Lactococcus lactis KF140 Ameliorates Nonalcoholic Fatty Liver Disease Induced by Nε‐Carboxymethyl‐Lysine and High‐Fat Diet

Scope Long‐term consumption of excessive dietary advanced glycation end‐products such as Nε‐carboxymethyl‐lysine (CML), which are produced by the Maillard reaction during food thermal processing, leads to nonalcoholic fatty liver disease (NAFLD) along with high fat consumption. The study previously...

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Veröffentlicht in:Molecular nutrition & food research 2024-08, Vol.68 (16), p.e2400260-n/a
Hauptverfasser: Lee, Hye‐Bin, Park, Miri, Lee, So‐Young, Ha, Sang Keun, Kim, Yoonsook, Lee, Kwang‐Won, Park, Ho‐Young
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container_title Molecular nutrition & food research
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creator Lee, Hye‐Bin
Park, Miri
Lee, So‐Young
Ha, Sang Keun
Kim, Yoonsook
Lee, Kwang‐Won
Park, Ho‐Young
description Scope Long‐term consumption of excessive dietary advanced glycation end‐products such as Nε‐carboxymethyl‐lysine (CML), which are produced by the Maillard reaction during food thermal processing, leads to nonalcoholic fatty liver disease (NAFLD) along with high fat consumption. The study previously finds that administration of Lactococcus lactis KF140 (LL‐KF140) detoxifies CML by decreasing CML absorption both in a rat model and clinical trial. Methods and results The present study evaluates the ameliorative effect of LL‐KF140 on NAFLD and fatty liver‐related biomarkers in a mouse model induced by CML and high fat. LL‐KF140 is orally administered to mice at a concentration of 1 × 107 or 1 × 108 colony‐forming unit (CFU) per mouse for 8 weeks. LL‐KF140 administration ameliorates the NAFLD‐related symptoms by reducing body weight and fat mass gain along with levels of serum aspartate transaminase, alanine transferase, and lipids as well as glucose intolerance and insulin resistance in CML‐treated mice. In addition, histological analysis including staining and western blotting shows that LL‐KF140 suppresses the lipogenesis pathway and CML absorption, thereby suppressing CML‐induced NAFLD. Conclusion These findings suggest that LL‐KF140 attenuates dietary CML‐induced NAFLD by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain. Lactococcus lactis KF140 (LL‐KF140) attenuates dietary CML‐induced nonalcoholic fatty liver disease by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain.
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The study previously finds that administration of Lactococcus lactis KF140 (LL‐KF140) detoxifies CML by decreasing CML absorption both in a rat model and clinical trial. Methods and results The present study evaluates the ameliorative effect of LL‐KF140 on NAFLD and fatty liver‐related biomarkers in a mouse model induced by CML and high fat. LL‐KF140 is orally administered to mice at a concentration of 1 × 107 or 1 × 108 colony‐forming unit (CFU) per mouse for 8 weeks. LL‐KF140 administration ameliorates the NAFLD‐related symptoms by reducing body weight and fat mass gain along with levels of serum aspartate transaminase, alanine transferase, and lipids as well as glucose intolerance and insulin resistance in CML‐treated mice. In addition, histological analysis including staining and western blotting shows that LL‐KF140 suppresses the lipogenesis pathway and CML absorption, thereby suppressing CML‐induced NAFLD. Conclusion These findings suggest that LL‐KF140 attenuates dietary CML‐induced NAFLD by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain. Lactococcus lactis KF140 (LL‐KF140) attenuates dietary CML‐induced nonalcoholic fatty liver disease by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain.</description><identifier>ISSN: 1613-4125</identifier><identifier>ISSN: 1613-4133</identifier><identifier>EISSN: 1613-4133</identifier><identifier>DOI: 10.1002/mnfr.202400260</identifier><identifier>PMID: 38962859</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Absorption ; advanced glycation end products ; Advanced glycosylation end products ; Alanine ; Alanine Transaminase - blood ; animal models ; Animals ; Aspartate transaminase ; Biomarkers ; blood serum ; Body fat ; Body weight ; Body weight gain ; clinical trials ; Diet, High-Fat - adverse effects ; fat intake ; Fatty liver ; Food consumption ; Food processing ; food research ; glucose ; Glucose tolerance ; High fat diet ; histology ; Insulin Resistance ; Lactococcus lactis ; Lipids ; Lipogenesis ; Lipogenesis - drug effects ; Liver ; Liver - drug effects ; Liver - metabolism ; Liver diseases ; Lysine ; Lysine - analogs &amp; derivatives ; Lysine - pharmacology ; Maillard reaction ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease - drug therapy ; Non-alcoholic Fatty Liver Disease - etiology ; nonalcoholic fatty liver disease ; Nε‐carboxymethyl‐lysine ; Oral administration ; Probiotics ; Probiotics - pharmacology ; Transaminase ; Western blotting</subject><ispartof>Molecular nutrition &amp; food research, 2024-08, Vol.68 (16), p.e2400260-n/a</ispartof><rights>2024 The Author(s). Molecular Nutrition &amp; Food Research published by Wiley‐VCH GmbH</rights><rights>2024 The Author(s). Molecular Nutrition &amp; Food Research published by Wiley‐VCH GmbH.</rights><rights>2024. This article is published under http://creativecommons.org/licenses/by-nc/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><cites>FETCH-LOGICAL-c2861-6265fa55fd126259c605a072b830edb82dba97d65aa76135d7ae35919e3d780d3</cites><orcidid>0000-0002-3329-2279 ; 0000-0002-9966-9059</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmnfr.202400260$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmnfr.202400260$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38962859$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Hye‐Bin</creatorcontrib><creatorcontrib>Park, Miri</creatorcontrib><creatorcontrib>Lee, So‐Young</creatorcontrib><creatorcontrib>Ha, Sang Keun</creatorcontrib><creatorcontrib>Kim, Yoonsook</creatorcontrib><creatorcontrib>Lee, Kwang‐Won</creatorcontrib><creatorcontrib>Park, Ho‐Young</creatorcontrib><title>Lactococcus lactis KF140 Ameliorates Nonalcoholic Fatty Liver Disease Induced by Nε‐Carboxymethyl‐Lysine and High‐Fat Diet</title><title>Molecular nutrition &amp; food research</title><addtitle>Mol Nutr Food Res</addtitle><description>Scope Long‐term consumption of excessive dietary advanced glycation end‐products such as Nε‐carboxymethyl‐lysine (CML), which are produced by the Maillard reaction during food thermal processing, leads to nonalcoholic fatty liver disease (NAFLD) along with high fat consumption. The study previously finds that administration of Lactococcus lactis KF140 (LL‐KF140) detoxifies CML by decreasing CML absorption both in a rat model and clinical trial. Methods and results The present study evaluates the ameliorative effect of LL‐KF140 on NAFLD and fatty liver‐related biomarkers in a mouse model induced by CML and high fat. LL‐KF140 is orally administered to mice at a concentration of 1 × 107 or 1 × 108 colony‐forming unit (CFU) per mouse for 8 weeks. LL‐KF140 administration ameliorates the NAFLD‐related symptoms by reducing body weight and fat mass gain along with levels of serum aspartate transaminase, alanine transferase, and lipids as well as glucose intolerance and insulin resistance in CML‐treated mice. In addition, histological analysis including staining and western blotting shows that LL‐KF140 suppresses the lipogenesis pathway and CML absorption, thereby suppressing CML‐induced NAFLD. Conclusion These findings suggest that LL‐KF140 attenuates dietary CML‐induced NAFLD by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain. Lactococcus lactis KF140 (LL‐KF140) attenuates dietary CML‐induced nonalcoholic fatty liver disease by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain.</description><subject>Absorption</subject><subject>advanced glycation end products</subject><subject>Advanced glycosylation end products</subject><subject>Alanine</subject><subject>Alanine Transaminase - blood</subject><subject>animal models</subject><subject>Animals</subject><subject>Aspartate transaminase</subject><subject>Biomarkers</subject><subject>blood serum</subject><subject>Body fat</subject><subject>Body weight</subject><subject>Body weight gain</subject><subject>clinical trials</subject><subject>Diet, High-Fat - adverse effects</subject><subject>fat intake</subject><subject>Fatty liver</subject><subject>Food consumption</subject><subject>Food processing</subject><subject>food research</subject><subject>glucose</subject><subject>Glucose tolerance</subject><subject>High fat diet</subject><subject>histology</subject><subject>Insulin Resistance</subject><subject>Lactococcus lactis</subject><subject>Lipids</subject><subject>Lipogenesis</subject><subject>Lipogenesis - drug effects</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver diseases</subject><subject>Lysine</subject><subject>Lysine - analogs &amp; derivatives</subject><subject>Lysine - pharmacology</subject><subject>Maillard reaction</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Non-alcoholic Fatty Liver Disease - drug therapy</subject><subject>Non-alcoholic Fatty Liver Disease - etiology</subject><subject>nonalcoholic fatty liver disease</subject><subject>Nε‐carboxymethyl‐lysine</subject><subject>Oral administration</subject><subject>Probiotics</subject><subject>Probiotics - pharmacology</subject><subject>Transaminase</subject><subject>Western blotting</subject><issn>1613-4125</issn><issn>1613-4133</issn><issn>1613-4133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNqFkstu1DAUhi0EoqWwZYksselmpr7ElyyrKUOrhkFCsI4c-4RxlcTFTijZwRvwMrwGD8GT4NGUWbDp6lz0nV865z8IvaRkSQlhZ_3QxiUjrMiFJI_QMZWULwrK-eNDzsQRepbSDSGcsoI_RUdcl5JpUR6jH5WxY7DB2inhLuc-4es1LQg-76HzIZoREt6EwXQ2bEPnLV6bcZxx5b9CxBc-gUmArwY3WXC4mfHm968_33-uTGzCt7mHcTt3ua7m5AfAZnD40n_e5k6WyeMwPkdPWtMleHEfT9Cn9ZuPq8tF9f7t1eq8WlimJV1IJkVrhGgdZZKJ0koiDFGs0ZyAazRzjSmVk8IYldcWThngoqQlcKc0cfwEne51b2P4MkEa694nC11nBghTqjkVXBFKOHkYJUooUkjFMvr6P_QmTDFfa0eVSlNKtcjUck_ZGFKK0Na30fcmzjUl9c7HeudjffAxD7y6l52aHtwB_2dcBoo9cOc7mB-Qq99t1h8Knb_iL7EFqx8</recordid><startdate>202408</startdate><enddate>202408</enddate><creator>Lee, Hye‐Bin</creator><creator>Park, Miri</creator><creator>Lee, So‐Young</creator><creator>Ha, Sang Keun</creator><creator>Kim, Yoonsook</creator><creator>Lee, Kwang‐Won</creator><creator>Park, Ho‐Young</creator><general>Wiley Subscription Services, Inc</general><scope>24P</scope><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>7QO</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-3329-2279</orcidid><orcidid>https://orcid.org/0000-0002-9966-9059</orcidid></search><sort><creationdate>202408</creationdate><title>Lactococcus lactis KF140 Ameliorates Nonalcoholic Fatty Liver Disease Induced by Nε‐Carboxymethyl‐Lysine and High‐Fat Diet</title><author>Lee, Hye‐Bin ; Park, Miri ; Lee, So‐Young ; Ha, Sang Keun ; Kim, Yoonsook ; Lee, Kwang‐Won ; Park, Ho‐Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2861-6265fa55fd126259c605a072b830edb82dba97d65aa76135d7ae35919e3d780d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Absorption</topic><topic>advanced glycation end products</topic><topic>Advanced glycosylation end products</topic><topic>Alanine</topic><topic>Alanine Transaminase - blood</topic><topic>animal models</topic><topic>Animals</topic><topic>Aspartate transaminase</topic><topic>Biomarkers</topic><topic>blood serum</topic><topic>Body fat</topic><topic>Body weight</topic><topic>Body weight gain</topic><topic>clinical trials</topic><topic>Diet, High-Fat - adverse effects</topic><topic>fat intake</topic><topic>Fatty liver</topic><topic>Food consumption</topic><topic>Food processing</topic><topic>food research</topic><topic>glucose</topic><topic>Glucose tolerance</topic><topic>High fat diet</topic><topic>histology</topic><topic>Insulin Resistance</topic><topic>Lactococcus lactis</topic><topic>Lipids</topic><topic>Lipogenesis</topic><topic>Lipogenesis - drug effects</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver diseases</topic><topic>Lysine</topic><topic>Lysine - analogs &amp; derivatives</topic><topic>Lysine - pharmacology</topic><topic>Maillard reaction</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Non-alcoholic Fatty Liver Disease - drug therapy</topic><topic>Non-alcoholic Fatty Liver Disease - etiology</topic><topic>nonalcoholic fatty liver disease</topic><topic>Nε‐carboxymethyl‐lysine</topic><topic>Oral administration</topic><topic>Probiotics</topic><topic>Probiotics - pharmacology</topic><topic>Transaminase</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Hye‐Bin</creatorcontrib><creatorcontrib>Park, Miri</creatorcontrib><creatorcontrib>Lee, So‐Young</creatorcontrib><creatorcontrib>Ha, Sang Keun</creatorcontrib><creatorcontrib>Kim, Yoonsook</creatorcontrib><creatorcontrib>Lee, Kwang‐Won</creatorcontrib><creatorcontrib>Park, Ho‐Young</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium &amp; 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food research</jtitle><addtitle>Mol Nutr Food Res</addtitle><date>2024-08</date><risdate>2024</risdate><volume>68</volume><issue>16</issue><spage>e2400260</spage><epage>n/a</epage><pages>e2400260-n/a</pages><issn>1613-4125</issn><issn>1613-4133</issn><eissn>1613-4133</eissn><abstract>Scope Long‐term consumption of excessive dietary advanced glycation end‐products such as Nε‐carboxymethyl‐lysine (CML), which are produced by the Maillard reaction during food thermal processing, leads to nonalcoholic fatty liver disease (NAFLD) along with high fat consumption. The study previously finds that administration of Lactococcus lactis KF140 (LL‐KF140) detoxifies CML by decreasing CML absorption both in a rat model and clinical trial. Methods and results The present study evaluates the ameliorative effect of LL‐KF140 on NAFLD and fatty liver‐related biomarkers in a mouse model induced by CML and high fat. LL‐KF140 is orally administered to mice at a concentration of 1 × 107 or 1 × 108 colony‐forming unit (CFU) per mouse for 8 weeks. LL‐KF140 administration ameliorates the NAFLD‐related symptoms by reducing body weight and fat mass gain along with levels of serum aspartate transaminase, alanine transferase, and lipids as well as glucose intolerance and insulin resistance in CML‐treated mice. In addition, histological analysis including staining and western blotting shows that LL‐KF140 suppresses the lipogenesis pathway and CML absorption, thereby suppressing CML‐induced NAFLD. Conclusion These findings suggest that LL‐KF140 attenuates dietary CML‐induced NAFLD by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain. Lactococcus lactis KF140 (LL‐KF140) attenuates dietary CML‐induced nonalcoholic fatty liver disease by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>38962859</pmid><doi>10.1002/mnfr.202400260</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-3329-2279</orcidid><orcidid>https://orcid.org/0000-0002-9966-9059</orcidid><oa>free_for_read</oa></addata></record>
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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Absorption
advanced glycation end products
Advanced glycosylation end products
Alanine
Alanine Transaminase - blood
animal models
Animals
Aspartate transaminase
Biomarkers
blood serum
Body fat
Body weight
Body weight gain
clinical trials
Diet, High-Fat - adverse effects
fat intake
Fatty liver
Food consumption
Food processing
food research
glucose
Glucose tolerance
High fat diet
histology
Insulin Resistance
Lactococcus lactis
Lipids
Lipogenesis
Lipogenesis - drug effects
Liver
Liver - drug effects
Liver - metabolism
Liver diseases
Lysine
Lysine - analogs & derivatives
Lysine - pharmacology
Maillard reaction
Male
Mice
Mice, Inbred C57BL
Non-alcoholic Fatty Liver Disease - drug therapy
Non-alcoholic Fatty Liver Disease - etiology
nonalcoholic fatty liver disease
Nε‐carboxymethyl‐lysine
Oral administration
Probiotics
Probiotics - pharmacology
Transaminase
Western blotting
title Lactococcus lactis KF140 Ameliorates Nonalcoholic Fatty Liver Disease Induced by Nε‐Carboxymethyl‐Lysine and High‐Fat Diet
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