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Liraglutide suppresses postprandial triglyceride and apolipoprotein B48 elevations after a fat-rich meal in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled, cross-over trial
Aims Postprandial triglyceridaemia is a risk factor for cardiovascular disease (CVD). This study investigated the effects of steady‐state liraglutide 1.8 mg versus placebo on postprandial plasma lipid concentrations after 3 weeks of treatment in patients with type 2 diabetes mellitus (T2DM). Methods...
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Published in: | Diabetes, obesity & metabolism obesity & metabolism, 2013-11, Vol.15 (11), p.1040-1048 |
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creator | Hermansen, K. Bækdal, T. A. Düring, M. Pietraszek, A. Mortensen, L. S. Jørgensen, H. Flint, A. |
description | Aims
Postprandial triglyceridaemia is a risk factor for cardiovascular disease (CVD). This study investigated the effects of steady‐state liraglutide 1.8 mg versus placebo on postprandial plasma lipid concentrations after 3 weeks of treatment in patients with type 2 diabetes mellitus (T2DM).
Methods
In a cross‐over trial, patients with T2DM (n = 20, 18–75 years, BMI 18.5–40 kg/m2) were randomized to once‐daily subcutaneous liraglutide (weekly dose escalation from 0.6 to 1.8 mg) and placebo. After each 3‐week period, a standardized fat‐rich meal was provided, and the effects of liraglutide on triglyceride (primary endpoint AUC0–8h), apolipoprotein B48, non‐esterified fatty acids, glycaemic responses and gastric emptying were assessed. ClinicalTrials.gov ID: NCT00993304. Funding: Novo Nordisk A/S.
Results
After 3 weeks, mean postprandial triglyceride (AUC0–8h liraglutide/placebo treatment‐ratio 0.72, 95% CI [0.62–0.83], p = 0.0004) and apolipoprotein B48 (AUC0–8h ratio 0.65 [0.58–0.73], p |
doi_str_mv | 10.1111/dom.12133 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1458529914</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1458529914</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4873-5e2c6232d146b655de89eb0c2edab9e97252f65fdfb82a6c3c96e34962bb9a483</originalsourceid><addsrcrecordid>eNqNkstu1TAQQCMEoqWw4AeQJTYgkdav-Mbd0UJbRKEbHkvLcSatixMb22m5_CI_he-9bRdIILzxQ2fOeEZTVU8J3iVl7fV-3CWUMHav2iZcsJowKu6vz7RuJaZb1aOULjHGnLWLh9UWZaJlWMjt6tepjfrczdn2gNIcQoSUIKHgUw5RT73VDuVoz93SQFxB5Q3p4J0NPkSfwU7ogLcIHFzpbP2UkB4yRKTRoHMdrblAIxRJ4UIBYMoJXdt8gfIyAKKoZOggQ9ovEauEfrQ_oX-Fej93DurO2ancgtMGOl8bP-XonVsRJvqUan9VkpUfave4ejBol-DJzb5TfT56--nwpD49O353-Pq0NrxdsLoBagRltC_t6UTT9NBK6LCh0OtOglzQhg6iGfqha6kWhhkpgHEpaNdJzVu2U73YeEv932dIWY02GXBOT-DnpAhv2oZKSfh_oJwxKTjBBX3-B3rp5ziVQhTDjeSMcNr-iyouTFj5_cr1ckOtWxRhUCHaUcelIlitRkaVNqv1yBT22Y1x7kbo78jbGSnA3ga4tg6WfzepN2cfbpX1JsKmDD_uInT8psSCLRr19eOxao9OvhyUutV79hvWUdw4</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1440137250</pqid></control><display><type>article</type><title>Liraglutide suppresses postprandial triglyceride and apolipoprotein B48 elevations after a fat-rich meal in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled, cross-over trial</title><source>Wiley</source><creator>Hermansen, K. ; Bækdal, T. A. ; Düring, M. ; Pietraszek, A. ; Mortensen, L. S. ; Jørgensen, H. ; Flint, A.</creator><creatorcontrib>Hermansen, K. ; Bækdal, T. A. ; Düring, M. ; Pietraszek, A. ; Mortensen, L. S. ; Jørgensen, H. ; Flint, A.</creatorcontrib><description>Aims
Postprandial triglyceridaemia is a risk factor for cardiovascular disease (CVD). This study investigated the effects of steady‐state liraglutide 1.8 mg versus placebo on postprandial plasma lipid concentrations after 3 weeks of treatment in patients with type 2 diabetes mellitus (T2DM).
