Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes

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Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes. / Pietraszek, A; Gregersen, S; Pedersen, S B; Holst, Jens Juul; Hermansen, K.

In: European Journal of Clinical Nutrition, Vol. 68, 14.05.2014, p. 1022-28.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Pietraszek, A, Gregersen, S, Pedersen, SB, Holst, JJ & Hermansen, K 2014, 'Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes', European Journal of Clinical Nutrition, vol. 68, pp. 1022-28. https://doi.org/10.1038/ejcn.2014.64

APA

Pietraszek, A., Gregersen, S., Pedersen, S. B., Holst, J. J., & Hermansen, K. (2014). Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes. European Journal of Clinical Nutrition, 68, 1022-28. https://doi.org/10.1038/ejcn.2014.64

Vancouver

Pietraszek A, Gregersen S, Pedersen SB, Holst JJ, Hermansen K. Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes. European Journal of Clinical Nutrition. 2014 May 14;68:1022-28. https://doi.org/10.1038/ejcn.2014.64

Author

Pietraszek, A ; Gregersen, S ; Pedersen, S B ; Holst, Jens Juul ; Hermansen, K. / Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes. In: European Journal of Clinical Nutrition. 2014 ; Vol. 68. pp. 1022-28.

Bibtex

@article{eb3a81b8fa3d4c39958214ec5546a651,
title = "Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes",
abstract = "Background/Objectives:Subjects with type 2 diabetes (T2D) and their nondiabetic first-degree relatives (REL) have increased risk of cardiovascular disease (CVD). Postprandial triglyceridemia (PPL), influenced by diet, is an independent risk factor for CVD. Dietary fat elicits increased PPL in T2D compared with nondiabetic controls, but our knowledge of PPL responses to fat in REL is sparse. Our aim was to test the hypothesis that REL respond to a monounsaturated fatty acid (MUFA) challenge with a higher PPL response compared with controls who have no family history of T2D (CON) and that MUFAs exert a differential impact on incretin responses and on the expression of genes involved in carbohydrate and lipid metabolism in muscle and adipose tissues of REL and CON.Subjects/Methods:A total of 17 REL and 17 CON consumed a meal with 72 energy percent derived from MUFAs (macadamia nut oil). Plasma triglycerides, free fatty acids, insulin, glucose, glucagon-like peptide 1, glucose-dependent insulintropic peptide and ghrelin were measured at baseline and regular intervals until 4 h postprandially. Muscle and adipose tissue biopsies were collected at baseline and at 210 min after the meal.Results:The MUFA-rich meal did not elicit different responses (P>0.05) in PPL, insulin, glucose, incretins or ghrelin in REL and CON. Several genes were differentially regulated in muscle and adipose tissues of REL and CON.Conclusions:A MUFA-rich meal elicits similar PPL, insulin and incretin responses in REL and CON. MUFAs have a differential impact on gene expression in muscle and adipose tissues in a pattern pointing toward early defects in lipid metabolism in REL.European Journal of Clinical Nutrition advance online publication, 14 May 2014; doi:10.1038/ejcn.2014.64.",
author = "A Pietraszek and S Gregersen and Pedersen, {S B} and Holst, {Jens Juul} and K Hermansen",
year = "2014",
month = may,
day = "14",
doi = "10.1038/ejcn.2014.64",
language = "English",
volume = "68",
pages = "1022--28",
journal = "European Journal of Clinical Nutrition",
issn = "0954-3007",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Acute effects of monounsaturated fat on postprandial lipemia and gene expression in first-degree relatives of subjects with type 2 diabetes

AU - Pietraszek, A

AU - Gregersen, S

AU - Pedersen, S B

AU - Holst, Jens Juul

AU - Hermansen, K

PY - 2014/5/14

Y1 - 2014/5/14

N2 - Background/Objectives:Subjects with type 2 diabetes (T2D) and their nondiabetic first-degree relatives (REL) have increased risk of cardiovascular disease (CVD). Postprandial triglyceridemia (PPL), influenced by diet, is an independent risk factor for CVD. Dietary fat elicits increased PPL in T2D compared with nondiabetic controls, but our knowledge of PPL responses to fat in REL is sparse. Our aim was to test the hypothesis that REL respond to a monounsaturated fatty acid (MUFA) challenge with a higher PPL response compared with controls who have no family history of T2D (CON) and that MUFAs exert a differential impact on incretin responses and on the expression of genes involved in carbohydrate and lipid metabolism in muscle and adipose tissues of REL and CON.Subjects/Methods:A total of 17 REL and 17 CON consumed a meal with 72 energy percent derived from MUFAs (macadamia nut oil). Plasma triglycerides, free fatty acids, insulin, glucose, glucagon-like peptide 1, glucose-dependent insulintropic peptide and ghrelin were measured at baseline and regular intervals until 4 h postprandially. Muscle and adipose tissue biopsies were collected at baseline and at 210 min after the meal.Results:The MUFA-rich meal did not elicit different responses (P>0.05) in PPL, insulin, glucose, incretins or ghrelin in REL and CON. Several genes were differentially regulated in muscle and adipose tissues of REL and CON.Conclusions:A MUFA-rich meal elicits similar PPL, insulin and incretin responses in REL and CON. MUFAs have a differential impact on gene expression in muscle and adipose tissues in a pattern pointing toward early defects in lipid metabolism in REL.European Journal of Clinical Nutrition advance online publication, 14 May 2014; doi:10.1038/ejcn.2014.64.

AB - Background/Objectives:Subjects with type 2 diabetes (T2D) and their nondiabetic first-degree relatives (REL) have increased risk of cardiovascular disease (CVD). Postprandial triglyceridemia (PPL), influenced by diet, is an independent risk factor for CVD. Dietary fat elicits increased PPL in T2D compared with nondiabetic controls, but our knowledge of PPL responses to fat in REL is sparse. Our aim was to test the hypothesis that REL respond to a monounsaturated fatty acid (MUFA) challenge with a higher PPL response compared with controls who have no family history of T2D (CON) and that MUFAs exert a differential impact on incretin responses and on the expression of genes involved in carbohydrate and lipid metabolism in muscle and adipose tissues of REL and CON.Subjects/Methods:A total of 17 REL and 17 CON consumed a meal with 72 energy percent derived from MUFAs (macadamia nut oil). Plasma triglycerides, free fatty acids, insulin, glucose, glucagon-like peptide 1, glucose-dependent insulintropic peptide and ghrelin were measured at baseline and regular intervals until 4 h postprandially. Muscle and adipose tissue biopsies were collected at baseline and at 210 min after the meal.Results:The MUFA-rich meal did not elicit different responses (P>0.05) in PPL, insulin, glucose, incretins or ghrelin in REL and CON. Several genes were differentially regulated in muscle and adipose tissues of REL and CON.Conclusions:A MUFA-rich meal elicits similar PPL, insulin and incretin responses in REL and CON. MUFAs have a differential impact on gene expression in muscle and adipose tissues in a pattern pointing toward early defects in lipid metabolism in REL.European Journal of Clinical Nutrition advance online publication, 14 May 2014; doi:10.1038/ejcn.2014.64.

U2 - 10.1038/ejcn.2014.64

DO - 10.1038/ejcn.2014.64

M3 - Journal article

C2 - 24824014

VL - 68

SP - 1022

EP - 1028

JO - European Journal of Clinical Nutrition

JF - European Journal of Clinical Nutrition

SN - 0954-3007

ER -

ID: 117854085