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Meeting Abstract: 576

Protein elicits a stronger early (30 min) glucose-dependent insulinotropic polypeptide (GIP) response than fat ingestion in lean individuals, with no difference in glucagon-like peptide-1 (GLP-1). We assessed the incretin hormone response to protein versus fat ingestion in obesity. Equicaloric (8 kcal/kg) fat (olive oil) or protein (whey protein) was ingested by non-diabetic obese male volunteers [body mass index (BMI) >30 kg/m(2) ; n = 12] and plasma GIP and GLP-1 were determined. We found no difference in the early GIP or GLP-1 responses to fat versus protein. However, the total 300-min GIP response was greater after fat than after protein ingestion (20.3 ± 3.9 vs. 10.0 ± 2.8 nmol/l × min; p = 0.026), whereas the 300-min GLP-1 responses were the same. Thus, in obesity, protein and fat ingestion elicit similar early (30 min) incretin hormone responses, whereas 300-min GIP secretion is more pronounced after fat than protein ingestion.

The two incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are key factors in the regulation of islet function and glucose metabolism, and incretin-based therapy for type 2 diabetes has gained considerable interest during recent years. Regulation of incretin hormone secretion is less well characterized. The main stimulus for incretin hormone secretion is presence of nutrients in the intestinal lumen, and carbohydrate, fat as well as protein all have the capacity to stimulate GIP and GLP-1 secretion. More recently, it has been established that a diurnal regulation exists with incretin hormone secretion to an identical meal being greater when the meal is served in the morning compared to in the afternoon. Finally, whether incretin hormone secretion is altered in disease states is an area with, so far, controversial results in different studies, although some studies have demonstrated reduced incretin hormone secretion in type 2 diabetes. This review summarizes our knowledge on regulation of incretin hormone secretion and its potential changes in disease states.

Milk fat is high in saturated fatty acids (SFA) and high intakes of SFA are associated with cardiovascular diseases. The aim of the present study was to prospectively evaluate the potential risk of a first-ever acute myocardial infarction (AMI) in relation to the estimated milk-fat intake, reflected as the proportions of pentadecanoic acid (15 : 0) and heptadecanoic acid (17 : 0) in serum lipid esters. This was evaluated in a study population selected within the Västerbotten Intervention Program and the northern Sweden 'Monitoring of Trends and Determinants in Cardiovascular disease' survey populations. A prospective case-control design was used. The proportions of the biomarkers were lower in the cases (n 78) than in the controls (n 156), who were matched for age, sex, sampling time and geographical region. The standardised odds ratios of becoming an AMI case were between 0.7 and 0.8 for the biomarkers. The proportions of 15 : 0 and 17 : 0 in serum phospholipids were significantly and negatively correlated to serum concentrations of plasminogen activator inhibitor-1, tissue-type plasminogen activator, triacylglycerols, insulin, specific insulin, pro-insulin and leptin (all P<0.0001), suggesting a negative relationship to the insulin-resistance syndrome and the risk of CHD. Adjustment for BMI did not materially change the relationships. Although there seems to be a negative association between milk-fat intake as mirrored by the proportions of 15 : 0 and 17 : 0 in serum lipid esters and a first-ever AMI, adjustment for clinical risk factors removed this relationship.

Subjects with impaired glucose tolerance (IGT) are usually overweight and exhibit insulin resistance with a defective compensation of insulin secretion. In this study, we sought to establish the interrelation between insulin secretion and insulin sensitivity after oral glucose in non-obese subjects with IGT and we also examined this interrelation in relation to the 2 main incretins, glucagon-like peptide (GLP-1) and gastric inhibitory polypeptide (GIP). To that end, 13 women with IGT and 17 women with normal glucose tolerance (NGT) underwent an oral glucose tolerance test (OGTT) with measurements of glucose, insulin, C-peptide, GLP-1, and GIP. Insulin secretion (TIS) and insulin sensitivity (OGIS) were assessed using models describing the relationship between glucose, insulin and C-peptide data. These models allowed estimation also of the hepatic extraction of insulin. The age (54.2 +/- 9.7 [mean +/- SD] years) and body mass index (BMI; 26.0 +/- 4.0 kg/m(2)) did not differ between the groups. Subjects with IGT displayed lower TIS during the initial 30 minutes after oral glucose (0.97 +/- 0.17 [mean +/- SEM] v 1.75 +/- 0.23 nmol/L in NGT; P = .018) and lower OGIS (397 21 v 463 12 mL/min/m(2); P = .005). The incremental 30-minute TIS times OGIS (reflecting insulin secretion in relation to insulin sensitivity) was significantly reduced in IGT (359 51 v 774 91 nmol/min/m(2), p = .001). This measure correlated inversely to the 2-hour glucose level (r = -0.71; P < .001). In contrast, TIS over the whole 180-minute period was higher in IGT (26.2 +/- 2.4 v 20.0 +/- 2.0 nmol/L; P = .035). Hepatic insulin extraction correlated linearly with OGIS (r = 0.71; P < .001), but was not significantly different between the groups although there was a trend with lower extraction in IGT (P = .055). Plasma levels of GLP-1 and GIP increased after oral glucose. Total secretion of these incretin hormones during the 3-hour test did not differ between the 2 groups. However, the 30-minute