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At least 865 records · Page 48Linked to original sources
PubMed1996

Progress toward hormonal therapy of gastrointestinal cancer.

OBJECTIVE: The authors discuss ongoing research to determine the mechanisms by which peptide hormones regulate growth of gastrointestinal cancer and ways in which this information might be used to develop noncytotoxic therapy. SUMMARY BACKGROUND: Approximately 100,000 people die of cancer of the gastrointestinal (GI) tract each year. Surgery is curative only when the tumor is localized. Chemotherapy and radiotherapy have limited efficacy for locally advanced or widespread disease. Various peptide hormones regulate the growth of these tumors. As for breast and prostate cancer, the growth regulatory effect of these hormones is being studied as a potential mechanism of hormonal therapy. CONCLUSION: Gut peptide hormones regulate the growth of GI malignancies through all-specific receptors and signal transduction pathways. Interruption or modification of these growth regulatory mechanisms may lead to specific noncytotoxic therapy. In combination with surgical extirpation, such hormonally based treatment may be curative of advanced GI cancer.

Animals↗
PubMed1990

[Regulation of food intake].

Regulation of food intake is commonly treated as a negative feedback-loop. Hunger and/or appetite lead man and animals to ingest food. The subsequent meal-contingent activation of pre- and postabsorptive mechanisms then leads to satiety. The activation of oral and gastrointestinal chemo- and mechanoreceptors is important on the preabsorptive site. The gastrointestinal hormone cholecystokinin may also have a physiological satiety effect. Preabsorptive satiety mechanisms are influenced by the rate of gastrointestinal transit. The pancreatic hormone glucagon, which is released during meal taking, and various metabolites contribute to the postabsorptive regulation of food intake through activation of hepatic chemoreceptors, which are connected to the brain via predominantly vagal afferents. In addition, glucoreceptors in the brain, in particular in the nucleus of the solitary tract, contribute to food intake regulation by monitoring blood glucose concentration or, more specifically, glucose utilization. The nucleus of the solitary tract, which relays vagal afferents from gut and liver and also gustatory afferents, projects to the hypothalamus and to other forebrain structures. In this neural network the informations from the periphery are integrated by various neurotransmitters and neuropeptides, but the exact role of the substances involved is not fully understood yet. Body weight and, hence, body fat presumably affects feeding through modulation of a postabsorptive mechanism.

Animals↗
PubMed1988

Treatment of severe cryptosporidium-related diarrhea with octreotide in a patient with AIDS.

Cryptosporidiosis commonly causes severe diarrhea in immunosuppressed patients. There currently are no antiparasitic drugs consistently effective for this infection. This case describes a 26-year-old hemophiliac patient with acquired immunodeficiency syndrome and cryptosporidiosis whose diarrhea improved with continuous intravenous administration of a long-acting somatostatin analog, octreotide. Somatostatin has a variety of inhibitory effects on gastrointestinal hormones as well as a possible nonspecific effect on gastrointestinal mucosal fluid and electrolyte secretion. The somatostatin analog should be considered for patients with secretory diarrhea refractory to other forms of therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Malnutrition after gastric surgery. Association with exaggerated distal intestinal hormone release.

This study was designed to investigate the mechanism of excessive weight loss following gastric surgery. Twelve weight-stable and six weight-losing postoperative subjects were studied. The weight-losing subjects had lesser body mass based upon anthropometric measurements. All weight-losing subjects and six weight-stable subjects excreted excess breath hydrogen after a standard meal. The quantities of hydrogen excreted by the weight-losing subjects and weight-stable subjects with positive tests were not different, implying similar degrees of carbohydrate malabsorption. Peak breath hydrogen concentration occurred earlier in weight-losing subjects than in weight-stable subjects (2 vs 5 hr), indicating more rapid oral-cecal transit of the test meal in weight-losing subjects. Analyses of postprandial blood samples for eight different gastrointestinal hormones demonstrated exaggerated postprandial elevations in the concentrations of enteroglucagon and neurotensin. The results of these studies demonstrate close correlations between excessive weight loss after gastric surgery, rapid gastrointestinal transit as measured by excess breath hydrogen excretion, and increased release of hormones from the distal intestine. We conclude that these hormones are secreted in excess due to the rapid gastrointestinal transit and that rapid gastrointestinal transit may play a role in excessive weight loss after gastric surgery.

Aged↗