Acute effects of casein on postprandial lipemia and incretin responses in type 2 diabetic subjects☆
Received 22 October 2008; received in revised form 22 December 2008; accepted 10 March 2009. published online 28 May 2009.
Abstract
Background and aims
Exaggerated and prolonged postprandial lipemia is potentially atherogenic and associated with type 2 diabetes. Limited data exist regarding the influence of dietary protein on postprandial lipemia in type 2 diabetes. We investigated, over 8-h, the acute effects of casein alone or in combination with carbohydrate on postprandial lipid and incretin responses to a fat-rich meal in type 2 diabetes.
Methods and results
Eleven type 2 diabetic subjects ingested four test meals in random order: an energy-free soup plus 80g of fat (control-meal); control-meal plus 45g carbohydrates (CHO-meal); control-meal plus 45g of casein (PRO-meal); and PRO-meal plus 45g carbohydrates (CHO+PRO-meal). Triglyceride and retinyl palmitate responses were measured in plasma and in a chylomicron-rich and chylomicron-poor fraction. We found no significant differences in triglyceride responses to PRO- and CHO+PRO-meal compared to the control-meal. However, the addition of casein to the CHO-meal reduced the raised triglyceride response in the chylomicron-rich fraction. Retinyl palmitate responses did not differ significantly between meals in the chylomicron-rich fraction, whereas the PRO-meal increased retinyl palmitate in the chylomicron-poor fraction. PRO- and PRO+CHO-meal increased insulin and glucagon compared to the control-meal. PRO+CHO-meal increased the glucose-dependent insulinotropic peptide response while no change in glucagon-like peptide-1 responses was detected.
Conclusions
The data presented suggest that casein per se did not modulate the postprandial triglyceride response in type 2 diabetes. When added to carbohydrate, casein suppressed the triglyceride response in the chylomicron-rich fraction, increased insulin and glucagon but did not affect the incretin responses.
aDepartment of Endocrinology and Metabolism, Aarhus University Hospital, Aarhus Sygehus THG, Denmark
bResearch Department of Human Nutrition, University of Copenhagen, Denmark
cDepartment of Biomedical Sciences, The Panum Institute, University of Copenhagen, Denmark
dInstitute of Physiology and Biochemistry of Nutrition, Federal Research Centre of Nutrition and Food, Kiel, Germany
Correspondence to: Kjeld Hermansen, Department of Endocrinology and Metabolism, Aarhus University Hospital, Aarhus Sygehus THG, 8000 Aarhus C, Denmark. Tel.: +45 89497650; fax: +45 86193807.
☆ Sponsorship: this work is carried out as part of the research program of the Danish Obesity Research Centre (DanORC, see www.danorc.dk). It is furthermore supported by the Nordic Centre of Excellence (NCoE) programme (Systems biology in controlled dietary interventions and cohort studies – SYSDIET, P No., 070014) and the Danish Diabetes Association.
ABSTRACT