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The most convincing evidence for a genetic component for obesity comes from twin and
adoption studies supporting that the genetic transmission of obesity is at least as
important as the non-genetic factors (1). Using genetic approaches, a number of
candidate genes for obesity have been identified and the importance of several of these
genes was ascertained through genetically engineered mice (2). Overall, genes that may
contribute to obesity susceptibility can be considered in three broad areas. These include
genes that i) regulate food intake (3), ii) participate in adipogenesis (4), and iii) influence
energy expenditure including mitochondrial proton leak and adaptive thermogenesis (5).
In the category of food intake regulation, functional studies both in humans and rodents
indicate a potentially important role for peptide YY (PYY) in decreasing food intake (6-
8). Following food intake and in proportion to meal size, PYY is secreted into the blood
stream from L-cells in the gastrointestinal tract in two forms, PYY1-36 and PYY3-36 (9),
and binds to neuropeptide receptors within the brain to reduce food intake. PYY3-36 was
previously shown to bind in vitro with highest affinity to the neuropeptide Y receptor Y2
(NPY2R) (10), an observation that was further established in vivo using Npy2r-deficient
mice, in which peripheral administration of PYY3-36 failed to reduce food intake (7). In
rodents, intravenous administration of PYY3-36 led to a reduction in food intake (6, 7, 11)
and in both obese and lean human subjects, PYY3-36 infusion markedly decreased food
intake (8). Combined, these studies support an important physiological role for PYY in
the regulation of feeding behavior.
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Ruhl, J.E.; Ade, P.A.R.; Carlstrom, J.E.; Cho, H.M.; Crawford,T.; Dobbs, M. et al. The South Pole Telescope, article, November 4, 2004; (digital.library.unt.edu/ark:/67531/metadc885152/m1/3/: accessed October 18, 2018), University of North Texas Libraries, Digital Library, digital.library.unt.edu; crediting UNT Libraries Government Documents Department.