Browsing by Subject "Endocrinology, Diabetes, and Metabolism"
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Item Calcium Sensitivy of β-cell Transcription Factor Binding to an Insulin Enhancer(1998-06-01) Scott, Gary Frank; Easom, Richard; Lacko, Andras G.; Wu, Ming-ChiGary Frank Scott, Calcium Sensitivity of β-cell Transcription Factor Binding to an Insulin Enhancer. Master of Science (Biochemistry and Molecular Biology), June 1998, 104 pp., 16 illustrations, bibliography, 94 titles. Insulin is an essential hormone and is produced exclusively in endocrine pancreas β-cells for the control of glucose homeostasis in mammals. The hypothesis tested in this thesis is that increased intracellular Ca2+ ([Ca2+]i) contributes to activation of glucose-induced insulin gene transcription. Glucose-induced insulin transcription has been mapped to binding of transcription factors by β-cell sequence motifs from -197 to -247, a glucose-response-enchancer (GRE), in the rat insulin1 gene (rINS1) promoter. Using oligonucleotide probes representing this glucose-response-enhancer (GRE) in electrophorectic mobility shift assays (EMSA), we have examined the Ca2+-sensitivity of transcription factor binding to nuclear extracts from cultured rat insulinoma β-cells (INS-1). In the presence or absence of kinase inhibitors, Ca2+ chelators, and Ca2+ channel blockers, binding was assayed for the following cell conditions: 1) in situ permeabilized cells exposed to Ca2+; 2) in vitro 32p-phosphorylated nuclear extracts; and 3) in situ glucose-stimulated and K+-depolarized intact cells. Binding was Ca2+-sensitive due to activation by K+depolarization as well as inhibition by a Ca2+-chelator, a Ca2+-channel blocker, and KN-93, specific for Ca2+/calmodulin kinases, suggesting a phosphorylation-dependent mechanism. Taken together, these findings identify a role for the Ca2+ second messenger in the glucose regulation of the insulin gene which points to novel treatments for type II diabetes.Item Effect of Short-Term Alpha Lipoic Acid Supplementation on Age Related Cognitive and Motor Deficits(2001-08-01) Shetty, Ritu A.; Forster, Michael J.; Dillon, Glenn H.; Das, HridayRitu A. Shetty. Effect of short-term antioxidant supplementation on age related cognitive and motor deficits. Master of Science (Biomedical Sciences), August, 2001, 24 pp, 2 tables, 11 figures, 30 references. During aging there is an increase in oxidative damage and loss of brain function that may reflect and increased level of oxidative stress. Studies have suggested that the increased oxidative damage in old rodents can be reversed, relatively rapidly, by experimental interventions like caloric restrictions and antioxidants capable of lowering oxidative stress (Forster et.al., Joseph et.al., 1995). Based on those findings, it was hypothesized that age-related declines in cognitive and/or psychomotor function are the result of molecular damage associated with oxidative stress. The current study addressed the possibility a decreasing oxidative damage could be produced with the antioxidant alpha lipoic acid, in aged mice, leading to a reversal of age-related impairments of psychomotor and cognitive functions. C57BL/6 mice aged 6 or 23 months were gavaged daily with 100mg/kg alpha-lipoic acid or the vehicle (0.9% saline; 2% methylcellulose). After 3 weeks of treatment, the animals were subjected to a battery of behavioral tests for motor and cognitive functions. Following the behavioral tests the animals were sacrificed brains were dissected and frozen for analysis of carbonyl concentration. The results showed significant age-related deficits in spatial learning, accuracy for spatial memory, recent memory, and psychomotor performance. None of these age-related deficits was reversed following the treatment with alpha lipoic acid. There was no reduction in carbonyl concentration with alpha lipoic acid supplementation. Thus we concluded that alpha lipoic acid supplementation had neither beneficial nor detrimental effects in reducing oxidative damage in brain or in reversal the age-related decline in function.Item Menopause Clinical Education Aid(2008-01-01)Item North Texas Health & Science - 2011, Issue 2(University of North Texas Health Science Center at Fort Worth, 2011-01-01)Item Synergy 2008: Annual Research Report(2008-01-01)Item Synergy 2011: Annual Research Report(2011-01-01)