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Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men.
PLoS One. 2016; 11(1):e0145890.Plos

Abstract

CONTEXT

Glucose and lipids stimulate the gut-hormones glucagon-like peptide (GLP)-1, GLP-2 and glucose-dependent insulinotropic polypeptide (GIP) but the effect of these on human postprandial lipid metabolism is not fully clarified.

OBJECTIVE

To explore the responses of GLP-1, GLP-2 and GIP after a fat-rich meal compared to the same responses after an oral glucose tolerance test (OGTT) and to investigate possible relationships between incretin response and triglyceride-rich lipoprotein (TRL) response to a fat-rich meal.

DESIGN

Glucose, insulin, GLP-1, GLP-2 and GIP were measured after an OGTT and after a fat-rich meal in 65 healthy obese (BMI 26.5-40.2 kg/m(2)) male subjects. Triglycerides (TG), apoB48 and apoB100 in TG-rich lipoproteins (chylomicrons, VLDL1 and VLDL2) were measured after the fat-rich meal.

MAIN OUTCOME MEASURES

Postprandial responses (area under the curve, AUC) for glucose, insulin, GLP-1, GLP-2, GIP in plasma, and TG, apoB48 and apoB100 in plasma and TG-rich lipoproteins.

RESULTS

The GLP-1, GLP-2 and GIP responses after the fat-rich meal and after the OGTT correlated strongly (r = 0.73, p<0.0001; r = 0.46, p<0.001 and r = 0.69, p<0.001, respectively). Glucose and insulin AUCs were lower, but the AUCs for GLP-1, GLP-2 and GIP were significantly higher after the fat-rich meal than after the OGTT. The peak value for all hormones appeared at 120 minutes after the fat-rich meal, compared to 30 minutes after the OGTT. After the fat-rich meal, the AUCs for GLP-1, GLP-2 and GIP correlated significantly with plasma TG- and apoB48 AUCs but the contribution was very modest.

CONCLUSIONS

In obese males, GLP-1, GLP-2 and GIP responses to a fat-rich meal are greater than following an OGTT. However, the most important explanatory variable for postprandial TG excursion was fasting triglycerides. The contribution of endogenous GLP-1, GLP-2 and GIP to explaining the variance in postprandial TG excursion was minor.

Authors+Show Affiliations

Research programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland. Endocrinology, Abdominal Center, Helsinki University Hospital, Helsinki, Finland.Department of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.Research programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.Department of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.Department of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.Research programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland. Endocrinology, Abdominal Center, Helsinki University Hospital, Helsinki, Finland.Research programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy.Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy.Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada.Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada.NNF Centre for Basic Metabolic Research, and Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.NNF Centre for Basic Metabolic Research, and Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.Department of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.Research programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.

Pub Type(s)

Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26752550

Citation

Matikainen, Niina, et al. "Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men." PloS One, vol. 11, no. 1, 2016, pp. e0145890.
Matikainen N, Björnson E, Söderlund S, et al. Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men. PLoS One. 2016;11(1):e0145890.
Matikainen, N., Björnson, E., Söderlund, S., Borén, C., Eliasson, B., Pietiläinen, K. H., Bogl, L. H., Hakkarainen, A., Lundbom, N., Rivellese, A., Riccardi, G., Després, J. P., Alméras, N., Holst, J. J., Deacon, C. F., Borén, J., & Taskinen, M. R. (2016). Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men. PloS One, 11(1), e0145890. https://doi.org/10.1371/journal.pone.0145890
Matikainen N, et al. Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men. PLoS One. 2016;11(1):e0145890. PubMed PMID: 26752550.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men. AU - Matikainen,Niina, AU - Björnson,Elias, AU - Söderlund,Sanni, AU - Borén,Christofer, AU - Eliasson,Björn, AU - Pietiläinen,Kirsi H, AU - Bogl,Leonie H, AU - Hakkarainen,Antti, AU - Lundbom,Nina, AU - Rivellese,Angela, AU - Riccardi,Gabriele, AU - Després,Jean-Pierre, AU - Alméras,Natalie, AU - Holst,Jens Juul, AU - Deacon,Carolyn F, AU - Borén,Jan, AU - Taskinen,Marja-Riitta, Y1 - 2016/01/11/ PY - 2015/10/26/received PY - 2015/12/09/accepted PY - 2016/1/12/entrez PY - 2016/1/12/pubmed PY - 2016/7/1/medline SP - e0145890 EP - e0145890 JF - PloS one JO - PLoS One VL - 11 IS - 1 N2 - CONTEXT: Glucose and lipids stimulate the gut-hormones glucagon-like peptide (GLP)-1, GLP-2 and glucose-dependent insulinotropic polypeptide (GIP) but the effect of these on human postprandial lipid metabolism is not fully clarified. OBJECTIVE: To explore the responses of GLP-1, GLP-2 and GIP after a fat-rich meal compared to the same responses after an oral glucose tolerance test (OGTT) and to investigate possible relationships between incretin response and triglyceride-rich lipoprotein (TRL) response to a fat-rich meal. DESIGN: Glucose, insulin, GLP-1, GLP-2 and GIP were measured after an OGTT and after a fat-rich meal in 65 healthy obese (BMI 26.5-40.2 kg/m(2)) male subjects. Triglycerides (TG), apoB48 and apoB100 in TG-rich lipoproteins (chylomicrons, VLDL1 and VLDL2) were measured after the fat-rich meal. MAIN OUTCOME MEASURES: Postprandial responses (area under the curve, AUC) for glucose, insulin, GLP-1, GLP-2, GIP in plasma, and TG, apoB48 and apoB100 in plasma and TG-rich lipoproteins. RESULTS: The GLP-1, GLP-2 and GIP responses after the fat-rich meal and after the OGTT correlated strongly (r = 0.73, p<0.0001; r = 0.46, p<0.001 and r = 0.69, p<0.001, respectively). Glucose and insulin AUCs were lower, but the AUCs for GLP-1, GLP-2 and GIP were significantly higher after the fat-rich meal than after the OGTT. The peak value for all hormones appeared at 120 minutes after the fat-rich meal, compared to 30 minutes after the OGTT. After the fat-rich meal, the AUCs for GLP-1, GLP-2 and GIP correlated significantly with plasma TG- and apoB48 AUCs but the contribution was very modest. CONCLUSIONS: In obese males, GLP-1, GLP-2 and GIP responses to a fat-rich meal are greater than following an OGTT. However, the most important explanatory variable for postprandial TG excursion was fasting triglycerides. The contribution of endogenous GLP-1, GLP-2 and GIP to explaining the variance in postprandial TG excursion was minor. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/26752550/Minor_Contribution_of_Endogenous_GLP_1_and_GLP_2_to_Postprandial_Lipemia_in_Obese_Men_ L2 - https://dx.plos.org/10.1371/journal.pone.0145890 DB - PRIME DP - Unbound Medicine ER -