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Enteric peptide hormones orchestrate appetite, food-seeking behaviors, caloric intake, physical and chemical digestion, and the absorption of the nutrients, intricately linking the brain, the intestines, and multiple endocrine organs to sustain the energy balance of the human body. Many enteric hormones arise from tissue-specific mechanisms, known as prohormone processing, to yield a variety of end products from a common precursor. These “alternative splicing” mechanisms create unique mediators with specific functions. Precursor hormones and their derivatives are referred to as a hormone family. These enteric hormone “families” include the gastrin, secretin, and somatostatin (SRIH) families, among others (Table 11-1). These families represent conservation of precursors over centuries of species’ evolution. Despite the unique chemistry derived from the tissue-specific processing, similar signaling may occur at receptor sites within/between these families. In recent years, gastrointestinal (GI) research has led to the realization of the role of the gut microbiome in neuropsychology, malignancy, obesity, and many other conditions. This chapter summarizes how microbiome and enteric hormone interplay in health and illness.

Table 11-1.Enteric Hormone Families

In addition to roles in nutrient digestion, absorption, and satiety, many of the GI hormones, including cholecystokinin (CCK), gastrin, and glucagonlike-peptide (GLP-1), provide a “trophic” signal to organs of the GI system. This trophic effect helps maintain tissue in the GI tract; however, if pathologic concentrations are present, trophism can lead to overproduction of tissue, such as hypertrophied gastric mucosa in gastrinomas arising in the presence of an abnormality in the menin gene.

Enteric hormone regulation involves negative feedback loops, products of digestion, direct hormonal signaling, and neurotransmission. One example of a negative feedback loop involves reduction of gastrin secretion in the stomach due to low pH encountered in the small intestine. Somatostatin (also known as somatotropin-releasing inhibitory hormone [SRIH] is secreted in response to gastric acidity, inhibiting gastrin release. Additionally, duodenal inhibitory signals are transmitted by the enteric nerves, resulting in inhibition of vagal stimulation and stimulation of sympathetic nerves to inhibit gastric action. Partially digested proteins yield polypeptides, which, when sensed in the small intestine, stimulate secretion of several hormones, including the incretins. Additional mechanisms for regulation of GI hormones include a hormonal “off” signal; for example, secretion of SRIH from the pancreas and other cells halts secretion of several secondary hormones including CCK, gastrin, and secretin. The central nervous system (CNS) plays a significant role in the regulation of the GI system, and vice versa. Neuropeptides such as vasoactive intestinal peptide (VIP), substance P, and CCK are used by the brain to regulate GI system activity, including, but not limited to, motility, secretion, ...

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