Glycyrrhizin ameliorates high fat diet-induced obesity in rats by activating NrF2 pathway
Obesity based on insulin resistance is a state of chronic oxidative stress and inflammation that are highly regulated through nuclear factor Erythroid 2-related factor 2 (NrF2) pathway. 70 male Wistar rats were randomized into two models. The prophylactic model was 10weeks and rats were grouped into...
Gespeichert in:
| Veröffentlicht in: | Life sciences (1973) 2018-01, Vol.193, p.159-170 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 170 |
|---|---|
| container_issue | |
| container_start_page | 159 |
| container_title | Life sciences (1973) |
| container_volume | 193 |
| creator | Abo El-Magd, Nada F. El-Mesery, Mohamed El-Karef, Amro El-Shishtawy, Mamdouh M. |
| description | Obesity based on insulin resistance is a state of chronic oxidative stress and inflammation that are highly regulated through nuclear factor Erythroid 2-related factor 2 (NrF2) pathway.
70 male Wistar rats were randomized into two models. The prophylactic model was 10weeks and rats were grouped into: normal group, GL group (received glycyrrhizin 50mg/kg/day orally along with normal pellet diet), HFD group and HFD+ GL group (received glycyrrhizin along with HFD). The treatment model was 14weeks and rats were grouped into: normal group, HFD group and HFD+GL group (received glycyrrhizin from the week 10).
Glycyrrhizin decreased significantly rat weights and insulin resistance, normalized lipid profile and reduced significantly the adipocytes size in adipose tissue and lipid deposition in the liver tissue through histopathologic examination. Furthermore, glycyrrhizin ameliorated obesity-induced oxidative stress which indicated by significant decrease in liver malondialdehyde level (P |
| doi_str_mv | 10.1016/j.lfs.2017.11.005 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1963474638</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0024320517305829</els_id><sourcerecordid>2013397264</sourcerecordid><originalsourceid>FETCH-LOGICAL-c447t-6b6eb92820cc8937ee99c92ec0292b3797a800347533f150b922d5ce582d198c3</originalsourceid><addsrcrecordid>eNp90DtPwzAUhmELgaBcfgALssTCkuBLEsdiQogCEoIFBibLcU5aV2lSbAcUfj2uWhgYmLw835H1InRKSUoJLS4Xadv4lBEqUkpTQvIdNKGlkAkpON1FE0JYlnBG8gN06P2CRJELvo8OmKRMCsEm6O2uHc3o3Nx-2Q7rJbS2dzqAx3M7m-NGB1xbCInt6sFAjfsKvA0jjjgyj6sRaxPshw62m-EnN2V4pcP8U4_HaK_RrYeT7XuEXqe3Lzf3yePz3cPN9WNiskyEpKgKqCQrGTGmlFwASGkkA0OYZBUXUuiSEJ6JnPOG5iRaVucG8pLVVJaGH6GLzd2V698H8EEtrTfQtrqDfvCKyiKus4KXkZ7_oYt-cF38nYoROZeCFVlUdKOM67130KiVs0vtRkWJWndXCxW7rydCUapi1bg5214eqiXUv4uf0BFcbQDEFB8WnPLGQheTWgcmqLq3_5z_Bl4rkbo</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2013397264</pqid></control><display><type>article</type><title>Glycyrrhizin ameliorates high fat diet-induced obesity in rats by activating NrF2 pathway</title><source>Elsevier ScienceDirect Journals Complete - AutoHoldings</source><source>MEDLINE</source><creator>Abo El-Magd, Nada F. ; El-Mesery, Mohamed ; El-Karef, Amro ; El-Shishtawy, Mamdouh M.</creator><creatorcontrib>Abo El-Magd, Nada F. ; El-Mesery, Mohamed ; El-Karef, Amro ; El-Shishtawy, Mamdouh M.</creatorcontrib><description>Obesity based on insulin resistance is a state of chronic oxidative stress and inflammation that are highly regulated through nuclear factor Erythroid 2-related factor 2 (NrF2) pathway.
70 male Wistar rats were randomized into two models. The prophylactic model was 10weeks and rats were grouped into: normal group, GL group (received glycyrrhizin 50mg/kg/day orally along with normal pellet diet), HFD group and HFD+ GL group (received glycyrrhizin along with HFD). The treatment model was 14weeks and rats were grouped into: normal group, HFD group and HFD+GL group (received glycyrrhizin from the week 10).
