Liraglutide Increases the Catabolism of Apolipoprotein B100-Containing Lipoproteins in Patients With Type 2 Diabetes and Reduces Proprotein Convertase Subtilisin/Kexin Type 9 Expression
Dyslipidemia observed in type 2 diabetes (T2D) is atherogenic. Important features of diabetic dyslipidemia are increased levels of triglyceride-rich lipoproteins and small dense LDL particles, which all have apolipoprotein B100 (apoB100) as a major apolipoprotein. This prompted us to study the effec...
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| Veröffentlicht in: | Diabetes care 2021-04, Vol.44 (4), p.1027-1037 |
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| creator | Vergès, Bruno Duvillard, Laurence Pais de Barros, Jean Paul Bouillet, Benjamin Baillot-Rudoni, Sabine Rouland, Alexia Petit, Jean Michel Degrace, Pascal Demizieux, Laurent |
| description | Dyslipidemia observed in type 2 diabetes (T2D) is atherogenic. Important features of diabetic dyslipidemia are increased levels of triglyceride-rich lipoproteins and small dense LDL particles, which all have apolipoprotein B100 (apoB100) as a major apolipoprotein. This prompted us to study the effect of the GLP-1 agonist liraglutide on the metabolism of apoB100-containing lipoproteins.
We performed an in vivo kinetic study with stable isotopes (L-[1-
C]leucine) in 10 patients with T2D before and after 6 months of treatment with liraglutide (1.2 mg/day). We also evaluated in mice the effect of liraglutide on the expression of genes involved in apoB100-containing lipoprotein clearance.
In patients with T2D, liraglutide treatment significantly reduced plasma apoB100 (0.93 ± 0.13 vs. 1.09 ± 0.11 g/L,
= 0.011) and fasting triglycerides (1.76 ± 0.37 vs. 2.48 ± 0.69 mmol/L,
= 0.005). The kinetic study showed a significant increase in indirect catabolism of VLDL
-apoB100 (4.11 ± 1.91 vs. 2.96 ± 1.61 pools/day,
= 0.005), VLDL
-apoB100 (5.17 ± 2.53 vs. 2.84 ± 1.65 pools/day,
= 0.008), and IDL-apoB100 (5.27 ± 2.77 vs. 3.74 ± 1.85 pools/day,
= 0.017) and in catabolism of LDL-apoB100 (0.72 ± 0.22 vs. 0.56 ± 0.22 pools/day,
= 0.005). In mice, liraglutide increased lipoprotein lipase (LPL) gene expression and reduced proprotein convertase subtilisin/kexin type 9 (PCSK9), retinol-binding protein 4 (RBP4), and tumor necrosis factor-α (TNF-α) gene expression in adipose tissue and decreased PCSK9 mRNA and increased LDL receptor protein expression in liver. In vitro, liraglutide directly reduced the expression of
in the liver.
Treatment with liraglutide induces a significant acceleration of the catabolism of triglyceride-rich lipoproteins (VLDL
, VLDL
, IDL) and LDL. Liraglutide modifies the expression of genes involved in apoB100-containing lipoprotein catabolism. These positive effects on lipoprotein metabolism may reduce cardiovascular risk in T2D. |
| doi_str_mv | 10.2337/DC20-1843 |
| format | Article |
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We performed an in vivo kinetic study with stable isotopes (L-[1-
C]leucine) in 10 patients with T2D before and after 6 months of treatment with liraglutide (1.2 mg/day). We also evaluated in mice the effect of liraglutide on the expression of genes involved in apoB100-containing lipoprotein clearance.
