Aerobic endurance training improves insulin sensitivity, and is of great importance in the prevention and treatment of type 2 diabetes. The improvement in insulin sensitivity and cardiovascular function through exercise is highly variable among individuals, and is probably partly determined by genetic components. This study evaluated the peroxisome proliferation-activated receptor-gamma2 ( PPAR-gamma2) Pro12Ala polymorphism and the angiotensin converting enzyme ( ACE) I/D polymorphism with respect to any potential influence that these highly prevalent polymorphisms may impose on changes in insulin sensitivity and maximal aerobic capacity induced by exercise. Seventy-nine healthy first-degree relatives of type 2 diabetic patients were compared to a control group consisting of 54 subjects without any family history of type 2 diabetes. All subjects had a normal OGTT. The groups were comparable with respect to age (34 +/- 7 vs. 33 +/- 7 years), gender ((m/f) 43/36 vs. 30/24) and BMI (25.7 +/- 2.6 vs. 25.3 +/- 2.5 kg/m (2)); p (all) = NS. Furthermore, a subgroup of 29 offspring and 17 control subjects were engaged in a standardized training program lasting ten weeks. Insulin sensitivity (hyperinsulinemic euglycemic clamp technique) and VO (2)max (exhaustive exercise test) was assessed before and after the training period. We will demonstrate the allelic frequency of the Ala-allele of the Pro12Ala polymorphism to be lower in offspring to type 2 diabetic patients (13.3 %) compared to control subjects (21.3 %); p < 0.05. In offspring only, the Pro12Ala polymorphism of the PPAR-gamma2 gene appeared to enhance weight changes brought about by exercise (Deltaweight = - 0.3 +/- 1.4 kg vs. - 1.8 +/- 1.8 kg; p < 0.05; (Pro/Pro vs. Pro/Ala + Ala/Ala) - suggesting possible gene-environment or gene-gene interactions. The ACE I/D polymorphism was not of significant importance in determining the capability of responding to exercise in terms of improvement in insulin sensitivity or maximal aerobic capacity.
IgG, IgA, and IgM serum antibody activities to gluten, a gluten fraction called glyc-gli, and antigens from egg and cow’s milk were monitored by an enzyme-linked immunosorbent assay (ELISA) in children with coeliac disease during treatment and gluten challenge. The IgA activity to gluten antigens showed in most patients a rapid and significant reduction after gluten withdrawal, whereas the IgG activity decreased more slowly. During gluten challenge, both these activities rose significantly, and the increases could usually be detected several months before overt clinical relapse. Such determinations, therefore, represent a valuable adjunct in the follow-up of children with coeliac disease. IgA activities to egg and cow’s milk antigens likewise tended to decrease after gluten withdrawal and increase during challenge, but the changes were less consistent for individual antigens. Nevertheless, monitoring of IgA activities to a selection of dietary antigens other than gluten may be particularly valuable when it comes to evaluation of intestinal responses in patients on a glutenfree diet.
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