Glycyrrhizin decreased significantly rat weights and insulin resistance, normalized lipid profile and reduced significantly the adipocytes size in adipose tissue and lipid deposition in the liver tissue through histopathologic examination. Furthermore, glycyrrhizin ameliorated obesity-induced oxidative stress which indicated by significant decrease in liver malondialdehyde level (P<0.001) and increase in the total antioxidant capacity (P<0.001). Interestingly, molecular mechanism of glycyrrhizin was explored, that included significant reduction of liver gluconeogenic enzymes mRNA expression (P<0.001), a significant increase of liver insulin receptor, NrF2 and homooxygenase-1 mRNA expressions (P<0.001) and significant increase and nuclear translocation of NrF2 in liver tissue.
Glycyrrhizin ameliorates HFD-induced obesity in rats that may be attributed to its ability to increase insulin receptor expression and to activate NrF2 and subsequent homooxygenase-1 pathway. Thus, this work represents a safe natural compound (glycyrrhizin) that has a great role either as prophylaxis or treatment for insulin resistance related to obesity.
The effect of high fat diet (HFD) feeding either for 10 or 14weeks on rats (A), the proposed mechanism of glycyrrhizin either as prophylaxis or treatment in amelioration of obesity-associated with insulin resistance induced by high fat diet (HFD) feeding in rats (B).
G6Pase: glucose-6-phosphatase, HDL-C: high density lipoprotein-cholesterol, HO-1: homooxygenase-1, HOMA IR: homeostatic model assessment of insulin resistance, LDL-C: low density lipoprotein-cholesterol, MDA: malondialdehyde, NrF2: nuclear factor erythroid-derived factor 2-related factor 2, PEPCK: phosphoenolpyruvate carboxykinase, TAC: total antioxidant capacity. [Display omitted]</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2017.11.005</identifier><identifier>PMID: 29129772</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Adipocytes ; Adipocytes - metabolism ; Adipose tissue ; Adipose Tissue - metabolism ; Adipose tissues ; Animal models ; Animals ; Antioxidants ; Diet ; Diet, High-Fat ; Gene expression ; Gluconeogenic enzymes ; Glycyrrhizic Acid - metabolism ; Glycyrrhizic Acid - pharmacology ; Glycyrrhizic Acid - therapeutic use ; Glycyrrhizin ; High fat diet ; Inflammation - pathology ; Insulin ; Insulin - metabolism ; Insulin receptor ; Insulin resistance ; Insulin Resistance - physiology ; Liver ; Liver - metabolism ; Male ; Malondialdehyde ; NF-E2-Related Factor 2 - metabolism ; Nuclear factor erythroid-2 related factor-2 ; Nuclear transport ; Obesity ; Obesity - metabolism ; Obesity - prevention & control ; Oxidation resistance ; Oxidative stress ; Oxidative Stress - physiology ; Oxygen ; Prophylaxis ; Rats ; Rats, Wistar ; Receptor, Insulin - metabolism ; Translocation</subject><ispartof>Life sciences (1973), 2018-01, Vol.193, p.159-170</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Jan 15, 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-6b6eb92820cc8937ee99c92ec0292b3797a800347533f150b922d5ce582d198c3</citedby><cites>FETCH-LOGICAL-c447t-6b6eb92820cc8937ee99c92ec0292b3797a800347533f150b922d5ce582d198c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2017.11.005$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3541,27915,27916,45986</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29129772$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Abo El-Magd, Nada F.</creatorcontrib><creatorcontrib>El-Mesery, Mohamed</creatorcontrib><creatorcontrib>El-Karef, Amro</creatorcontrib><creatorcontrib>El-Shishtawy, Mamdouh M.</creatorcontrib><title>Glycyrrhizin ameliorates high fat diet-induced obesity in rats by activating NrF2 pathway</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Obesity based on insulin resistance is a state of chronic oxidative stress and inflammation that are highly regulated through nuclear factor Erythroid 2-related factor 2 (NrF2) pathway.
70 male Wistar rats were randomized into two models. The prophylactic model was 10weeks and rats were grouped into: normal group, GL group (received glycyrrhizin 50mg/kg/day orally along with normal pellet diet), HFD group and HFD+ GL group (received glycyrrhizin along with HFD). The treatment model was 14weeks and rats were grouped into: normal group, HFD group and HFD+GL group (received glycyrrhizin from the week 10).
Glycyrrhizin decreased significantly rat weights and insulin resistance, normalized lipid profile and reduced significantly the adipocytes size in adipose tissue and lipid deposition in the liver tissue through histopathologic examination. Furthermore, glycyrrhizin ameliorated obesity-induced oxidative stress which indicated by significant decrease in liver malondialdehyde level (P<0.001) and increase in the total antioxidant capacity (P<0.001). Interestingly, molecular mechanism of glycyrrhizin was explored, that included significant reduction of liver gluconeogenic enzymes mRNA expression (P<0.001), a significant increase of liver insulin receptor, NrF2 and homooxygenase-1 mRNA expressions (P<0.001) and significant increase and nuclear translocation of NrF2 in liver tissue.