In patients with T2D, liraglutide treatment significantly reduced plasma apoB100 (0.93 ± 0.13 vs. 1.09 ± 0.11 g/L,
= 0.011) and fasting triglycerides (1.76 ± 0.37 vs. 2.48 ± 0.69 mmol/L,
= 0.005). The kinetic study showed a significant increase in indirect catabolism of VLDL
-apoB100 (4.11 ± 1.91 vs. 2.96 ± 1.61 pools/day,
= 0.005), VLDL
-apoB100 (5.17 ± 2.53 vs. 2.84 ± 1.65 pools/day,
= 0.008), and IDL-apoB100 (5.27 ± 2.77 vs. 3.74 ± 1.85 pools/day,
= 0.017) and in catabolism of LDL-apoB100 (0.72 ± 0.22 vs. 0.56 ± 0.22 pools/day,
= 0.005). In mice, liraglutide increased lipoprotein lipase (LPL) gene expression and reduced proprotein convertase subtilisin/kexin type 9 (PCSK9), retinol-binding protein 4 (RBP4), and tumor necrosis factor-α (TNF-α) gene expression in adipose tissue and decreased PCSK9 mRNA and increased LDL receptor protein expression in liver. In vitro, liraglutide directly reduced the expression of
in the liver.
Treatment with liraglutide induces a significant acceleration of the catabolism of triglyceride-rich lipoproteins (VLDL
, VLDL
, IDL) and LDL. Liraglutide modifies the expression of genes involved in apoB100-containing lipoprotein catabolism. These positive effects on lipoprotein metabolism may reduce cardiovascular risk in T2D.</description><identifier>ISSN: 0149-5992</identifier><identifier>EISSN: 1935-5548</identifier><identifier>DOI: 10.2337/DC20-1843</identifier><identifier>PMID: 33531418</identifier><language>eng</language><publisher>United States: American Diabetes Association</publisher><subject>Adipose tissue ; Antidiabetics ; Apolipoproteins ; Cardiovascular diseases ; Catabolism ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Dyslipidemia ; Gene expression ; Genes ; GLP-1 receptor agonists ; Health risks ; In vivo methods and tests ; Isotopes ; Kexin ; Leucine ; Lipid metabolism ; Lipoprotein lipase ; Lipoproteins ; Liver ; Low density lipoprotein ; Metabolic disorders ; Metabolism ; Pools ; Proteins ; Research design ; Retinol-binding protein ; Stable isotopes ; Subtilisin ; Triglycerides ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Vitamin A</subject><ispartof>Diabetes care, 2021-04, Vol.44 (4), p.1027-1037</ispartof><rights>2021 by the American Diabetes Association.</rights><rights>Copyright American Diabetes Association Apr 1, 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c348t-d49a158ef734f072d988d419fbeeb1a7480d4217a6f6f5adc00f46a76c9bc5cf3</citedby><cites>FETCH-LOGICAL-c348t-d49a158ef734f072d988d419fbeeb1a7480d4217a6f6f5adc00f46a76c9bc5cf3</cites><orcidid>0000-0001-8957-629X ; 0000-0002-4317-6714 ; 0000-0002-1809-2455</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33531418$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vergès, Bruno</creatorcontrib><creatorcontrib>Duvillard, Laurence</creatorcontrib><creatorcontrib>Pais de Barros, Jean Paul</creatorcontrib><creatorcontrib>Bouillet, Benjamin</creatorcontrib><creatorcontrib>Baillot-Rudoni, Sabine</creatorcontrib><creatorcontrib>Rouland, Alexia</creatorcontrib><creatorcontrib>Petit, Jean Michel</creatorcontrib><creatorcontrib>Degrace, Pascal</creatorcontrib><creatorcontrib>Demizieux, Laurent</creatorcontrib><title>Liraglutide Increases the Catabolism of Apolipoprotein B100-Containing Lipoproteins in Patients With Type 2 Diabetes and Reduces Proprotein Convertase Subtilisin/Kexin Type 9 Expression</title><title>Diabetes care</title><addtitle>Diabetes Care</addtitle><description>Dyslipidemia observed in type 2 diabetes (T2D) is atherogenic. Important features of diabetic dyslipidemia are increased levels of triglyceride-rich lipoproteins and small dense LDL particles, which all have apolipoprotein B100 (apoB100) as a major apolipoprotein. This prompted us to study the effect of the GLP-1 agonist liraglutide on the metabolism of apoB100-containing lipoproteins.
