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Liver repair diet

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https://www.readbyqxmd.com/read/27749006/an-extra-virgin-olive-oil-rich-diet-intervention-ameliorates-the-non-alcoholic-steatohepatitis-induced-by-a-high-fat-western-type-diet-in-mice
#1
Enrique Jurado-Ruiz, Lourdes M Varela, Amparo Luque, Genoveva Berná, Gladys Cahuana, Enrique Martinez-Force, Rocío Gallego-Durán, Bernat Soria, Baukje de Roos, Manuel Romero Gómez, Franz Martín
SCOPE: We evaluated the protective effect of extra virgin olive oil (EVOO) in high-fat diets (HFDs) on the inflammatory response and liver damage in a non-alcoholic fatty liver disease (NAFLD) mouse model. METHODS AND RESULTS: C57BL/6J mice fed a standard diet or a lard-based HFD (HFD-L) for 12 weeks to develop NAFLD. HFD fed mice were then divided into four groups and fed for 24 weeks with: HFD-L; HFD-EVOO; HFD-OL (phenolics-rich EVOO) and R (reversion; standard diet)...
October 17, 2016: Molecular Nutrition & Food Research
https://www.readbyqxmd.com/read/27635189/liver-cholesterol-overload-aggravates-obstructive-cholestasis-by-inducing-oxidative-stress-and-premature-death-in-mice
#2
Natalia Nuño-Lámbarri, Mayra Domínguez-Pérez, Anna Baulies-Domenech, Maria J Monte, Jose J G Marin, Patricia Rosales-Cruz, Verónica Souza, Roxana U Miranda, Leticia Bucio, Eduardo E Montalvo-Jave, María Concepción Gutiérrez-Ruiz, Carmen García-Ruiz, José C Fernández-Checa, Luis Enrique Gomez-Quiroz
Nonalcoholic steatohepatitis is one of the leading causes of liver disease. Dietary factors determine the clinical presentation of steatohepatitis and can influence the progression of related diseases. Cholesterol has emerged as a critical player in the disease and hence consumption of cholesterol-enriched diets can lead to a progressive form of the disease. The aim was to investigate the impact of liver cholesterol overload on the progression of the obstructive cholestasis in mice subjected to bile duct ligation surgery...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27609769/weight-loss-following-diet-induced-obesity-does-not-alter-colon-tumorigenesis-in-the-aom-mouse-model
#3
Kandy T Velázquez, Reilly T Enos, Meredith S Carson, Taryn L Cranford, Jackie E Bader, Ioulia Chatzistamou, Udai P Singh, Prakash S Nagarkatti, Mitzi Nagarkatti, J Mark Davis, James A Carson, E Angela Murphy
Obesity presents a significant public health concern given its association with increased cancer incidence, unfavorable prognosis, and metastasis. However, there is very little literature on the effects of weight loss, following obesity, on risk for colon cancer or liver cancer. Therefore, we sought to study whether intentional weight loss through diet manipulation was capable of mitigating colon and liver cancer in mice. We fed mice with a high-fat diet (HFD) comprised of 47% carbohydrates, 40% fat, and 13% protein for 20 wk to mimic human obesity...
October 1, 2016: American Journal of Physiology. Gastrointestinal and Liver Physiology
https://www.readbyqxmd.com/read/27556946/restricted-diet-delays-accelerated-ageing-and-genomic-stress-in-dna-repair-deficient-mice
#4
W P Vermeij, M E T Dollé, E Reiling, D Jaarsma, C Payan-Gomez, C R Bombardieri, H Wu, A J M Roks, S M Botter, B C van der Eerden, S A Youssef, R V Kuiper, B Nagarajah, C T van Oostrom, R M C Brandt, S Barnhoorn, S Imholz, J L A Pennings, A de Bruin, Á Gyenis, J Pothof, J Vijg, H van Steeg, J H J Hoeijmakers
Mice deficient in the DNA excision-repair gene Ercc1 (Ercc1(∆/-)) show numerous accelerated ageing features that limit their lifespan to 4-6 months. They also exhibit a 'survival response', which suppresses growth and enhances cellular maintenance. Such a response resembles the anti-ageing response induced by dietary restriction (also known as caloric restriction). Here we report that a dietary restriction of 30% tripled the median and maximal remaining lifespans of these progeroid mice, strongly retarding numerous aspects of accelerated ageing...
