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Therapeutic effect of autophagy induced by rapamycin versus intermittent fasting in animal model of fatty liver
High-fructose, high-fat diet consumption (HFHF) is one of the primary causes of non-alcoholic fatt liver disease (NAFLD), which is due to impaired beta-oxidation or apolipoprotein secretion by hepatocytes. Activation of autophagy in hepatocytes could be a therapeutic method against hepatic complicat...
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Published in: | Folia histochemica et cytobiologica 2023-01, Vol.61 (4), p.205-216 |
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description | High-fructose, high-fat diet consumption (HFHF) is one of the primary causes of non-alcoholic fatt liver disease (NAFLD), which is due to impaired beta-oxidation or apolipoprotein secretion by hepatocytes. Activation of autophagy in hepatocytes could be a therapeutic method against hepatic complications. This study was designed to compare effects of rapamycin and intermittent fasting-inducing autophagy in rats with experimentally induced nonalcoholic fatty liver.
Male rats were divided into five groups: C (control, n = 6), the experimental group (EX) subdivided, EXIa (HFHF, n = 6), EXIb (recovery, n = 6), EXII (rapamycin, n = 6) and EXIII (intermittent fasting, n = 6). All rats in the experimental group received HFHF diet for 8 weeks to induce nonalcoholic-fatty liver and obesity. Then, for the next 8 weeks the animals received either a daily oral dose of rapamycin (EXII group) or to intermittent fasting (IF) for 16 hours daily (EXIII group). Blood samples were drawn, and serum TG concentration as well as ALT and AST activities were determined. Hepatic sections were examined by light and electron microscopy. LC3B immunohistochemical staining, morphometric and statistical studies were performed.
Subgroups EXIa (HFHF subgroup) and EXIb (Recovery subgroup) showed marked increase in TG, ALT, and AST levels associated with loss of normal hepatic architecture, cytoplasmic vacuolations and faint LC3B immunoreactivity. Ultrathin sections exhibited many autophagosomes in hepatocytes. On the other hand, rapamycin (EXII) and IF (EXIII) groups showed significant improvement to a variable extent in comparison to EXI groups.
It could be concluded that rapamycin and intermittent fasting significantly improved NAFLD-induced changes of liver structure and function by inducing autophagy in hepatocytes. |
doi_str_mv | 10.5603/fhc.95905 |
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Male rats were divided into five groups: C (control, n = 6), the experimental group (EX) subdivided, EXIa (HFHF, n = 6), EXIb (recovery, n = 6), EXII (rapamycin, n = 6) and EXIII (intermittent fasting, n = 6). All rats in the experimental group received HFHF diet for 8 weeks to induce nonalcoholic-fatty liver and obesity. Then, for the next 8 weeks the animals received either a daily oral dose of rapamycin (EXII group) or to intermittent fasting (IF) for 16 hours daily (EXIII group). Blood samples were drawn, and serum TG concentration as well as ALT and AST activities were determined. Hepatic sections were examined by light and electron microscopy. LC3B immunohistochemical staining, morphometric and statistical studies were performed.
Subgroups EXIa (HFHF subgroup) and EXIb (Recovery subgroup) showed marked increase in TG, ALT, and AST levels associated with loss of normal hepatic architecture, cytoplasmic vacuolations and faint LC3B immunoreactivity. Ultrathin sections exhibited many autophagosomes in hepatocytes. On the other hand, rapamycin (EXII) and IF (EXIII) groups showed significant improvement to a variable extent in comparison to EXI groups.
It could be concluded that rapamycin and intermittent fasting significantly improved NAFLD-induced changes of liver structure and function by inducing autophagy in hepatocytes.</description><identifier>ISSN: 0239-8508</identifier><identifier>EISSN: 1897-5631</identifier><identifier>DOI: 10.5603/fhc.95905</identifier><identifier>PMID: 38013515</identifier><language>eng</language><publisher>Poland: Wydawnictwo Via Medica</publisher><subject>Animal models ; Animals ; Apolipoproteins ; Autophagy ; Diet ; Disease Models, Animal ; Electron microscopy ; Fasting ; Fatty liver ; Hepatocytes ; High fat diet ; Immunoreactivity ; Intermittent Fasting ; Liver ; Liver diseases ; Male ; Non-alcoholic Fatty Liver Disease - drug therapy ; Oxidation ; Phagosomes ; Rapamycin ; Rats ; Recovery ; Sirolimus - pharmacology ; Sirolimus - therapeutic use ; Structure-function relationships ; Subgroups</subject><ispartof>Folia histochemica et cytobiologica, 2023-01, Vol.61 (4), p.205-216</ispartof><rights>2023. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-8741-0050</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2917501969?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25753,27924,27925,37012,37013,44590</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38013515$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hosny, Sara Adel</creatorcontrib><creatorcontrib>Moustafa, Mohammed Hafez Ahmed</creatorcontrib><creatorcontrib>Mehina, Fatma Mahmoud</creatorcontrib><creatorcontrib>Sabry, Marwa Mohamed</creatorcontrib><title>Therapeutic effect of autophagy induced by rapamycin versus intermittent fasting in animal model of fatty liver</title><title>Folia histochemica et cytobiologica</title><addtitle>Folia Histochem Cytobiol</addtitle><description>High-fructose, high-fat diet consumption (HFHF) is one of the primary causes of non-alcoholic fatt liver disease (NAFLD), which is due to impaired beta-oxidation or apolipoprotein secretion by hepatocytes. Activation of autophagy in hepatocytes could be a therapeutic method against hepatic complications. This study was designed to compare effects of rapamycin and intermittent fasting-inducing autophagy in rats with experimentally induced nonalcoholic fatty liver.
