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Postprandial lipaemia is considered an emerging risk factor for cardiovascular disease also in the Type 2 diabetic population. However, little information exists on the daily triglyceride profile of these patients, especially during everyday life. The aim of the study was to evaluate the daily triglyceride profile of Type 2 diabetic patients during their everyday life.145 Type 2 diabetic patients (66 men/79 women, age range 45-65 years) at a health district near Naples, Italy, participating in a screening survey for the evaluation of diabetic complications, and 30 non-diabetic subjects of the same area underwent four daily capillary triglyceride profiles by Accutrend (Roche)-a previously validated method.Triglyceride values (mmol/l; Means +/- SE) were 2.22+/-0.08 at fasting, decreased before lunch (2.03+/-0.07), reached a peak 3 h after lunch (2.73+/-0.09) and remained substantially high before dinner (2.47+/-0.09) (all p0.001 vs fasting). The triglyceride profile of non-diabetic subjects was significantly lower at each point (average difference of 0.73 mmol/l). The percentage of patients with values above 2.25 mmol/l was 61% 3 h after lunch and 49% before dinner. Moreover, in 30% of patients with optimal fasting values (1.69 mmol/l) triglyceride concentrations 3 h after lunch ranged between 1.69 and 2.25 mmol/l, and in 31% they were above 2.25 mmol/l.Most Type 2 diabetic patients have postprandial triglycerides above optimal concentrations for several hours after meals. Moreover, optimal fasting concentrations are not always a good predictor of postprandial triglycerides.

Aims/hypothesis: Overexpression of the gene encoding phosphoprotein enriched in astrocytes 15 (PEA15), also known as phosphoprotein enriched in diabetes (PED), causes insulin resistance and diabetes in transgenic mice and has been observed in type 2 diabetic individuals. The aim of this study was to investigate whether PEA15 overexpression occurs in individuals at high risk of diabetes and whether it is associated with specific type 2 diabetes subphenotypes. Subjects and methods: We analysed PEA15 expression in euglycaemic first-degree relatives (FDR) of type 2 diabetic subjects. Results: The expression of PEA15 in peripheral blood leucocytes (PBLs) paralleled that in fat and skeletal muscle tissues. In PBLs from the FDR, PEA15 expression was two-fold higher than in euglycaemic individuals with no family history of diabetes (control subjects), both at the protein and the mRNA level (p < 0.001). The expression of PEA15 was comparable in FDR and type 2 diabetic subjects and in each group close to one-third of the subjects expressed PEA15 levels more than 2 SD higher than the mean of control subjects. Subjects with IFG with at least one type 2 diabetes-affected FDR also overexpressed PEA15 (p < 0.05). In all the groups analysed, PEA15 expression was independent of sex and unrelated to age, BMI, waist circumference, systolic and diastolic BP, and fasting cholesterol, triacylglycerol and glucose levels. However, in euglycaemic FDR of type 2 diabetic subjects, PEA15 expression was inversely correlated with insulin sensitivity (r = -557, p = 0.01). Conclusions/interpretation: We conclude that PEA15 overexpression represents a common defect in FDR of patients with type 2 diabetes and is correlated with reduced insulin sensitivity in these individuals.

This study evaluates prospectively the relationship between impaired glucose tolerance (IGT) and blood pressure. From a population of 1376 men and women aged 40-59 years, all those with IGT (n = 54) plus 133 age- weight- and sex-matched normoglycaemic control subjects were selected after excluding treated hypertensive patients. Blood pressure, fasting and postload blood glucose and plasma insulin were measured. At 11.5 years after the first visit 76% of the IGT patients and 80% of the control subjects were re-examined. At baseline blood pressure was significantly higher in IGT patients than in control subjects (systolic 135.5 +/- 2.3 vs 127.9 +/- 1.4 mmHg, p0.001; and diastolic 88.0 +/- 1.5 vs 84.7 +/- 0.7 mm Hg, p0.05) independent of age, gender, weight, antihypertensive medication and insulinaemia. Accordingly, hypertension was more frequent in subjects with IGT (odds ratio 2.1, 95% confidence, interval (CI) 0.9-4.9). Postload insulin was significantly associated with hypertension--both at univariate and multivariate analysis--in normoglycaemic subjects, but not in those with IGT. At follow-up systolic blood pressure increased in both groups; the increase was smaller in patients with IGT (6.0 +/- 2.4 vs 12.3 +/- 1.6 mm Hg p0.05). Likewise, the 11.5 years' cumulative incidence of hypertension was not significantly different in subjects with baseline IGT or normoglycaemia; if anything it was lower in the IGT group (odds ratio 0.36, 95% CI 0.1-1.2). In multivariate analysis incidence of hypertension was associated positively with baseline blood pressure (p0.0003) and negatively with IGT status p0.03), while no significant association was found with insulin. In conclusion, the findings of this study question IGT as a risk factor for hypertension. Furthermore, these data do not indicate a major role for hyperglycaemia and hyperinsulinaemia per se in the aetiology of hypertension and suggest that IGT and hypertension share one or more pathogenetic factor(s) (i.e., insulin resistance, hyperactivity of the sympathetic nervous system, etc.), which induce deterioration of blood pressure control first, and hyperglycaemia later.