August 24, 2016: Nature
https://www.readbyqxmd.com/read/27497985/berberine-attenuates-oxidative-stress-and-hepatocytes-apoptosis-via-protecting-mitochondria-in-blunt-snout-bream-megalobrama-amblycephala-fed-high-fat-diets
#5
Kang-Le Lu, Li-Na Wang, Ding-Dong Zhang, Wen-Bin Liu, Wei-Na Xu
High-fat diets may have favorable effects on growth and cost, but high-fat diets often induce excessive fat deposition, resulting in liver damage. This study aimed to identify the hepatoprotective of a Chinese herb (berberine) for blunt snout bream (Megalobrama amblycephala). Fish were fed with a normal diet (LFD, 5 % fat), high-fat diet (HFD, 15 % fat) or berberine-supplemented diets (BSD, 15 % fat with berberine 50 or 100 mg/kg level) for 8 weeks. After the feeding, histology, oxidative status and mitochondrial function of liver were assessed...
August 6, 2016: Fish Physiology and Biochemistry
https://www.readbyqxmd.com/read/27233965/the-ron-receptor-tyrosine-kinase-regulates-macrophage-heterogeneity-and-plays-a-protective-role-in-diet-induced-obesity-atherosclerosis-and-hepatosteatosis
#6
Shan Yu, Joselyn N Allen, Adwitia Dey, Limin Zhang, Gayathri Balandaram, Mary J Kennett, Mingcan Xia, Na Xiong, Jeffrey M Peters, Andrew Patterson, Pamela A Hankey-Giblin
Obesity is a chronic inflammatory disease mediated in large part by the activation of inflammatory macrophages. This chronic inflammation underlies a whole host of diseases including atherosclerosis, hepatic steatosis, insulin resistance, type 2 diabetes, and cancer, among others. Macrophages are generally classified as either inflammatory or alternatively activated. Some tissue-resident macrophages are derived from yolk sac erythromyeloid progenitors and fetal liver progenitors that seed tissues during embryogenesis and have the ability to repopulate through local proliferation...
July 1, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27126624/laparoscopic-redo-hepaticojejunostomy-for-children-with-choledochal-cysts
#7
Mei Diao, Long Li, Wei Cheng
BACKGROUND: The current study is to evaluate the long-term efficacy of laparoscopic redo hepaticojejunostomy (LRH) for children with cholecochal cysts (CDCs). METHODS: Between January 2006 and January 2016, 44 CDC children who had biliary re-obstructions after primary definitive surgeries successfully underwent LRH in our hospital. The hepatic arteries were repositioned behind Roux loop. Ductoplasties and wide hepaticojejunostomies were carried out. The operative time, postoperative recovery and complications were compared with our open redo hepaticojejunostomy (ORH, n = 16) between October 2001 and December 2005...
December 2016: Surgical Endoscopy
https://www.readbyqxmd.com/read/27096691/non-alcoholic-steatohepatitis-clinical-and-translational-research
#8
Manuela G Neuman, Mihai Voiculescu, Radu M Nanau, Yaakov Maor, Ehud Melzer, Lawrence B Cohen, Mihai Opris, Stephen Malnick
UNLABELLED: The present review includes translational and clinical research that characterize non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Clinical and experimental evidence led to the recognition of the key toxic role played by lipotoxicity in the pathogenesis of NAFLD. The current understanding of lipotoxicity suggests that organ injury is initiated by the generation of oxidative metabolites and the translocation of gut-derived endotoxin. These processes lead to cellular injury and stimulation of the inflammatory responses mediated through a variety of molecules...