Methods
In a cross‐over trial, patients with T2DM (n = 20, 18–75 years, BMI 18.5–40 kg/m2) were randomized to once‐daily subcutaneous liraglutide (weekly dose escalation from 0.6 to 1.8 mg) and placebo. After each 3‐week period, a standardized fat‐rich meal was provided, and the effects of liraglutide on triglyceride (primary endpoint AUC0–8h), apolipoprotein B48, non‐esterified fatty acids, glycaemic responses and gastric emptying were assessed. ClinicalTrials.gov ID: NCT00993304. Funding: Novo Nordisk A/S.
Results
After 3 weeks, mean postprandial triglyceride (AUC0–8h liraglutide/placebo treatment‐ratio 0.72, 95% CI [0.62–0.83], p = 0.0004) and apolipoprotein B48 (AUC0–8h ratio 0.65 [0.58–0.73], p < 0.0001) significantly decreased with liraglutide 1.8 mg versus placebo, as did iAUC0–8h and Cmax (p < 0.001). No significant treatment differences were observed for non‐esterified fatty acids. Mean postprandial glucose and glucagon AUC0–8h and Cmax were significantly reduced with liraglutide versus placebo. Postprandial gastric emptying rate [assessed by paracetamol absorption (liquid phase) and the 13C‐octanoate breath test (solid phase)] displayed no treatment differences. Mean low‐density lipoprotein and total cholesterol decreased significantly with liraglutide versus placebo.
Conclusions
Liraglutide treatment in patients with T2DM significantly reduced postprandial excursions of triglyceride and apolipoprotein B48 after a fat‐rich meal, independently of gastric emptying. Results indicate liraglutide's potential to reduce CVD risk via improvement of postprandial lipaemia.</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/dom.12133</identifier><identifier>PMID: 23683069</identifier><identifier>CODEN: DOMEF6</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Aged ; antidiabetic drug ; Antidiabetics ; Apolipoproteins ; Body Mass Index ; Cardiovascular diseases ; Cardiovascular Diseases - complications ; Cardiovascular Diseases - epidemiology ; Cardiovascular Diseases - prevention & control ; Cholesterol ; Cross-Over Studies ; Denmark - epidemiology ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - drug therapy ; Diet ; Diet, High-Fat - adverse effects ; Double-Blind Method ; Fatty acids ; Female ; Gastric emptying ; Gastric Emptying - drug effects ; Germany - epidemiology ; GLP-1 analogue ; Glucagon ; Glucagon-Like Peptide 1 - adverse effects ; Glucagon-Like Peptide 1 - analogs & derivatives ; Glucagon-Like Peptide 1 - blood ; Glucagon-Like Peptide 1 - pharmacokinetics ; Glucagon-Like Peptide 1 - therapeutic use ; Half-Life ; Humans ; Hyperlipidemias - complications ; Hyperlipidemias - etiology ; Hyperlipidemias - prevention & control ; Hypoglycemic Agents - adverse effects ; Hypoglycemic Agents - blood ; Hypoglycemic Agents - pharmacokinetics ; Hypoglycemic Agents - therapeutic use ; Hypolipidemic Agents - adverse effects ; Hypolipidemic Agents - blood ; Hypolipidemic Agents - pharmacokinetics ; Hypolipidemic Agents - therapeutic use ; lipid-lowering therapy ; Lipids ; Lipids - blood ; Liraglutide ; Male ; Middle Aged ; Obesity - complications ; Paracetamol ; phase I-II study ; Placebos ; Postprandial Period ; randomized trial ; Risk Factors ; type II diabetes</subject><ispartof>Diabetes, obesity & metabolism, 2013-11, Vol.15 (11), p.1040-1048</ispartof><rights>2013 The Authors. Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd</rights><rights>2013 The Authors. Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.</rights><rights>2013 John Wiley & Sons Ltd</rights><rights>2013. This article is published under http://creativecommons.org/licenses/by-nc/3.0/ (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><citedby>FETCH-LOGICAL-c4873-5e2c6232d146b655de89eb0c2edab9e97252f65fdfb82a6c3c96e34962bb9a483</citedby><cites>FETCH-LOGICAL-c4873-5e2c6232d146b655de89eb0c2edab9e97252f65fdfb82a6c3c96e34962bb9a483</cites></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/23683069$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hermansen, K.</creatorcontrib><creatorcontrib>Bækdal, T. A.</creatorcontrib><creatorcontrib>Düring, M.</creatorcontrib><creatorcontrib>Pietraszek, A.</creatorcontrib><creatorcontrib>Mortensen, L. S.</creatorcontrib><creatorcontrib>Jørgensen, H.</creatorcontrib><creatorcontrib>Flint, A.</creatorcontrib><title>Liraglutide suppresses postprandial triglyceride and apolipoprotein B48 elevations after a fat-rich meal in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled, cross-over trial</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>Aims
Postprandial triglyceridaemia is a risk factor for cardiovascular disease (CVD). This study investigated the effects of steady‐state liraglutide 1.8 mg versus placebo on postprandial plasma lipid concentrations after 3 weeks of treatment in patients with type 2 diabetes mellitus (T2DM).
Methods
In a cross‐over trial, patients with T2DM (n = 20, 18–75 years, BMI 18.5–40 kg/m2) were randomized to once‐daily subcutaneous liraglutide (weekly dose escalation from 0.6 to 1.8 mg) and placebo. After each 3‐week period, a standardized fat‐rich meal was provided, and the effects of liraglutide on triglyceride (primary endpoint AUC0–8h), apolipoprotein B48, non‐esterified fatty acids, glycaemic responses and gastric emptying were assessed. ClinicalTrials.gov ID: NCT00993304. Funding: Novo Nordisk A/S.
Results
After 3 weeks, mean postprandial triglyceride (AUC0–8h liraglutide/placebo treatment‐ratio 0.72, 95% CI [0.62–0.83], p = 0.0004) and apolipoprotein B48 (AUC0–8h ratio 0.65 [0.58–0.73], p < 0.0001) significantly decreased with liraglutide 1.8 mg versus placebo, as did iAUC0–8h and Cmax (p < 0.001). No significant treatment differences were observed for non‐esterified fatty acids. Mean postprandial glucose and glucagon AUC0–8h and Cmax were significantly reduced with liraglutide versus placebo. Postprandial gastric emptying rate [assessed by paracetamol absorption (liquid phase) and the 13C‐octanoate breath test (solid phase)] displayed no treatment differences. Mean low‐density lipoprotein and total cholesterol decreased significantly with liraglutide versus placebo.
