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.