sprague-Dawley rats were treadmill trained for 8 wk while consuming either a high-fat (F) diet or high-carbohydrate (C) diet. The diets were switched for one-half the number of rats in each group 3 days before the animals were killed, during which feeding time the rats did not exercise. One-half of rats receiving each of the four diet combinations were taken at rest (R) or exhaustion (E), resulting in eight groups: CCR, CFR, FFR, FCR, CCE CFE, FFE, and FCE. An analysis of variance revealed that resting glycogen in the FCR group was enhanced in muscle (19-33%) and liver (23%) compared with controls. Each F group's exercise time to exhaustion [CFE, 322.9 +/- 25.0; FFE, 356.8 +/- 37.8; FCE, 467.0 +/- 32.6 (SE) min] was different (P < 0.05) from control (CCE, 257.5 +/- 29.2 min). Postexercise glycogen was equivalent among all dietary groups, were muscle triglycerides. The FF and FC groups had higher 3-hydroxyacyl-CoA dehydrogenase activity in soleus muscle than either CC or CF animals. After training, body weights were similar between the two dietary groups; however, percent body fat was 17% greater after the F diet, even though F diet animals voluntarily consumed 12% less energy than did C diet animals. These data suggest that exercise endurance time is optimized in trained rats that receive a carbohydrate load after adaptation to a F diet. However, despite intense exercise training, the F diet promotes body fat deposition, and the health consequences of following such a regimen are still unknown.
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Santoro Leonardi-Carvalho, Daphne. "Metabolic Differences in the Steatosis Induced by a High-Fat Diet and High-Protein-Fat Diet in Rats." Advances in Biochemistry 3, no. 6 (2015): 86. http://dx.doi.org/10.11648/j.ab.20150306.14.

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Chicco, Adam J., Genevieve C. Sparagna, Sylvia A. McCune, Christopher A. Johnson, Robert C. Murphy, David A. Bolden, Meredith L. Rees, Ryan T. Gardner, and Russell L. Moore. "Linoleate-Rich High-Fat Diet Decreases Mortality in Hypertensive Heart Failure Rats Compared With Lard and Low-Fat Diets." Hypertension 52, no. 3 (September 2008): 549–55. http://dx.doi.org/10.1161/hypertensionaha.108.114264.

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Recent studies indicate that high-fat diets may attenuate cardiac hypertrophy and contractile dysfunction in chronic hypertension. However, it is unclear whether consuming a high-fat diet improves prognosis in aged individuals with advanced hypertensive heart disease or the extent to which differences in its fatty acid composition modulate its effects in this setting. In this study, aged spontaneously hypertensive heart failure rats were administered a standard high-carbohydrate diet or high-fat diet (42% of kilocalories) supplemented with high-linoleate safflower oil or lard until death to determine their effects on disease progression and mortality. Both high-fat diets attenuated cardiac hypertrophy, left ventricular chamber dilation, and systolic dysfunction observed in rats consuming the high-carbohydrate diet. However, the lard diet significantly hastened heart failure mortality compared with the high-carbohydrate diet, whereas the linoleate diet significantly delayed mortality. Both high-fat diets elicited changes in the myocardial fatty acid profile, but neither had any effect on thromboxane excretion or blood pressure. The prosurvival effect of the linoleate diet was associated with a greater myocardial content and linoleate-enrichment of cardiolipin, an essential mitochondrial phospholipid known to be deficient in the failing heart. This study demonstrates that, despite having favorable effects on cardiac morphology and function in hypertension, a high-fat diet may accelerate or attenuate mortality in advanced hypertensive heart disease depending on its fatty acid composition. The precise mechanisms responsible for the divergent effects of the lard and linoleate-enriched diets merit further investigation but may involve diet-induced changes in the content and/or composition of cardiolipin in the heart.
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Chiang Morales, Milton D., Chao-Yuan Chang, Van Long Le, I.-Tao Huang, I.-Lin Tsai, Hung-Jen Shih, and Chun-Jen Huang. "High-Fructose/High-Fat Diet Downregulates the Hepatic Mitochondrial Oxidative Phosphorylation Pathway in Mice Compared with High-Fat Diet Alone." Cells 11, no. 21 (October 29, 2022): 3425. http://dx.doi.org/10.3390/cells11213425.

