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Short Bowel Syndrome
Published in John K. DiBaise, Carol Rees Parrish, Jon S. Thompson, Short Bowel Syndrome Practical Approach to Management, 2017
Many hormones are produced by cells within in the GI tract. These hormones participate in many physiological roles, including the control of secretomotor activity, and are closely linked with the nervous system. Most of the gut hormones fall into one of two families according to their molecular structure: the gastrin family (e.g., gastrin and cholecystokinin) or the secretin family (e.g., gastric inhibitory peptide [GIP], GLP, secretin, and vasoactive intestinal peptide). The hormones are produced in response to luminal stimuli (primarily nutrient contact) and have five main areas of function, including the control of gastric emptying/secretion (gastrin, somatostatin), regulating the rate of digestion (cholecystokinin, secretin, GIP, and motilin), slowing the rate of GI transit (GLP-1, neurotensin, and peptide YY), promoting intestinal growth (GLP-2 and neurotensin), and control of blood glucose (insulin, GLP-1, GIP).
Applied physiology of nociception
Published in Pamela E Macintyre, Suellen M Walker, David J Rowbotham, Clinical Pain Management, 2008
Cholecystokinin (CCK) belongs to the gastrin family of peptides and is widely distributed in the nervous system, where it has been shown to be a neurotransmitter mediating many important functions. CCK appears to have an important but complex involvement in nociceptive transmission and modulation. The most well-defined and apparently physiological role for CCK is that it is a functional antagonist of opioid-induced analgesia.65 The sites of interaction between CCK and opioids are clearly multiple, but the spinal cord is an important site. It has been suggested that CCK does not alter baseline pain threshold but reduces the binding affinity of MOR (μ opioid receptor) ligands and also counteracts intracellular events subsequent to opioid receptor activation. Thus, CCK antagonists are a potential interesting target to enhance opioid analgesia.66
Phage display selection of fully human antibody fragments to inhibit growth-promoting effects of glycine-extended gastrin 17 on human colorectal cancer cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Shirin Khajeh, Mohammad Reza Tohidkia, Ayuob Aghanejad, Tayebeh Mehdipour, Farzaneh Fathi, Yadollah Omidi
Among gastrointestinal (GI) tumors, colorectal cancers (CRCs) is considered as one of the most common cancers worldwide and the fourth most common cause of cancer-associated deaths [1]. Although multiple factors mediate development of CRCs, various studies have demonstrated that gastrin family hormones play a crucial role in CRCs pathogenesis [2]. Gastrin family-derived peptides including progastrin (81 amino acid), C-terminal flanking peptide (6 amino acids), glycine-extended gastrin (34 and17 amino acids, G34-Gly and G17-Gly), and amidated gastrin (17 amino acids, G17) are immature and mature products which are processed through multiple posttranslational modifications (i.e. phosphorylation, sulfation, amidation) from a large precursor molecule called preprogastrin with 101 amino acids. The peptide hormone G17 is frequently recognized as a mature form of gastrin processing, however, it has been demonstrated that G17-Gly is the main end-product in premalignant and malignant colonic lesions due to immature processing arising from deficiency of amidation enzyme by which G17-Gly is converted to amidated G17 [3]. Different cumulative in vitro studies have shown that G17-Gly promotes proliferation of different GI cell lines including pancreatic carcinoma cell line (AR4–2J) [4], gastric carcinoma cell lines (AGS and SIIA), and colon carcinoma cell lines (HCT-116, LoVo and HT29) [5]. Moreover, there is in vivo evidence that G17-Gly mediates hyperproliferation of colonic mucosa and formation of aberrant crypt foci in different animal models such as xenograft tumor models of DLD-1, G17-Gly overexpressed transgenic mice and gastrin-deficient mice perfused with this peptide [6]. It was proposed that growth effects of G17-Gly on CRC cells are mediated by distinct receptor from classical gastrin/cholecystokinin B receptor (CCKB-R) [7] and, to date, no specific receptor has been identified definitely.