Male rats were divided into five groups: C (control, n = 6), the experimental group (EX) subdivided, EXIa (HFHF, n = 6), EXIb (recovery, n = 6), EXII (rapamycin, n = 6) and EXIII (intermittent fasting, n = 6). All rats in the experimental group received HFHF diet for 8 weeks to induce nonalcoholic-fatty liver and obesity. Then, for the next 8 weeks the animals received either a daily oral dose of rapamycin (EXII group) or to intermittent fasting (IF) for 16 hours daily (EXIII group). Blood samples were drawn, and serum TG concentration as well as ALT and AST activities were determined. Hepatic sections were examined by light and electron microscopy. LC3B immunohistochemical staining, morphometric and statistical studies were performed.
Subgroups EXIa (HFHF subgroup) and EXIb (Recovery subgroup) showed marked increase in TG, ALT, and AST levels associated with loss of normal hepatic architecture, cytoplasmic vacuolations and faint LC3B immunoreactivity. Ultrathin sections exhibited many autophagosomes in hepatocytes. On the other hand, rapamycin (EXII) and IF (EXIII) groups showed significant improvement to a variable extent in comparison to EXI groups.
It could be concluded that rapamycin and intermittent fasting significantly improved NAFLD-induced changes of liver structure and function by inducing autophagy in hepatocytes.</description><subject>Animal models</subject><subject>Animals</subject><subject>Apolipoproteins</subject><subject>Autophagy</subject><subject>Diet</subject><subject>Disease Models, Animal</subject><subject>Electron microscopy</subject><subject>Fasting</subject><subject>Fatty liver</subject><subject>Hepatocytes</subject><subject>High fat diet</subject><subject>Immunoreactivity</subject><subject>Intermittent Fasting</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Non-alcoholic Fatty Liver Disease - drug therapy</subject><subject>Oxidation</subject><subject>Phagosomes</subject><subject>Rapamycin</subject><subject>Rats</subject><subject>Recovery</subject><subject>Sirolimus - pharmacology</subject><subject>Sirolimus - therapeutic use</subject><subject>Structure-function relationships</subject><subject>Subgroups</subject><issn>0239-8508</issn><issn>1897-5631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpd0ctOJCEUBmBinIxtzyx8AUPiZlyUc4CigKXpOGpi4qZnXaGog12mLi1QJvX24nXhigQ-_nD4CTlhcCErEH_9zl0YaUAekBXTRhWyEuyQrIALU2gJ-ogcx_gIkHXJfpIjoYEJyeSKTNsdBrvHOXWOovfoEp08tXOa9jv7sNBubGeHLW0Wmp0dFteN9BlDnGM-SxiGLiUcE_U2pm58yJvUjt1gezpMLfavad6mtNC-y9d-kR_e9hF_f6xr8v_f1XZzU9zdX99uLu8Kx5VIhfIArISq5E3p0TeGgwVvVWW1l8zIsvHGtQ1XgCVrBTrTKie1RCGd5l6JNfnznrsP09OMMdVDFx32vR1xmmPNtSkVL5WGTM--0cdpDmN-Xc0NUxKYqUxW5-_KhSnGgL7ehzxlWGoG9WsLdW6hfmsh29OPxLkZsP2Sn98uXgDRCIOo</recordid><startdate>20230101</startdate><enddate>20230101</enddate><creator>Hosny, Sara Adel</creator><creator>Moustafa, Mohammed Hafez Ahmed</creator><creator>Mehina, Fatma Mahmoud</creator><creator>Sabry, Marwa Mohamed</creator><general>Wydawnictwo Via Medica</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>4T-</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BYOGL</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8741-0050</orcidid></search><sort><creationdate>20230101</creationdate><title>Therapeutic effect of autophagy induced by rapamycin versus intermittent fasting in animal model of fatty liver</title><author>Hosny, Sara Adel ; Moustafa, Mohammed Hafez Ahmed ; Mehina, Fatma Mahmoud ; Sabry, Marwa Mohamed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c273t-7f00140642b4fefb920a0fa76a8f51954bf9cdb270e41d3ec9d7c585e35c82f73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Apolipoproteins</topic><topic>Autophagy</topic><topic>Diet</topic><topic>Disease Models, Animal</topic><topic>Electron microscopy</topic><topic>Fasting</topic><topic>Fatty liver</topic><topic>Hepatocytes</topic><topic>High fat diet</topic><topic>Immunoreactivity</topic><topic>Intermittent Fasting</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Non-alcoholic Fatty Liver Disease - drug