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Both high-fat diet (HFD) alone and high-fructose plus HFD (HFr/HFD) cause diet-induced non-alcoholic fatty liver disease in murine models. However, the mechanisms underlying their impacts on inducing different levels of liver injury are yet to be elucidated. This study employed a proteomic approach to elucidate further on this issue. Adult male C57BL/6J mice were allocated to the HFD or the HFr/HFD group. After feeding for 12 weeks, all mice were euthanized and samples were collected. The proteomic profiles in liver tissues were analyzed using liquid chromatography–tandem mass spectrometry followed by canonical pathway analysis. We demonstrated that the mitochondrial oxidative phosphorylation (OXPHOS) pathway was the most significantly downregulated canonical pathway in the HFr/HFD group when compared with the HFD group. Within the OXPHOS pathway, the HFr/HFD group demonstrated significant downregulation of complexes I and III and significant upregulation of complex IV when compared with the HFD group. Moreover, the HFr/HFD group had lower protein levels of NADH: ubiquinone oxidoreductase subunits S3, S6, A5, and A12 in complex I (p < 0.001, =0.03, <0.001, and <0.001, respectively), lower protein level of cytochrome C in complex III (p < 0.001), and higher protein level of cytochrome C oxidase subunit 2 in complex IV (p = 0.002), when compared with the HFD group. To summarize, we have demonstrated that the hepatic mitochondrial OXPHOS pathway is significantly downregulated in long-term HFr/HFD feeding when compared with long-term HFD feeding. These data support the concept that the hepatic mitochondrial OXPHOS pathway should be involved in mediating the effects of HFr/HFD on inducing more severe liver injury than HFD alone.
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Kim, Jong-Yeon, Lorraine A. Nolte, Polly A. Hansen, Dong-Ho Han, Kevin Ferguson, Paul A. Thompson, and John O. Holloszy. "High-fat diet-induced muscle insulin resistance: relationship to visceral fat mass." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2057—R2065. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2057.

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It has been variously hypothesized that the insulin resistance induced in rodents by a high-fat diet is due to increased visceral fat accumulation, to an increase in muscle triglyceride (TG) content, or to an effect of diet composition. In this study we used a number of interventions: fish oil, leptin, caloric restriction, and shorter duration of fat feeding, to try to disassociate an increase in visceral fat from muscle insulin resistance. Substituting fish oil (18% of calories) for corn oil in the high-fat diet partially protected against both the increase in visceral fat and muscle insulin resistance without affecting muscle TG content. Injections of leptin during the last 4 days of a 4-wk period on the high-fat diet partially reversed the increase in visceral fat and the muscle insulin resistance, while completely normalizing muscle TG. Restricting intake of the high-fat diet to 75% of ad libitum completely prevented the increase in visceral fat and muscle insulin resistance. Maximally insulin-stimulated glucose transport was negatively correlated with visceral fat mass ( P < 0.001) in both the soleus and epitrochlearis muscles and with muscle TG concentration in the soleus ( P < 0.05) but not in the epitrochlearis. Thus we were unable to dissociate the increase in visceral fat from muscle insulin resistance using a variety of approaches. These results support the hypothesis that an increase in visceral fat is associated with development of muscle insulin resistance.
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Sleem, Ibtesam, Ashley Toney, QinYin Shi, Soonkyu Chung, and Vicki Schlegel. "Red Kidney Beans Ameliorate the High Fat Diet-Induced Hepatic Fat Accumulation and Inflammation." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 778. http://dx.doi.org/10.1093/cdn/nzaa052_047.