Glycyrrhizin ameliorates HFD-induced obesity in rats that may be attributed to its ability to increase insulin receptor expression and to activate NrF2 and subsequent homooxygenase-1 pathway. Thus, this work represents a safe natural compound (glycyrrhizin) that has a great role either as prophylaxis or treatment for insulin resistance related to obesity.
The effect of high fat diet (HFD) feeding either for 10 or 14weeks on rats (A), the proposed mechanism of glycyrrhizin either as prophylaxis or treatment in amelioration of obesity-associated with insulin resistance induced by high fat diet (HFD) feeding in rats (B).
G6Pase: glucose-6-phosphatase, HDL-C: high density lipoprotein-cholesterol, HO-1: homooxygenase-1, HOMA IR: homeostatic model assessment of insulin resistance, LDL-C: low density lipoprotein-cholesterol, MDA: malondialdehyde, NrF2: nuclear factor erythroid-derived factor 2-related factor 2, PEPCK: phosphoenolpyruvate carboxykinase, TAC: total antioxidant capacity. [Display omitted]</description><subject>Adipocytes</subject><subject>Adipocytes - metabolism</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose tissues</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Gene expression</subject><subject>Gluconeogenic enzymes</subject><subject>Glycyrrhizic Acid - metabolism</subject><subject>Glycyrrhizic Acid - pharmacology</subject><subject>Glycyrrhizic Acid - therapeutic use</subject><subject>Glycyrrhizin</subject><subject>High fat diet</subject><subject>Inflammation - pathology</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin receptor</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nuclear factor erythroid-2 related factor-2</subject><subject>Nuclear transport</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Obesity - prevention & control</subject><subject>Oxidation resistance</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Oxygen</subject><subject>Prophylaxis</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Insulin - metabolism</subject><subject>Translocation</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90DtPwzAUhmELgaBcfgALssTCkuBLEsdiQogCEoIFBibLcU5aV2lSbAcUfj2uWhgYmLw835H1InRKSUoJLS4Xadv4lBEqUkpTQvIdNKGlkAkpON1FE0JYlnBG8gN06P2CRJELvo8OmKRMCsEm6O2uHc3o3Nx-2Q7rJbS2dzqAx3M7m-NGB1xbCInt6sFAjfsKvA0jjjgyj6sRaxPshw62m-EnN2V4pcP8U4_HaK_RrYeT7XuEXqe3Lzf3yePz3cPN9WNiskyEpKgKqCQrGTGmlFwASGkkA0OYZBUXUuiSEJ6JnPOG5iRaVucG8pLVVJaGH6GLzd2V698H8EEtrTfQtrqDfvCKyiKus4KXkZ7_oYt-cF38nYoROZeCFVlUdKOM67130KiVs0vtRkWJWndXCxW7rydCUapi1bg5214eqiXUv4uf0BFcbQDEFB8WnPLGQheTWgcmqLq3_5z_Bl4rkbo</recordid><startdate>20180115</startdate><enddate>20180115</enddate><creator>Abo El-Magd, Nada F.</creator><creator>El-Mesery, Mohamed</creator><creator>El-Karef, Amro</creator><creator>El-Shishtawy, Mamdouh M.</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20180115</creationdate><title>Glycyrrhizin ameliorates high fat diet-induced obesity in rats by activating NrF2 pathway</title><author>Abo El-Magd, Nada F. ; El-Mesery, Mohamed ; El-Karef, Amro ; El-Shishtawy, Mamdouh M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-6b6eb92820cc8937ee99c92ec0292b3797a800347533f150b922d5ce582d198c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adipocytes</topic><topic>Adipocytes - metabolism</topic><topic>Adipose tissue</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose tissues</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Diet</topic><topic>Diet, High-Fat</topic><topic>Gene expression</topic><topic>Gluconeogenic enzymes</topic><topic>Glycyrrhizic Acid - metabolism</topic><topic>Glycyrrhizic Acid - pharmacology</topic><topic>Glycyrrhizic Acid - therapeutic use</topic><topic>Glycyrrhizin</topic><topic>High fat diet</topic><topic>Inflammation - pathology</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin receptor</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nuclear factor erythroid-2 related factor-2</topic><topic>Nuclear transport</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>Obesity - prevention & control</topic><topic>Oxidation resistance</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - physiology</topic><topic>Oxygen</topic><topic>Prophylaxis</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Insulin - metabolism</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Abo El-Magd, Nada F.</creatorcontrib><creatorcontrib>El-Mesery, Mohamed</creatorcontrib><creatorcontrib>El-Karef, Amro</creatorcontrib><creatorcontrib>El-Shishtawy, Mamdouh M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abo El-Magd, Nada F.</au><au>El-Mesery, Mohamed</au><au>El-Karef, Amro</au><au>El-Shishtawy, Mamdouh M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glycyrrhizin ameliorates high fat diet-induced obesity in rats by activating NrF2 pathway</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2018-01-15</date><risdate>2018</risdate><volume>193</volume><spage>159</spage><epage>170</epage><pages>159-170</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Obesity based on insulin resistance is a state of chronic oxidative stress and inflammation that are highly regulated through nuclear factor Erythroid 2-related factor 2 (NrF2) pathway.