2016: Journal of Pharmacy & Pharmaceutical Sciences: a Publication of the Canadian Society for Pharmaceutical Sciences
https://www.readbyqxmd.com/read/26670291/attrition-of-hepatic-damage-inflicted-by-angiotensin-ii-with-%C3%AE-tocopherol-and-%C3%AE-carotene-in-experimental-apolipoprotein-e-knock-out-mice
#9
Kaliappan Gopal, Munusamy Gowtham, Singh Sachin, Mani Ravishankar Ram, Esaki M Shankar, Tunku Kamarul
Angiotensin II is one of the key regulatory peptides implicated in the pathogenesis of liver disease. The mechanisms underlying the salubrious role of α-tocopherol and β-carotene on liver pathology have not been comprehensively assessed. Here, we investigated the mechanisms underlying the role of Angiotensin II on hepatic damage and if α-tocopherol and β-carotene supplementation attenuates hepatic damage. Hepatic damage was induced in Apoe(-/-)mice by infusion of Angiotensin II followed by oral administration with α-tocopherol and β-carotene-enriched diet for 60 days...
December 16, 2015: Scientific Reports
https://www.readbyqxmd.com/read/26622336/biological-effects-of-pyrroloquinoline-quinone-on-liver-damage-in-bmi-1-knockout-mice
#10
Yuanqing Huang, Ning Chen, Dengshun Miao
Pyrroloquinoline quinone (PQQ) has been demonstrated to function as an antioxidant by scavenging free radicals and subsequently protecting the mitochondria from oxidative stress-induced damage. The aim of the present study was to investigate whether PQQ is able to rescue premature senescence in the liver, induced by the deletion of B cell-specific Moloney MLV insertion site-1 (Bmi-1), by inhibiting oxidative stress. In vivo, the mice were allocated into three groups that underwent the following treatment protocols...
August 2015: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/26599547/glycoprotein-nonmetastatic-melanoma-b-gpnmb-positive-macrophages-contribute-to-the-balance-between-fibrosis-and-fibrolysis-during-the-repair-of-acute-liver-injury-in-mice
#11
Kotaro Kumagai, Kazuaki Tabu, Fumisato Sasaki, Yoichiro Takami, Yuko Morinaga, Seiichi Mawatari, Shinichi Hashimoto, Shiroh Tanoue, Shuji Kanmura, Tsutomu Tamai, Akihiro Moriuchi, Hirofumi Uto, Hirohito Tsubouchi, Akio Ido
BACKGROUND AND AIMS: Glycoprotein nonmetastatic melanoma B (Gpnmb), a transmembrane glycoprotein that is expressed in macrophages, negatively regulates inflammation. We have reported that Gpnmb is strongly expressed in the livers of rats fed a choline-deficient, L-amino acid-defined (CDAA) diet. However, the role of macrophage-expressed Gpnmb in liver injury is still unknown. This study aimed to clarify the characteristics of infiltrating macrophages that express Gpnmb, and the involvement of Gpnmb in the repair process in response to liver injury...
2015: PloS One
https://www.readbyqxmd.com/read/26496771/a-modified-choline-deficient-ethionine-supplemented-diet-reduces-morbidity-and-retains-a-liver-progenitor-cell-response-in-mice
#12
Adam M Passman, Robyn P Strauss, Sarah B McSpadden, Megan L Finch-Edmondson, Ken H Woo, Luke A Diepeveen, Roslyn London, Bernard A Callus, George C Yeoh
The choline-deficient, ethionine-supplemented (CDE) dietary model induces chronic liver damage, and stimulates liver progenitor cell (LPC)-mediated repair. Long-term CDE administration leads to hepatocellular carcinoma in rodents and lineage-tracing studies show that LPCs differentiate into functional hepatocytes in this model. The CDE diet was first modified for mice by our laboratory by separately administering choline-deficient chow and ethionine in the drinking water (CD+E diet). Although this CD+E diet is widely used, concerns with variability in weight loss, morbidity, mortality and LPC response have been raised by researchers who have adopted this model...