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Abstract Objectives High fat diet (HFD)-induced obesity links with prevalence of metabolic dysfunction, including low-grade chronic inflammation, insulin resistance, and hepatic steatosis. Dry edible beans (DEBs) play a significant role in human nutrition as a rich source of proteins, carbohydrates, fibers, and various micronutrients. The aim of this study is to evaluate the ability of red kidney beans (RKBs) to attenuate the deleterious effects of HFD in the liver. Methods Syrian hamsters were randomly assigned with one of five experimental diet groups; low fat diet (control), high fat diet, high fat diet with 5% whole beans (HFD + B), high fat diet with 4.5% dehulled beans (HFD + DHB) and high fat diet with 0.5% hull of beans (HFD + HB) and fed for 4 weeks. Results Supplementation of RKB resulted in lower body weight, liver weight, and glucose levels (P &lt; 0.001) in HFD + B and HFD + DHB group compared to HFD group. Adding RKBs downregulated gene expressions related to inflammation (e.g., interleukin 6 (IL-6)) and lipogenesis (e.g., hepatic fatty acid synthase (FASN)) in the liver. Furthermore, RKBs supplemented groups showed reduced hepatic fat accumulation in comparison with the HFD group. Conclusions Supplementation of RKBs and their hulls attenuates hepatic stresses by decreasing the lipogenesis and inflammation, which contribute to enhancing insulin sensitivity. Funding Sources USDA Multi-Hatch, Program: W-3150.
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Melyana, Cantika Putri, Sony Wibisono Mudjanarko, Lilik Herawati, Mohammad Anam Al-Arif, and Purwo Sri Rejeki. "Effect of High Fat Diet on Body Weight, Visceral Fat Weight, and PPARG Expressions on Visceral Fat in Mice." Folia Medica Indonesiana 57, no. 3 (September 5, 2021): 186. http://dx.doi.org/10.20473/fmi.v57i3.16213.

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Obesity becomes a global epidemic nowadays. The high-fat diet is used as an alternative therapy for obesity. The optimal composition of a high-fat diet to reduce body weight is still unknown. This study aimed to determine which components of a high-fat diet can decrease body weight, visceral fat, and PPARG expression of visceral fat. This study was conducted at the Faculty of Veterinary Medicine, Universitas Airlangga, for three months by using a randomized post-test only control group design. Fifty male mice, 2-3 months old, 18-30 grams were adapted for one week given standard diet AIN93-M, then mice were divided into five groups, namely K1 (control group, 12% fat, 20% protein, 62% carbs); K2 (30% fat, 60% proteins, 0% carbs); K3 (45% fat, 45% protein, 0% carbs); K4 (60% fat, 30% protein, 0% carbs); and K5 (75% fat, 15% protein, 0% carbs). Bodyweight was measured before and after treatment, then the visceral fat and PPARG expressions were evaluated. Statistical comparisons were performed using Statistical Package for the Social Sciences (SPSS) software. After treatment, there were forty-three mice. The body weight and visceral fat weight of the mice with a high-fat diet were decreased. The most significant changes in body weight were in K4 with -9,60 ± 3,806 grams reduction. The bodyweight of mice in K5, slightly increased than K2-K4. This could be caused by the hormesis phenomenon. PPARG expressions decreased in groups with a high-fat diet but increased in K5. The composition of a high-fat diet in group K4 was the most optimal to decrease the body weight, visceral fat, and PPARG expressions in mice
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Schrauwen, P., W. D. van Marken Lichtenbelt, W. H. Saris, and K. R. Westerterp. "Changes in fat oxidation in response to a high-fat diet." American Journal of Clinical Nutrition 66, no. 2 (August 1, 1997): 276–82. http://dx.doi.org/10.1093/ajcn/66.2.276.

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Smith, Steven R., Lilian de Jonge, Jeffery J. Zachwieja, Heli Roy, Tuong Nguyen, Jennifer C. Rood, Marlene M. Windhauser, and George A. Bray. "Fat and carbohydrate balances during adaptation to a high-fat diet." American Journal of Clinical Nutrition 71, no. 2 (February 1, 2000): 450–57. http://dx.doi.org/10.1093/ajcn/71.2.450.

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Xu, Lingyan, Xinran Ma, Jieli Li, Xiaoying Li, Jianming Xu, Shu Wang, and Guang Ning. "SRC-3 deficient mice developed fat redistribution under high-fat diet." Endocrine 38, no. 1 (May 7, 2010): 60–66. http://dx.doi.org/10.1007/s12020-010-9344-2.

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Schrauwen, Patrick, Wouter D. van Marken Lichtenbelt, and Klaas R. Westerterp. "Fat and carbohydrate balances during adaptation to a high-fat diet." American Journal of Clinical Nutrition 72, no. 5 (November 1, 2000): 1239–40. http://dx.doi.org/10.1093/ajcn/72.5.1239.