70 male Wistar rats were randomized into two models. The prophylactic model was 10weeks and rats were grouped into: normal group, GL group (received glycyrrhizin 50mg/kg/day orally along with normal pellet diet), HFD group and HFD+ GL group (received glycyrrhizin along with HFD). The treatment model was 14weeks and rats were grouped into: normal group, HFD group and HFD+GL group (received glycyrrhizin from the week 10).
Glycyrrhizin decreased significantly rat weights and insulin resistance, normalized lipid profile and reduced significantly the adipocytes size in adipose tissue and lipid deposition in the liver tissue through histopathologic examination. Furthermore, glycyrrhizin ameliorated obesity-induced oxidative stress which indicated by significant decrease in liver malondialdehyde level (P<0.001) and increase in the total antioxidant capacity (P<0.001). Interestingly, molecular mechanism of glycyrrhizin was explored, that included significant reduction of liver gluconeogenic enzymes mRNA expression (P<0.001), a significant increase of liver insulin receptor, NrF2 and homooxygenase-1 mRNA expressions (P<0.001) and significant increase and nuclear translocation of NrF2 in liver tissue.
Glycyrrhizin ameliorates HFD-induced obesity in rats that may be attributed to its ability to increase insulin receptor expression and to activate NrF2 and subsequent homooxygenase-1 pathway. Thus, this work represents a safe natural compound (glycyrrhizin) that has a great role either as prophylaxis or treatment for insulin resistance related to obesity.
The effect of high fat diet (HFD) feeding either for 10 or 14weeks on rats (A), the proposed mechanism of glycyrrhizin either as prophylaxis or treatment in amelioration of obesity-associated with insulin resistance induced by high fat diet (HFD) feeding in rats (B).
G6Pase: glucose-6-phosphatase, HDL-C: high density lipoprotein-cholesterol, HO-1: homooxygenase-1, HOMA IR: homeostatic model assessment of insulin resistance, LDL-C: low density lipoprotein-cholesterol, MDA: malondialdehyde, NrF2: nuclear factor erythroid-derived factor 2-related factor 2, PEPCK: phosphoenolpyruvate carboxykinase, TAC: total antioxidant capacity. [Display omitted]</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>29129772</pmid><doi>10.1016/j.lfs.2017.11.005</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0024-3205 |
| ispartof | Life sciences (1973), 2018-01, Vol.193, p.159-170 |
| issn | 0024-3205 1879-0631 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1963474638 |
| source | Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE |
| subjects | Adipocytes Adipocytes - metabolism Adipose tissue Adipose Tissue - metabolism Adipose tissues Animal models Animals Antioxidants Diet Diet, High-Fat Gene expression Gluconeogenic enzymes Glycyrrhizic Acid - metabolism Glycyrrhizic Acid - pharmacology Glycyrrhizic Acid - therapeutic use Glycyrrhizin High fat diet Inflammation - pathology Insulin Insulin - metabolism Insulin receptor Insulin resistance Insulin Resistance - physiology Liver Liver - metabolism Male Malondialdehyde NF-E2-Related Factor 2 - metabolism Nuclear factor erythroid-2 related factor-2 Nuclear transport Obesity Obesity - metabolism Obesity - prevention & control Oxidation resistance Oxidative stress Oxidative Stress - physiology Oxygen Prophylaxis Rats Rats, Wistar Receptor, Insulin - metabolism Translocation |
| title | Glycyrrhizin ameliorates high fat diet-induced obesity in rats by activating NrF2 pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-15T07%3A39%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Glycyrrhizin%20ameliorates%20high%20fat%20diet-induced%20obesity%20in%20rats%20by%20activating%20NrF2%20pathway&rft.jtitle=Life%20sciences%20(1973)&rft.au=Abo%20El-Magd,%20Nada%20F.&rft.date=2018-01-15&rft.volume=193&rft.spage=159&rft.epage=170&rft.pages=159-170&rft.issn=0024-3205&rft.eissn=1879-0631&rft_id=info:doi/10.1016/j.lfs.2017.11.005&rft_dat=%3Cproquest_cross%3E2013397264%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2013397264&rft_id=info:pmid/29129772&rft_els_id=S0024320517305829&rfr_iscdi=true |