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Ullamari Pesonen

Researcher at University of Turku

Publications -  94
Citations -  3187

Ullamari Pesonen is an academic researcher from University of Turku. The author has contributed to research in topics: Neuropeptide Y receptor & Insulin. The author has an hindex of 32, co-authored 92 publications receiving 3042 citations. Previous affiliations of Ullamari Pesonen include Orion Corporation.

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Inverse Correlation between Serum Testosterone and Leptin in Men

TL;DR: It is concluded that testosterone has a suppressive effect on leptin production, as reflected by circulating levels of this hormone in elderly men.
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Association of a leucine(7)-to-proline(7) polymorphism in the signal peptide of neuropeptide Y with high serum cholesterol and LDL cholesterol levels

TL;DR: Evidence is provided that NPY is linked to cholesterol metabolism and that the polymorphism producing Pro(7) inNPY is one of the strongest genetic factors identified thus far affecting serum cholesterol, particularly in obese subjects.
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Altered intracellular processing and release of neuropeptide Y due to leucine 7 to proline 7 polymorphism in the signal peptide of preproneuropeptide Y in humans.

TL;DR: The functional role of the recently found leucine 7 to proline 7 (Leu7Pro) polymorphism in the signal peptide of preproneuropeptide Y, sympathetic responses, including neuropeptic responses, are studied.
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C957T polymorphism of the human dopamine D2 receptor gene predicts extrastriatal dopamine receptor availability in vivo.

TL;DR: The findings indicate that the DRD2 SNPs regulateDRD2 availability in the human cortex and in the thalamus in vivo, however, the regulation pattern is different from that observed previously for striatal DRD1 availability in vivo.
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Identification of a three-amino acid deletion in the alpha2B-adrenergic receptor that is associated with reduced basal metabolic rate in obese subjects.

TL;DR: A genetic polymorphism of the alpha2B-adrenoceptor subtype can partly explain the variation in basal metabolic rate in an obese population and may therefore contribute to the pathogenesis of obesity.