We performed an in vivo kinetic study with stable isotopes (L-[1-
C]leucine) in 10 patients with T2D before and after 6 months of treatment with liraglutide (1.2 mg/day). We also evaluated in mice the effect of liraglutide on the expression of genes involved in apoB100-containing lipoprotein clearance.
In patients with T2D, liraglutide treatment significantly reduced plasma apoB100 (0.93 ± 0.13 vs. 1.09 ± 0.11 g/L,
= 0.011) and fasting triglycerides (1.76 ± 0.37 vs. 2.48 ± 0.69 mmol/L,
= 0.005). The kinetic study showed a significant increase in indirect catabolism of VLDL
-apoB100 (4.11 ± 1.91 vs. 2.96 ± 1.61 pools/day,
= 0.005), VLDL
-apoB100 (5.17 ± 2.53 vs. 2.84 ± 1.65 pools/day,
= 0.008), and IDL-apoB100 (5.27 ± 2.77 vs. 3.74 ± 1.85 pools/day,
= 0.017) and in catabolism of LDL-apoB100 (0.72 ± 0.22 vs. 0.56 ± 0.22 pools/day,
= 0.005). In mice, liraglutide increased lipoprotein lipase (LPL) gene expression and reduced proprotein convertase subtilisin/kexin type 9 (PCSK9), retinol-binding protein 4 (RBP4), and tumor necrosis factor-α (TNF-α) gene expression in adipose tissue and decreased PCSK9 mRNA and increased LDL receptor protein expression in liver. In vitro, liraglutide directly reduced the expression of
in the liver.
Treatment with liraglutide induces a significant acceleration of the catabolism of triglyceride-rich lipoproteins (VLDL
, VLDL
, IDL) and LDL. Liraglutide modifies the expression of genes involved in apoB100-containing lipoprotein catabolism. These positive effects on lipoprotein metabolism may reduce cardiovascular risk in T2D.</description><subject>Adipose tissue</subject><subject>Antidiabetics</subject><subject>Apolipoproteins</subject><subject>Cardiovascular diseases</subject><subject>Catabolism</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Dyslipidemia</subject><subject>Gene expression</subject><subject>Genes</subject><subject>GLP-1 receptor agonists</subject><subject>Health risks</subject><subject>In vivo methods and tests</subject><subject>Isotopes</subject><subject>Kexin</subject><subject>Leucine</subject><subject>Lipid metabolism</subject><subject>Lipoprotein lipase</subject><subject>Lipoproteins</subject><subject>Liver</subject><subject>Low density lipoprotein</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Pools</subject><subject>Proteins</subject><subject>Research design</subject><subject>Retinol-binding protein</subject><subject>Stable isotopes</subject><subject>Subtilisin</subject><subject>Triglycerides</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Vitamin A</subject><issn>0149-5992</issn><issn>1935-5548</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNpdkc1qFTEYhoMo9lhdeAMScKOLsfmdSZZ1WrV4wKIVl0Mm-dKmzMlMk4y0l-bdmdpawVU-eB-evPAi9JKSd4zz7uCoZ6ShSvBHaEM1l42UQj1GG0KFbqTWbA89y_mSECKEUk_RHueSU0HVBv3ahmTOp7UEB_gk2gQmQ8blAnBvihnnKeQdnj0-XOq5zEuaC4SI31NCmn6OxYQY4jne_ssyrvmpKQFiyfhHKBf47GYBzPBRMCOUqjfR4a_gVlvv0_Qgrb6fkEptgL-tYwn17xAPPsN1zf4oND6-XhLkHOb4HD3xZsrw4v7dR98_HJ_1n5rtl48n_eG2sVyo0jihDZUKfMeFJx1zWiknqPYjwEhNJxRxgtHOtL710jhLiBet6VqrRyut5_vozZ23trxaIZdhF7KFaTIR5jUPTKiWCkI6WdHX_6GX85pibTcwSTraEa5Upd7eUTbNOSfww5LCzqSbgZLhds_BWUaG2z0r--reuI47cA_k3wH5bz6wnXo</recordid><startdate>202104</startdate><enddate>202104</enddate><creator>Vergès, Bruno</creator><creator>Duvillard, Laurence</creator><creator>Pais de Barros, Jean Paul</creator><creator>Bouillet, Benjamin</creator><creator>Baillot-Rudoni, Sabine</creator><creator>Rouland, Alexia</creator><creator>Petit, Jean