Abstract
Increased postprandial lipemia is a risk marker of cardiovascular disease (CVD). While
moderate alcohol drinking is associated with a reduced risk of CVD in nondiabetic
and type 2 diabetic patients, it is also known that alcohol increases postprandial
triacylglycerol levels. The incretins, glucose-dependent insulinotropic polypeptide
(GIP) and glucagon-like peptide 1 (GLP-1), are important hormones from the gut that
enhance nutrient-stimulated insulin secretion. Their responses to a moderate alcohol
dose in type 2 diabetes have not previously been studied. We sought to determine how
alcohol influences postprandial lipid and incretin levels in patients with type 2
diabetes when taken in combination with a fat-rich mixed meal. Eleven patients with
type 2 diabetes ingested on 3 separate days in random order 3 different meals containing:
100 g butter alone or 100 g butter in combination with 40 g alcohol and 50 g carbohydrate,
or 100 g butter and 120 g carbohydrate. The meal with alcohol and 50 g carbohydrate
was isocaloric to that of 120 g carbohydrate. Triacylglycerol levels were measured
after separation by ultracentrifugation into a chylomicron-rich fraction with Svedberg
flotation unit values (Sf) > 1,000, and a chylomicron-poor fraction with Sf < 1,000.
Supplementation of a fat-rich mixed meal with alcohol in type 2 diabetic subjects
suppressed GLP-1 early in the postprandial phase and increased the late triacylglycerol
responses compared with the 2 other meals. In the chylomicron-rich fraction, both
triacylglycerol and cholesterol were increased by alcohol. No significant differences
in high-density lipoprotein (HDL)-cholesterol levels were seen. Isocaloric amounts
of carbohydrate and alcohol suppressed equally the postprandial free fatty acid levels,
but carbohydrate increased the postprandial glucose, GIP, and insulin levels the most.
Early in the postprandial phase, alcohol suppresses the incretin responses and increases
the late postprandial triacylglycerol levels in type 2 diabetic patients. Whether
this reflects an alcohol-induced suppression of the incretin response, which adds
to the alcohol-induced impairment of triacylglycerol clearance in type 2 diabetic
patients, remains to be elucidated.
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Article info
Publication history
Accepted:
August 25,
2003
Received:
April 8,
2003
Footnotes
☆Supported by the Danish Diabetes Association, Eli Lilly Diabetes Research Foundation, Helga og Peter Kornings Fond, and the Institute of Clinical Experimental Research, Aarhus University.
Identification
Copyright
© 2004 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