Conclusions
Liraglutide treatment in patients with T2DM significantly reduced postprandial excursions of triglyceride and apolipoprotein B48 after a fat‐rich meal, independently of gastric emptying. Results indicate liraglutide's potential to reduce CVD risk via improvement of postprandial lipaemia.</description><subject>Aged</subject><subject>antidiabetic drug</subject><subject>Antidiabetics</subject><subject>Apolipoproteins</subject><subject>Body Mass Index</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular Diseases - complications</subject><subject>Cardiovascular Diseases - epidemiology</subject><subject>Cardiovascular Diseases - prevention & control</subject><subject>Cholesterol</subject><subject>Cross-Over Studies</subject><subject>Denmark - epidemiology</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diet</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Double-Blind Method</subject><subject>Fatty acids</subject><subject>Female</subject><subject>Gastric emptying</subject><subject>Gastric Emptying - drug effects</subject><subject>Germany - epidemiology</subject><subject>GLP-1 analogue</subject><subject>Glucagon</subject><subject>Glucagon-Like Peptide 1 - adverse effects</subject><subject>Glucagon-Like Peptide 1 - analogs & derivatives</subject><subject>Glucagon-Like Peptide 1 - blood</subject><subject>Glucagon-Like Peptide 1 - pharmacokinetics</subject><subject>Glucagon-Like Peptide 1 - therapeutic use</subject><subject>Half-Life</subject><subject>Humans</subject><subject>Hyperlipidemias - complications</subject><subject>Hyperlipidemias - etiology</subject><subject>Hyperlipidemias - prevention & control</subject><subject>Hypoglycemic Agents - adverse effects</subject><subject>Hypoglycemic Agents - blood</subject><subject>Hypoglycemic Agents - pharmacokinetics</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Hypolipidemic Agents - adverse effects</subject><subject>Hypolipidemic Agents - blood</subject><subject>Hypolipidemic Agents - pharmacokinetics</subject><subject>Hypolipidemic Agents - therapeutic use</subject><subject>lipid-lowering therapy</subject><subject>Lipids</subject><subject>Lipids - blood</subject><subject>Liraglutide</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Obesity - complications</subject><subject>Paracetamol</subject><subject>phase I-II study</subject><subject>Placebos</subject><subject>Postprandial Period</subject><subject>randomized trial</subject><subject>Risk Factors</subject><subject>type II diabetes</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNqNkstu1TAQQCMEoqWw4AeQJTYgkdav-Mbd0UJbRKEbHkvLcSatixMb22m5_CI_he-9bRdIILzxQ2fOeEZTVU8J3iVl7fV-3CWUMHav2iZcsJowKu6vz7RuJaZb1aOULjHGnLWLh9UWZaJlWMjt6tepjfrczdn2gNIcQoSUIKHgUw5RT73VDuVoz93SQFxB5Q3p4J0NPkSfwU7ogLcIHFzpbP2UkB4yRKTRoHMdrblAIxRJ4UIBYMoJXdt8gfIyAKKoZOggQ9ovEauEfrQ_oX-Fej93DurO2ancgtMGOl8bP-XonVsRJvqUan9VkpUfave4ejBol-DJzb5TfT56--nwpD49O353-Pq0NrxdsLoBagRltC_t6UTT9NBK6LCh0OtOglzQhg6iGfqha6kWhhkpgHEpaNdJzVu2U73YeEv932dIWY02GXBOT-DnpAhv2oZKSfh_oJwxKTjBBX3-B3rp5ziVQhTDjeSMcNr-iyouTFj5_cr1ckOtWxRhUCHaUcelIlitRkaVNqv1yBT22Y1x7kbo78jbGSnA3ga4tg6WfzepN2cfbpX1JsKmDD_uInT8psSCLRr19eOxao9OvhyUutV79hvWUdw4</recordid><startdate>201311</startdate><enddate>201311</enddate><creator>Hermansen, K.</creator><creator>Bækdal, T. A.</creator><creator>Düring, M.</creator><creator>Pietraszek, A.</creator><creator>Mortensen, L. S.</creator><creator>Jørgensen, H.</creator><creator>Flint, A.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>24P</scope><scope>WIN</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>7TS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>201311</creationdate><title>Liraglutide suppresses postprandial triglyceride and apolipoprotein B48 elevations after a fat-rich meal in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled, cross-over trial</title><author>Hermansen, K. ; Bækdal, T. A. ; Düring, M. ; Pietraszek, A. ; Mortensen, L. S. ; Jørgensen, H. ; Flint, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4873-5e2c6232d146b655de89eb0c2edab9e97252f65fdfb82a6c3c96e34962bb9a483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aged</topic><topic>antidiabetic