Michel</creator><creator>Degrace, Pascal</creator><creator>Demizieux, Laurent</creator><general>American Diabetes Association</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8957-629X</orcidid><orcidid>https://orcid.org/0000-0002-4317-6714</orcidid><orcidid>https://orcid.org/0000-0002-1809-2455</orcidid></search><sort><creationdate>202104</creationdate><title>Liraglutide Increases the Catabolism of Apolipoprotein B100-Containing Lipoproteins in Patients With Type 2 Diabetes and Reduces Proprotein Convertase Subtilisin/Kexin Type 9 Expression</title><author>Vergès, Bruno ; Duvillard, Laurence ; Pais de Barros, Jean Paul ; Bouillet, Benjamin ; Baillot-Rudoni, Sabine ; Rouland, Alexia ; Petit, Jean Michel ; Degrace, Pascal ; Demizieux, Laurent</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-d49a158ef734f072d988d419fbeeb1a7480d4217a6f6f5adc00f46a76c9bc5cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adipose tissue</topic><topic>Antidiabetics</topic><topic>Apolipoproteins</topic><topic>Cardiovascular diseases</topic><topic>Catabolism</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Dyslipidemia</topic><topic>Gene expression</topic><topic>Genes</topic><topic>GLP-1 receptor agonists</topic><topic>Health risks</topic><topic>In vivo methods and tests</topic><topic>Isotopes</topic><topic>Kexin</topic><topic>Leucine</topic><topic>Lipid metabolism</topic><topic>Lipoprotein lipase</topic><topic>Lipoproteins</topic><topic>Liver</topic><topic>Low density lipoprotein</topic><topic>Metabolic disorders</topic><topic>Metabolism</topic><topic>Pools</topic><topic>Proteins</topic><topic>Research design</topic><topic>Retinol-binding protein</topic><topic>Stable isotopes</topic><topic>Subtilisin</topic><topic>Triglycerides</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Vitamin A</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vergès, Bruno</creatorcontrib><creatorcontrib>Duvillard, Laurence</creatorcontrib><creatorcontrib>Pais de Barros, Jean Paul</creatorcontrib><creatorcontrib>Bouillet, Benjamin</creatorcontrib><creatorcontrib>Baillot-Rudoni, Sabine</creatorcontrib><creatorcontrib>Rouland, Alexia</creatorcontrib><creatorcontrib>Petit, Jean Michel</creatorcontrib><creatorcontrib>Degrace, Pascal</creatorcontrib><creatorcontrib>Demizieux, Laurent</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vergès, Bruno</au><au>Duvillard, Laurence</au><au>Pais de Barros, Jean Paul</au><au>Bouillet, Benjamin</au><au>Baillot-Rudoni, Sabine</au><au>Rouland, Alexia</au><au>Petit, Jean Michel</au><au>Degrace, Pascal</au><au>Demizieux, Laurent</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Liraglutide Increases the Catabolism of Apolipoprotein B100-Containing Lipoproteins in Patients With Type 2 Diabetes and Reduces Proprotein Convertase Subtilisin/Kexin Type 9 Expression</atitle><jtitle>Diabetes care</jtitle><addtitle>Diabetes Care</addtitle><date>2021-04</date><risdate>2021</risdate><volume>44</volume><issue>4</issue><spage>1027</spage><epage>1037</epage><pages>1027-1037</pages><issn>0149-5992</issn><eissn>1935-5548</eissn><abstract>Dyslipidemia observed in type 2 diabetes (T2D) is atherogenic. Important features of diabetic dyslipidemia are increased levels of triglyceride-rich lipoproteins and small dense LDL particles, which all have apolipoprotein B100 (apoB100) as a major apolipoprotein. This prompted us to study the effect of the GLP-1 agonist liraglutide on the metabolism of apoB100-containing lipoproteins.
