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This study examined the effects of exercise on glucose metabolism in adipocytes from female rats. Female rats were exercised by swimming six hours per day, five days per week for eight weeks. There was no variation in body weight gain (P > 0.05) between the exercise and control animals through the experimental period. The swimmers' fat cells were smaller (P < 0.05) than those of the sedentary controls of the same age. The rates of glucose oxidation of both C-1 and C-6 glucose were significantly higher (P < 0.05) in the exercise rats' adipocytes at all insulin concentrations. The sedentary control rats' adipocytes showed no significant response at any insulin concentration. Thus, exercise is a significant stimulus to cause increased oxidation rates in the adipocytes from exercising rats. These data also indicate that glucose transport, not defective glucose oxidation, is the limiting mechanism that accounts for the decreased responsiveness of adipocytes from sedentary control animals.

This purpose of this study was to determine the effects of vitamin E and/or resistance exercise on insulin resistance and glucose uptake. Nine subjects, who were currently active but not strength training, were assigned to either the vitamin E or placebo group based on their prescreening measurements. Subjects underwent a 3-week vitamin E washout period before testing. At baseline testing subjects were given a 75-gram glucose load and blood was drawn every 15-minutes for 2-hours to analyze insulin and glucose response. Another oral glucose tolerance test (OGTT) was performed 45minutes after a 50-minute full body progressive resistance training session to determine insulin and glucose response to exercise. Subjects ingested either the placebo (3 capsules of olive oil) or 1200 IU vitamin E (3 capsules) for 9-weeks. After 3-weeks of supplementation the subjects returned for another exercising OGTT. After this session the subjects began a 6-week progressive resistance exercise program, in which they performed another OGTT after the last session. Both groups showed a significant increase in strength gains pre and post resistance training. The statistical analysis failed to demonstrate any differences between groups in insulin or glucose response in any of the four OGTT trials, but there were multiple trends present. Combining vitamin E supplementation with resistance training increased insulin sensitivity and the disposal of glucose. Both groups also had significant strength gains from pre to post study. Future research is needed for verification of these trends. / School of Physical Education

Motivation: The detrimental effects of obesity and insulin resistance in Caucasians and African-Americans have been the focus of many recent publications, and the association between PAI-1act and markers of the metabolic syndrome is well established but data on African subjects are still lacking. Objectives: To investigate possible differences between the association of PAI-1act with markers of the metabolic syndrome in Caucasian and African women. Methods We used cross-sectional data from the POWIRS I and II studies, involving 95 African and 114 Caucasian women respectively in the Potchefstroom district of the North West Province, South Africa. Results: Mean plasma PAI-1act was significantly higher in the Caucasian than in the African subjects (p < 0.001). Markers for the metabolic syndrome explained 60% of the variance of PAI-1act in the Caucasian group, but only 2.8% of the variance of PAI-1act in the African group. Waist circumference emerged as the strongest independent predictor of PAI-1act in the Caucasian (34%) as well as the African subjects (11%). Conclusion: This study showed clear differences in PAI-1act between African and Caucasian subjects, along with differences in the association of PAI-1act with markers of the metabolic syndrome. Apparent genetic differences between the two groups (especially the role of the 4G/5G genotype) may have an important influence on PAI-1act The role of PAI-1act in the metabolic syndrome may differ between Caucasians and Africans. / Thesis (M.Sc. (Nutrition))--North-West University, Potchefstroom Campus, 2005.

Overnutrition causes many metabolic diseases including type 2 diabetes. PFKFB3/iPFK2 is a master regulator of adipocyte and intestinal nutrient metabolism. Using PFKFB3/iPFK2+/– mice and adipocyte-specific PFKFB3 over-expression mice, the present study investigated the role of PFKFB3/iPFK2 in regulating diet-induced adiposity, inflammation in adipose tissue and intestine, and systemic insulin resistance. On a high-fat diet (HFD), PFKFB3+/– mice gained much less body weight than did wild-type littermates. However, HFD-induced systemic insulin resistance in PFKFB3+/– mice was more severe than in wild-type littermates. In contrast, adipocyte-specific PFKFB3 over-expression increased adiposity but suppressed overnutrition induced adipose tissue inflammatory response and improved insulin sensitivity. In addition to adipose tissue, PFKFB3/iPFK2 also played a role in intestine events. Compared to wild-type littermates, PFKFB3+/– mice displayed a significant increase in the expression of intestinal inflammatory markers on a HFD. In conclusion, PFKFB3 protects against overnutrition-induced adipose tissue and intestine inflammatory response and systemic insulin resistance in an adiposity-independent manner. Selective PFKFB3 activation may be viable for treating and/or preventing insulin resistance and type 2 diabetes.

Title page, contents and abstract only. The complete thesis in print form is available from the University of Adelaide Library. / In human populations, perturbed growth in early life and ageing have been identified as risk factors for the development of Insulin resistance syndrome (IRS). The consequences of restricted prenatal growth on postnatal function have been investigated using numerous experimental models of intrauterine growth retardation, mainly in the rat. These studies have shown that some, but not all, aspects of postnatal function that are programmed in humans are also programmed in the rat. This study was designed to determine whether IRS develops with increasing age in the guinea pig as it does in the human and whether the development of the syndrome is more pronounced in aged offspring which have undergone spontaneous fetal growth restriction and accelerated growth in the neonatal period. It appeared that the guinea pig is a suitable animal model of ageing, displaying many of the metabolic, cardiovascular and anthropometric changes seen in humans. Furthermore, the effects of perturbed prenatal and early postnatal growth on the development of IRS in the aged guinea pig exhibit a sexually dimorphic pattern. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1297545 / Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2007

Title page, contents and abstract only. The complete thesis in print form is available from the University of Adelaide Library. / In human populations, perturbed growth in early life and ageing have been identified as risk factors for the development of Insulin resistance syndrome (IRS). The consequences of restricted prenatal growth on postnatal function have been investigated using numerous experimental models of intrauterine growth retardation, mainly in the rat. These studies have shown that some, but not all, aspects of postnatal function that are programmed in humans are also programmed in the rat. This study was designed to determine whether IRS develops with increasing age in the guinea pig as it does in the human and whether the development of the syndrome is more pronounced in aged offspring which have undergone spontaneous fetal growth restriction and accelerated growth in the neonatal period. It appeared that the guinea pig is a suitable animal model of ageing, displaying many of the metabolic, cardiovascular and anthropometric changes seen in humans. Furthermore, the effects of perturbed prenatal and early postnatal growth on the development of IRS in the aged guinea pig exhibit a sexually dimorphic pattern. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1297545 / Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2007

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Diss. (sammanfattning) Uppsala : Univ., 2001. / Härtill 4 uppsatser.