December 2015: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/26473743/inhibition-of-hedgehog-signaling-ameliorates-hepatic-inflammation-in-mice-with-nonalcoholic-fatty-liver-disease
#13
COMPARATIVE STUDY
Hyunjoo Kwon, Kyoungsub Song, Chang Han, Weina Chen, Ying Wang, Srikanta Dash, Kyu Lim, Tong Wu
UNLABELLED: Hedgehog (Hh) signaling plays a critical role in liver development, regeneration, injury repair, and carcinogenesis. Activation of Hh signaling has been observed in patients with nonalcoholic fatty liver diseases (NAFLD); however, the pathobiological function and regulatory mechanism of hepatic Hh signaling in the pathogenesis of NAFLD remain to be further defined. This study was designed to examine the effect and mechanism of hepatic Hh signaling in high-fat diet-induced NAFLD by using pharmacological Smoothened (Smo) inhibitors (GDC-0449 and LED225) and liver-specific Smo knockout mice...
April 2016: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/26290021/-cholesterol-overload-in-hepatocytes-affects-nicotinamide-adenine-dinucleotide-phosphate-oxidase-nadph-activity-abrogating-hepatocyte-growth-factor-hgf-induced-cellular-protection
#14
Alberto G López-Reyes, Karina Martínez-Flores, Denise Clavijo-Cornejo, Natalia Nuño-Lámbarri, Mayrel Palestino-Domínguez, Verónica Souza, Leticia Bucio, Arturo Panduro, Roxana U Miranda, Luis Enrique Gómez-Quiroz, María Concepción Gutiérrez-Ruiz
The increment in the prevalence of obesity incidence in Mexico is leading to the increase in many chronic maladies, including liver diseases. It is well known that lipid-induced liver sensitization is related to the kind of lipid rather than the amount of them in the organ. Cholesterol overload in the liver aggravates the toxic effects of canonical liver insults. However, the status on the repair and survival response elicited by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the hepatocyte growth factor (HGF) is not completely understood...
July 2015: Gaceta Médica de México
https://www.readbyqxmd.com/read/26260870/developmental-exposure-of-aflatoxin-b1-reversibly-affects-hippocampal-neurogenesis-targeting-late-stage-neural-progenitor-cells-through-suppression-of-cholinergic-signaling-in-rats
#15
Takeshi Tanaka, Sayaka Mizukami, Yasuko Hasegawa-Baba, Nobuhiko Onda, Yoshiko Sugita-Konishi, Toshinori Yoshida, Makoto Shibutani
To elucidate the maternal exposure effects of aflatoxin B1 (AFB1) and its metabolite aflatoxin M1, which is transferred into milk, on postnatal hippocampal neurogenesis, pregnant Sprague-Dawley rats were provided a diet containing AFB1 at 0, 0.1, 0.3, or 1.0 ppm from gestational day 6 to day 21 after delivery on weaning. Offspring were maintained through postnatal day (PND) 77 without AFB1 exposure. Following exposure to 1.0 ppm AFB1, offspring showed no apparent systemic toxicity at weaning, whereas dams showed increased liver weight and DNA repair gene upregulation in the liver...
October 2, 2015: Toxicology
https://www.readbyqxmd.com/read/26173184/kupffer-cell-monocyte-communication-is-essential-for-initiating-murine-liver-progenitor-cell-mediated-liver-regeneration
#16
Caryn L Elsegood, Chun Wei Chan, Mariapia A Degli-Esposti, Matthew E Wikstrom, Alice Domenichini, Kyren Lazarus, Nico van Rooijen, Ruth Ganss, John K Olynyk, George C T Yeoh
UNLABELLED: Liver progenitor cells (LPCs) are necessary for repair in chronic liver disease because the remaining hepatocytes cannot replicate. However, LPC numbers also correlate with disease severity and hepatocellular carcinoma risk. Thus, the progenitor cell response in diseased liver may be regulated to optimize liver regeneration and minimize the likelihood of tumorigenesis. How this is achieved is currently unknown. Human and mouse diseased liver contain two subpopulations of macrophages with different ontogenetic origins: prenatal yolk sac-derived Kupffer cells and peripheral blood monocyte-derived macrophages...