drug</topic><topic>Antidiabetics</topic><topic>Apolipoproteins</topic><topic>Body Mass Index</topic><topic>Cardiovascular diseases</topic><topic>Cardiovascular Diseases - complications</topic><topic>Cardiovascular Diseases - epidemiology</topic><topic>Cardiovascular Diseases - prevention & control</topic><topic>Cholesterol</topic><topic>Cross-Over Studies</topic><topic>Denmark - epidemiology</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diet</topic><topic>Diet, High-Fat - adverse effects</topic><topic>Double-Blind Method</topic><topic>Fatty acids</topic><topic>Female</topic><topic>Gastric emptying</topic><topic>Gastric Emptying - drug effects</topic><topic>Germany - epidemiology</topic><topic>GLP-1 analogue</topic><topic>Glucagon</topic><topic>Glucagon-Like Peptide 1 - adverse effects</topic><topic>Glucagon-Like Peptide 1 - analogs & derivatives</topic><topic>Glucagon-Like Peptide 1 - blood</topic><topic>Glucagon-Like Peptide 1 - pharmacokinetics</topic><topic>Glucagon-Like Peptide 1 - therapeutic use</topic><topic>Half-Life</topic><topic>Humans</topic><topic>Hyperlipidemias - complications</topic><topic>Hyperlipidemias - etiology</topic><topic>Hyperlipidemias - prevention & control</topic><topic>Hypoglycemic Agents - adverse effects</topic><topic>Hypoglycemic Agents - blood</topic><topic>Hypoglycemic Agents - pharmacokinetics</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Hypolipidemic Agents - adverse effects</topic><topic>Hypolipidemic Agents - blood</topic><topic>Hypolipidemic Agents - pharmacokinetics</topic><topic>Hypolipidemic Agents - therapeutic use</topic><topic>lipid-lowering therapy</topic><topic>Lipids</topic><topic>Lipids - blood</topic><topic>Liraglutide</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Obesity - complications</topic><topic>Paracetamol</topic><topic>phase I-II study</topic><topic>Placebos</topic><topic>Postprandial Period</topic><topic>randomized trial</topic><topic>Risk Factors</topic><topic>type II diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hermansen, K.</creatorcontrib><creatorcontrib>Bækdal, T. A.</creatorcontrib><creatorcontrib>Düring, M.</creatorcontrib><creatorcontrib>Pietraszek, A.</creatorcontrib><creatorcontrib>Mortensen, L. S.</creatorcontrib><creatorcontrib>Jørgensen, H.</creatorcontrib><creatorcontrib>Flint, A.</creatorcontrib><collection>Istex</collection><collection>Open Access: Wiley-Blackwell Open Access Journals</collection><collection>Wiley Online Library Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hermansen, K.</au><au>Bækdal, T. A.</au><au>Düring, M.</au><au>Pietraszek, A.</au><au>Mortensen, L. S.</au><au>Jørgensen, H.</au><au>Flint, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Liraglutide suppresses postprandial triglyceride and apolipoprotein B48 elevations after a fat-rich meal in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled, cross-over trial</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2013-11</date><risdate>2013</risdate><volume>15</volume><issue>11</issue><spage>1040</spage><epage>1048</epage><pages>1040-1048</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><coden>DOMEF6</coden><abstract>Aims
Postprandial triglyceridaemia is a risk factor for cardiovascular disease (CVD). This study investigated the effects of steady‐state liraglutide 1.8 mg versus placebo on postprandial plasma lipid concentrations after 3 weeks of treatment in patients with type 2 diabetes mellitus (T2DM).
Methods
In a cross‐over trial, patients with T2DM (n = 20, 18–75 years, BMI 18.5–40 kg/m2) were randomized to once‐daily subcutaneous liraglutide (weekly dose escalation from 0.6 to 1.8 mg) and placebo. After each 3‐week period, a standardized fat‐rich meal was provided, and the effects of liraglutide on triglyceride (primary endpoint AUC0–8h), apolipoprotein B48, non‐esterified fatty acids, glycaemic responses and gastric emptying were assessed. ClinicalTrials.gov ID: NCT00993304. Funding: Novo Nordisk A/S.
