(2013). Amylin and GLP-1 target different populations of area postrema neurons that are both modulated by nutrient stimuli. Physiology and Behavior,[112][113] This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPTThe area postrema mediates the hypophagic effect of the pancreatic hormone amylin and is also sensitive to glucagon-like peptide 1 (GLP-1). Protein seems to modulate amylin responsiveness because amylin seems to produce a stronger hypophagic effect and a stronger c-Fos expression when protein is absent from the diet. Accordingly, amylin induces a stronger c-Fos expression in the AP when injected in fasted compared to ad libitum fed rats.Here we tested the hypothesis that diet-derived protein attenuates the amylin dependent suppression of feeding and AP activation using isocaloric diets that differed in their protein content. Moreover, we investigated whether peripheral amino acid injection attenuates amylin-induced c-Fos expression in fasted rats. Since recent evidence suggests that GLP-1 may also reduce eating via the AP we tested whether 24h fasting also increases neuronal AP responsiveness to GLP-1 similar to the fasting-induced increase in amylin responsiveness. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT 2In conclusion, our findings support a protein-dependent modulation of behavioral and neuronal amylin responsiveness under equicaloric feeding conditions. Amino acids might contribute to the inhibitory effect of diet-derived protein to reduce amylin-induced neuronal AP activation. Neuronal AP responsiveness to GLP-1 is also increased in the fasted state suggesting that diet-derived nutrients may also interfere with AP-mediated GLP-1 effects.Nevertheless, the primary target neurons for amylin appear to be distinct from cells targeted by GLP-1 and by stimuli producing aversion (LiCl) or contributing to blood pressure regulation (AngII) via the AP. Since amylin and GLP-1 analogs are targets for the treatment of obesity, the nutrient-dependent modulation of AP responsiveness might entail implications for such therapeutic approaches.

Calcium ions are of irnportance for the function of every cell in the organism, and this applies also for the fat eells. In incubated slices of rabbit adipose tissue, ACTH-or epinephrine-stirnulated Iipolysis was accompanied by an increase in.tissue calcium (A/cgün and Rudman 1969). Werner and Löw (1973, 1974) investigated the effects of the hormones of calcium homeostasis, parathyroid hormone and calcitonin, upon lipolysis of incubated rat adipose tissue pieces and demonstrated that parathyroid hormone induced a 3 to 5 fold inerease in glycerol release, which was aecompanied by enhanced calcium aeeumulation in the tissue, whereas calcitonin exerted opposite effeets. As the question remained open whether these meehanisms were instrumental in the human organism, too, the influences of parathyroid hormone and of calcitonin upon incubated slices of human adipose tissue were studied.

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