This is the second revision of a competitive renewal seeking 4 years of support for a program aimed at identifying the physiological basis of a specific calcium appetite. Scant attention has been paid to the role of calcium intake and calcium homeostasis. This is a critical omission in light of the low calcium intake of most Americans, and the involvement of low calcium intake in many chronic diseases (e.g., osteoporosis, kidney disease, heart disease, and hypertension). In this project, it is proposed to take advantage of the biopsychological methods developed to study other ingestive behaviors to elucidate the physiological processes underlying the motivation to drink calcium.
Three specific aims are proposed. First, the hypothesis will be tested that circulating concentrations of calcium mediate calcium intake. This will be done by measuring calcium intake in rats given intracerebral ventricular infusions of calcium or calcium antagonists. Second, the hypothesis will be tested that one or more of the calcium regulatory hormones has direct effects on calcium intake. The contribution of each of the three hormones involved (parathyroid hormone, calcitonin, and 1,25-dihydroxy vitamin D) will be assessed by measuring the effect on calcium intake of 1,25-dihydroxy vitamin D infused into rats with plasma concentration of parathyroid hormone and calcitonin held constant. Third, the question of why calcium deprived rats drink sodium chloride and various other taste solutions will be addressed. It is hypothesized that calcium deprived rats ingest these solutions because they increase plasma calcium concentrations, which in turn, reinforces subsequent intake. This will be tested by a) screening a large number of compounds to determine whether they influence plasma calcium concentrations and b) using the electronic esophagus preparation to investigate whether rats find manipulations that increase plasma calcium rewarding. These studies will provide a solid foundation for understanding the physiological controls of calcium intake. This information from studies with rats will help identify the reasons for the low calcium intake of Americans, and provide strategies to help rectify this problem.
| Workman, Alan D; Carey, Ryan M; Chen, Bei et al. (2017) CALHM1-Mediated ATP Release and Ciliary Beat Frequency Modulation in Nasal Epithelial Cells. Sci Rep 7:6687 |
| Poole, Rachel L; Aleman, Tiffany R; Ellis, Hillary T et al. (2016) Maltodextrin Acceptance and Preference in Eight Mouse Strains. Chem Senses 41:45-52 |
| Subramaniam, Selvakumar; Ozdener, Mehmet Hakan; Abdoul-Azize, Souleymane et al. (2016) ERK1/2 activation in human taste bud cells regulates fatty acid signaling and gustatory perception of fat in mice and humans. FASEB J 30:3489-3500 |
| Tordoff, Michael G; Aleman, Tiffany R; Ellis, Hillary T et al. (2015) Normal Taste Acceptance and Preference of PANX1 Knockout Mice. Chem Senses 40:453-9 |
| Tordoff, Michael G; Downing, Arnelle; Voznesenskaya, Anna (2014) Macronutrient selection by seven inbred mouse strains and three taste-related knockout strains. Physiol Behav 135:49-54 |
| Voznesenskaya, Anna; Tordoff, Michael G (2013) Influence of cross-fostering on preference for calcium chloride in C57BL/6J and PWK/PhJ mice. Physiol Behav 122:159-62 |
| Ellis, Hillary T; Tordoff, Michael G; Parker, M Rockwell (2013) Itpr3 Is responsible for the mouse tufted (tf) locus. J Hered 104:295-7 |
| Voznesenskaya, Anna; Tordoff, Michael G (2013) Influence of estrous and circadian cycles on calcium intake of the rat. Physiol Behav 112-113:56-60 |
| Tordoff, Michael G; Ellis, Hillary T (2013) Taste dysfunction in BTBR mice due to a mutation of Itpr3, the inositol triphosphate receptor 3 gene. Physiol Genomics 45:834-55 |
| Tordoff, Michael G; Alarcón, Laura K; Valmeki, Sitaram et al. (2012) T1R3: a human calcium taste receptor. Sci Rep 2:496 |
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