Results
After 3 weeks, mean postprandial triglyceride (AUC0–8h liraglutide/placebo treatment‐ratio 0.72, 95% CI [0.62–0.83], p = 0.0004) and apolipoprotein B48 (AUC0–8h ratio 0.65 [0.58–0.73], p < 0.0001) significantly decreased with liraglutide 1.8 mg versus placebo, as did iAUC0–8h and Cmax (p < 0.001). No significant treatment differences were observed for non‐esterified fatty acids. Mean postprandial glucose and glucagon AUC0–8h and Cmax were significantly reduced with liraglutide versus placebo. Postprandial gastric emptying rate [assessed by paracetamol absorption (liquid phase) and the 13C‐octanoate breath test (solid phase)] displayed no treatment differences. Mean low‐density lipoprotein and total cholesterol decreased significantly with liraglutide versus placebo.
Conclusions
Liraglutide treatment in patients with T2DM significantly reduced postprandial excursions of triglyceride and apolipoprotein B48 after a fat‐rich meal, independently of gastric emptying. Results indicate liraglutide's potential to reduce CVD risk via improvement of postprandial lipaemia.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>23683069</pmid><doi>10.1111/dom.12133</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged antidiabetic drug Antidiabetics Apolipoproteins Body Mass Index Cardiovascular diseases Cardiovascular Diseases - complications Cardiovascular Diseases - epidemiology Cardiovascular Diseases - prevention & control Cholesterol Cross-Over Studies Denmark - epidemiology Diabetes Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - drug therapy Diet Diet, High-Fat - adverse effects Double-Blind Method Fatty acids Female Gastric emptying Gastric Emptying - drug effects Germany - epidemiology GLP-1 analogue Glucagon Glucagon-Like Peptide 1 - adverse effects Glucagon-Like Peptide 1 - analogs & derivatives Glucagon-Like Peptide 1 - blood Glucagon-Like Peptide 1 - pharmacokinetics Glucagon-Like Peptide 1 - therapeutic use Half-Life Humans Hyperlipidemias - complications Hyperlipidemias - etiology Hyperlipidemias - prevention & control Hypoglycemic Agents - adverse effects Hypoglycemic Agents - blood Hypoglycemic Agents - pharmacokinetics Hypoglycemic Agents - therapeutic use Hypolipidemic Agents - adverse effects Hypolipidemic Agents - blood Hypolipidemic Agents - pharmacokinetics Hypolipidemic Agents - therapeutic use lipid-lowering therapy Lipids Lipids - blood Liraglutide Male Middle Aged Obesity - complications Paracetamol phase I-II study Placebos Postprandial Period randomized trial Risk Factors type II diabetes |
title | Liraglutide suppresses postprandial triglyceride and apolipoprotein B48 elevations after a fat-rich meal in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled, cross-over trial |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T16%3A00%3A38IST&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=Liraglutide%20suppresses%20postprandial%20triglyceride%20and%20apolipoprotein%20B48%20elevations%20after%20a%20fat-rich%20meal%20in%20patients%20with%20type%202%20diabetes:%20a%20randomized,%20double-blind,%20placebo-controlled,%20cross-over%20trial&rft.jtitle=Diabetes,%20obesity%20&%20metabolism&rft.au=Hermansen,%20K.&rft.date=2013-11&rft.volume=15&rft.issue=11&rft.spage=1040&rft.epage=1048&rft.pages=1040-1048&rft.issn=1462-8902&rft.eissn=1463-1326&rft.coden=DOMEF6&rft_id=info:doi/10.1111/dom.12133&rft_dat=%3Cproquest_cross%3E1458529914%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4873-5e2c6232d146b655de89eb0c2edab9e97252f65fdfb82a6c3c96e34962bb9a483%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1440137250&rft_id=info:pmid/23683069&rfr_iscdi=true |