We performed an in vivo kinetic study with stable isotopes (L-[1-
C]leucine) in 10 patients with T2D before and after 6 months of treatment with liraglutide (1.2 mg/day). We also evaluated in mice the effect of liraglutide on the expression of genes involved in apoB100-containing lipoprotein clearance.
In patients with T2D, liraglutide treatment significantly reduced plasma apoB100 (0.93 ± 0.13 vs. 1.09 ± 0.11 g/L,
= 0.011) and fasting triglycerides (1.76 ± 0.37 vs. 2.48 ± 0.69 mmol/L,
= 0.005). The kinetic study showed a significant increase in indirect catabolism of VLDL
-apoB100 (4.11 ± 1.91 vs. 2.96 ± 1.61 pools/day,
= 0.005), VLDL
-apoB100 (5.17 ± 2.53 vs. 2.84 ± 1.65 pools/day,
= 0.008), and IDL-apoB100 (5.27 ± 2.77 vs. 3.74 ± 1.85 pools/day,
= 0.017) and in catabolism of LDL-apoB100 (0.72 ± 0.22 vs. 0.56 ± 0.22 pools/day,
= 0.005). In mice, liraglutide increased lipoprotein lipase (LPL) gene expression and reduced proprotein convertase subtilisin/kexin type 9 (PCSK9), retinol-binding protein 4 (RBP4), and tumor necrosis factor-α (TNF-α) gene expression in adipose tissue and decreased PCSK9 mRNA and increased LDL receptor protein expression in liver. In vitro, liraglutide directly reduced the expression of
in the liver.
Treatment with liraglutide induces a significant acceleration of the catabolism of triglyceride-rich lipoproteins (VLDL
, VLDL
, IDL) and LDL. Liraglutide modifies the expression of genes involved in apoB100-containing lipoprotein catabolism. These positive effects on lipoprotein metabolism may reduce cardiovascular risk in T2D.</abstract><cop>United States</cop><pub>American Diabetes Association</pub><pmid>33531418</pmid><doi>10.2337/DC20-1843</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-8957-629X</orcidid><orcidid>https://orcid.org/0000-0002-4317-6714</orcidid><orcidid>https://orcid.org/0000-0002-1809-2455</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetes care, 2021-04, Vol.44 (4), p.1027-1037 |
| issn | 0149-5992 1935-5548 |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adipose tissue Antidiabetics Apolipoproteins Cardiovascular diseases Catabolism Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Dyslipidemia Gene expression Genes GLP-1 receptor agonists Health risks In vivo methods and tests Isotopes Kexin Leucine Lipid metabolism Lipoprotein lipase Lipoproteins Liver Low density lipoprotein Metabolic disorders Metabolism Pools Proteins Research design Retinol-binding protein Stable isotopes Subtilisin Triglycerides Tumor necrosis factor-TNF Tumor necrosis factor-α Vitamin A |
| title | Liraglutide Increases the Catabolism of Apolipoprotein B100-Containing Lipoproteins in Patients With Type 2 Diabetes and Reduces Proprotein Convertase Subtilisin/Kexin Type 9 Expression |
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