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However,\n                    <jats:italic>in\u00a0vivo<\/jats:italic>\n                    analysis of somatostatin and\n                    <jats:styled-content style=\"fixed-case\">GHRH<\/jats:styled-content>\n                    release into the pituitary portal vasculature and peripheral\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    output demonstrates that the withdrawal of somatostatin or the appearance of\n                    <jats:styled-content style=\"fixed-case\">GHRH<\/jats:styled-content>\n                    into pituitary portal blood does not reliably dictate\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    release. Consequently, additional intermediates acting at the level of the hypothalamus and within the anterior pituitary gland are likely to contribute to the release of\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    , entraining\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    secretory patterns to meet physiological demand. The identification and validation of the actions of such intermediates is particularly important, given that the pattern of\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    release defines several of the physiological actions of\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    . This review highlights the actions of neuropeptide Y in regulating\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    release. It is acknowledged that pulsatile\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    release may not occur selectively in response to hypothalamic control of pituitary function. As such, interactions between somatotroph networks, the median eminence and pituitary microvasculature and blood flow, and the emerging role of tanycytes and pericytes as critical regulators of pulsatility are considered. It is argued that collective interactions between the hypothalamus, the median eminence and pituitary vasculature, and structural components within the pituitary gland dictate somatotroph function and thereby pulsatile\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    release. These interactions may override hypothalamic somatostatin and\n                    <jats:styled-content style=\"fixed-case\">GHRH<\/jats:styled-content>\n                    \u2010mediated\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    release, and modify pulsatile\n                    <jats:styled-content style=\"fixed-case\">GH<\/jats:styled-content>\n                    release relative to the peripheral glucose supply, and thereby physiological demand.\n                  <\/jats:p>","DOI":"10.1111\/jne.12278","type":"journal-article","created":{"date-parts":[[2015,3,24]],"date-time":"2015-03-24T13:36:26Z","timestamp":1427204186000},"page":"577-587","source":"Crossref","is-referenced-by-count":16,"title":["Nutrient Sensing Overrides Somatostatin and Growth Hormone\u2010Releasing Hormone to Control Pulsatile Growth Hormone Release"],"prefix":"10.1111","volume":"27","author":[{"given":"F. 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