therapy</topic><topic>Oxidation</topic><topic>Phagosomes</topic><topic>Rapamycin</topic><topic>Rats</topic><topic>Recovery</topic><topic>Sirolimus - pharmacology</topic><topic>Sirolimus - therapeutic use</topic><topic>Structure-function relationships</topic><topic>Subgroups</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hosny, Sara Adel</creatorcontrib><creatorcontrib>Moustafa, Mohammed Hafez Ahmed</creatorcontrib><creatorcontrib>Mehina, Fatma Mahmoud</creatorcontrib><creatorcontrib>Sabry, Marwa Mohamed</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Docstoc</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>East Europe, Central Europe Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Research Library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Folia histochemica et cytobiologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hosny, Sara Adel</au><au>Moustafa, Mohammed Hafez Ahmed</au><au>Mehina, Fatma Mahmoud</au><au>Sabry, Marwa Mohamed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic effect of autophagy induced by rapamycin versus intermittent fasting in animal model of fatty liver</atitle><jtitle>Folia histochemica et cytobiologica</jtitle><addtitle>Folia Histochem Cytobiol</addtitle><date>2023-01-01</date><risdate>2023</risdate><volume>61</volume><issue>4</issue><spage>205</spage><epage>216</epage><pages>205-216</pages><issn>0239-8508</issn><eissn>1897-5631</eissn><abstract>High-fructose, high-fat diet consumption (HFHF) is one of the primary causes of non-alcoholic fatt liver disease (NAFLD), which is due to impaired beta-oxidation or apolipoprotein secretion by hepatocytes. Activation of autophagy in hepatocytes could be a therapeutic method against hepatic complications. This study was designed to compare effects of rapamycin and intermittent fasting-inducing autophagy in rats with experimentally induced nonalcoholic fatty liver.
Male rats were divided into five groups: C (control, n = 6), the experimental group (EX) subdivided, EXIa (HFHF, n = 6), EXIb (recovery, n = 6), EXII (rapamycin, n = 6) and EXIII (intermittent fasting, n = 6). All rats in the experimental group received HFHF diet for 8 weeks to induce nonalcoholic-fatty liver and obesity. Then, for the next 8 weeks the animals received either a daily oral dose of rapamycin (EXII group) or to intermittent fasting (IF) for 16 hours daily (EXIII group). Blood samples were drawn, and serum TG concentration as well as ALT and AST activities were determined. Hepatic sections were examined by light and electron microscopy. LC3B immunohistochemical staining, morphometric and statistical studies were performed.
Subgroups EXIa (HFHF subgroup) and EXIb (Recovery subgroup) showed marked increase in TG, ALT, and AST levels associated with loss of normal hepatic architecture, cytoplasmic vacuolations and faint LC3B immunoreactivity. Ultrathin sections exhibited many autophagosomes in hepatocytes. On the other hand, rapamycin (EXII) and IF (EXIII) groups showed significant improvement to a variable extent in comparison to EXI groups.
It could be concluded that rapamycin and intermittent fasting significantly improved NAFLD-induced changes of liver structure and function by inducing autophagy in hepatocytes.</abstract><cop>Poland</cop><pub>Wydawnictwo Via Medica</pub><pmid>38013515</pmid><doi>10.5603/fhc.95905</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8741-0050</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animal models Animals Apolipoproteins Autophagy Diet Disease Models, Animal Electron microscopy Fasting Fatty liver Hepatocytes High fat diet Immunoreactivity Intermittent Fasting Liver Liver diseases Male Non-alcoholic Fatty Liver Disease - drug therapy Oxidation Phagosomes Rapamycin Rats Recovery Sirolimus - pharmacology Sirolimus - therapeutic use Structure-function relationships Subgroups |
title | Therapeutic effect of autophagy induced by rapamycin versus intermittent fasting in animal model of fatty liver |
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