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46

Blundell, John E., and John Cooling. "High-fat and low-fat (behavioural) phenotypes: biology or environment?" Proceedings of the Nutrition Society 58, no. 4 (November 1999): 773–77. http://dx.doi.org/10.1017/s0029665199001056.

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It is now widely accepted that obesity develops by way of genetic mechanisms conferring specific dispositions which interact with strong environmental pressures. It is also accepted that certain dispositions constitute metabolic risk factors for weight gain. It is less well accepted that certain patterns of behaviour (arising from biological demands or environmental influences) put individuals at risk of developing a positive energy balance and weight gain (behavioural risk factors). Relevant patterns of behaviour include long-lasting habits for selecting and eating particular types of foods. Such habits define two distinct groups characterized as high-fat (HF) and low-fat (LF) phenotypes. These habits are important because of the attention given to dietary macronutrients in body-weight gain and the worldwide epidemic of obesity. Considerable evidence indicates that the total amount of dietary fat consumed remains the most potent food-related risk factor for weight gain. However, although habitual intake of a high-fat diet is a behavioural risk factor for obesity, it does not constitute a biological inevitability. A habitual low-fat diet does seem to protect against the development of obesity, but a high-fat diet does not guarantee that an individual will be obese. Although obesity is much more prevalent among HF than LF, some HF are lean with BMI well within the normal range. The concept of 'different routes to obesity' through a variety of nutritional scenarios can be envisaged, with predisposed individuals varying in their susceptibility to different dietary inputs. In a particular subgroup of individuals (young adult males) HF and LF displayed quite different profiles of appetite control, response to nutrient challenges and physiological measures, including BMR, RQ, heart rate, plasma leptin levels and thermogenic responses to fat and carbohydrate meals. These striking differences suggest that HF and LF can be used as a conceptual tool to investigate the relationship between biology and the environment (diet) in the control of body weight.
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McAuley, K. A., C. M. Hopkins, K. J. Smith, R. T. McLay, S. M. Williams, R. W. Taylor, and J. I. Mann. "Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese women." Diabetologia 48, no. 1 (December 23, 2004): 8–16. http://dx.doi.org/10.1007/s00125-004-1603-4.

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McAuley, K. A., C. M. Hopkins, K. J. Smith, R. T. McLay, S. M. Williams, R. W. Taylor, and J. I. Mann. "Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese women." Diabetologia 48, no. 5 (April 16, 2005): 1033. http://dx.doi.org/10.1007/s00125-005-1746-y.

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Guyenet, Stephan J. "High-fat Diets: Details Matter." Obesity 17, no. 7 (July 2009): 1309. http://dx.doi.org/10.1038/oby.2009.48.

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Akowuah, Prince K., Carolina Lema, Rolando E. Rumbaut, and Alan R. Burns. "A Low-Fat/Sucrose Diet Rich in Complex Carbohydrates Reverses High-Fat/Sucrose Diet-Induced Corneal Dysregulation." International Journal of Molecular Sciences 24, no. 2 (January 4, 2023): 931. http://dx.doi.org/10.3390/ijms24020931.

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High-fat/sucrose diet feeding in mice causes loss of corneal nerve function and impairs corneal wound healing. While changing to a diet with a low fat/sugar composition and enrichments in complex carbohydrates mitigates the reduction in nerve function, it remains to be determined if it has an effect on corneal wound healing. In this study, 6-week-old C57BL/6 male mice were fed either a normal diet or a high-fat/sucrose diet for 20 weeks. A third group (diet reversal) was placed on a high-fat/sucrose diet for 10 weeks followed by a normal diet for an additional 10 weeks. A central corneal epithelial abrasion wound was created, and wound closure was monitored. Neutrophil and platelet recruitment was assessed by immunofluorescence microscopy. Mice fed the high-fat/sucrose diet-only had greater adiposity (p < 0.005) than normal diet-only fed mice; diet reversal markedly reduced adiposity. Following corneal abrasion, wound closure was delayed by ~6 h (p ≤ 0.01) and, at 30 h post-wounding, fewer neutrophils reached the wound center and fewer extravascular platelets were present at the limbus (p < 0.05). Diet restored normal wound closure and neutrophil and platelet influx in the injured cornea. These data suggest compositional changes to the diet may be an effective diet-based therapeutic strategy for maintaining or restoring corneal health.
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