October 2015: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/26076224/nonmedicinal-interventions-in-nonalcoholic-fatty-liver-disease
#17
REVIEW
Manuela G Neuman, Radu M Nanau, Lawrence B Cohen
Unhealthy diet and lack of physical exercise are responsible for fat accumulation in the liver, which may lead to liver disease. Histologically, the severity of the disease has two stages: nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). NAFLD is defined by the presence of steatosis with no evidence of cellular injury such as hepatocyte ballooning. NASH is a distinct entity from NAFLD, and is characterized by the presence of inflammation with hepatocytes damage, with or without fibrosis...
June 2015: Canadian Journal of Gastroenterology & Hepatology
https://www.readbyqxmd.com/read/26064446/biologically-active-high-levels-of-interleukin-22-inhibit-hepatic-gluconeogenesis-but-do-not-affect-obesity-and-its-metabolic-consequences
#18
Ogyi Park, Sung Hwan Ki, Mingjiang Xu, Hua Wang, Dechun Feng, Joseph Tam, Douglas Osei-Hyiaman, George Kunos, Bin Gao
BACKGROUND: Interleukin-22 (IL-22), a cytokine with important functions in anti-microbial defense and tissue repair, has been recently suggested to have beneficial effects in obesity and metabolic syndrome in some but not in other studies. Here, we re-examined the effects of IL-22 on obesity, insulin resistance, and hepatic glucose metabolism. RESULTS: Genetic deletion of IL-22 did not affect high-fat-diet (HFD)-induced obesity and insulin resistance. IL-22 transgenic mice with relatively high levels of circulating IL-22 (~600 pg/ml) were completely resistant to Concanavalin A-induced liver injury but developed the same degree of high fat diet (HFD)-induced obesity, insulin resistance, and fatty liver as the wild-type littermate controls...
2015: Cell & Bioscience
https://www.readbyqxmd.com/read/26059707/the-extracellular-matrix-and-insulin-resistance
#19
REVIEW
Ashley S Williams, Li Kang, David H Wasserman
The extracellular matrix (ECM) is a highly-dynamic compartment that undergoes remodeling as a result of injury and repair. Over the past decade, mounting evidence in humans and rodents suggests that ECM remodeling is associated with diet-induced insulin resistance in several metabolic tissues. In addition, integrin receptors for the ECM have also been implicated in the regulation of insulin action. This review addresses what is currently known about the ECM, integrins, and insulin action in the muscle, liver, and adipose tissue...
July 2015: Trends in Endocrinology and Metabolism: TEM
https://www.readbyqxmd.com/read/25903395/chronic-ethanol-induced-impairment-of-wnt-%C3%AE-catenin-signaling-is-attenuated-by-ppar-%C3%AE-agonist
#20
Chelsea Q Xu, Suzanne M de la Monte, Ming Tong, Chiung-Kuei Huang, Miran Kim
BACKGROUND: The Wnt/β-catenin pathway regulates liver growth, repair, and regeneration. Chronic ethanol (EtOH) exposure blunts normal liver regenerative responses, in part by inhibiting insulin/IGF signaling, and correspondingly, previous studies showed that EtOH-impaired liver regeneration could be restored by insulin sensitizer (proliferator-activated receptor [PPAR]-δ agonist) treatment. As Wnt/β-catenin functions overlap and cross talk with insulin/IGF pathways, we investigated the effects of EtOH exposure and PPAR-δ agonist treatment on Wnt pathway gene expression in relation to liver regeneration...
June 2015: Alcoholism, Clinical and Experimental Research
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