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Growth hormone (GH) is primarily produced in the pituitary gland, although GH gene expression also occurs in the central and autonomic nervous systems. GH-immunoreactive proteins are abundant in the brain, spinal cord, and peripheral nerves. The appearance of GH in these tissues occurs prior to the ontogenic differentiation of the pituitary gland and prior to the presence of GH in systemic circulation. Neural GH is also present in neonates, juveniles, and adults and is independent of changes in pituitary GH secretion. Neural GH is therefore likely to have local roles in neural development or neural function, especially as GH receptors (GHRs) are widespread in the nervous system. In recent studies, GH mRNA and GH immunoreactive proteins have been identified in the neural retina of embryonic chicks. GH immunoreactivity is present in the optic cup of chick embryos at embryonic day (ED) 3 of the 21-d incubation period. It is widespread in the neural retina by ED 7 but also present in the nonpigmented retina, choroid, sclera, and cornea. This immunoreactivity is associated with proteins in the neural retina comparable in size with those in the adult pituitary gland, although it is primarily associated with 15-16 kDa moieties rather than with the full-length molecule of approximately 22 kDa. These small GH moieties may reflect proteolytic fragments of "monomer" GH and (or) the presence of different GH gene transcripts, since full-length and truncated GH cDNAs are present in retinal tissue extracts. The GH immunoreactivity in the retina persists throughout embryonic development but is not present in juvenile birds (after 6 weeks of age). This immunoreactivity is also associated with the presence of GH receptor (GHR) immunoreactivity and GHR mRNA in ocular tissues of chick embryos. The retina is thus an extrapituitary site of GH gene expression during early development and is probably an autocrine or paracrine site of GH action. The marked ontogenic pattern of GH immunoreactivity in the retina suggests hitherto unsuspected roles for GH in neurogenesis or ocular development.

Diseases of the pancreas vary by type, etiology, pathophysiology, and outcomes. One of the principle therapeutic considerations in all types of pancreatic diseases is nutrition. This review will consider acute pancreatitis (AP). Choice of patient, type and composition of nutrition, and timing of initiation will be discussed as components for achieving the maximum benefits of nutrition therapy in AP. The paradigm of nutrition therapy in AP has shifted to early enteral and/or oral nutrition based on disease severity to help mitigate the underlying inflammatory cascade of events leading to AP, beginning with anatomic and functional intestinal changes. Additionally, newer research investigating the inflammatory changes that instigate, maintain, and propagate AP will be discussed in terms of the nutrition effects on systemic inflammation. Nutrition therapy can mitigate the inflammatory changes in the intestinal tract and help with intestinal motility, bacterial overgrowth and translocation. It can help maintain intestinal bacterial composition and abundance similar to predisease levels. This review will also discuss the changes in the intestinal microbiome and effects of probiotics in AP.

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