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At least 883 records · Page 49Linked to original sources
PubMed1973

Hormonal control of pancreatic growth.

Investigations have outlined pancreatic secretory and synthetic responses to gastrointestinal hormones. However, there is little information concerning hormonal influences on pancreatic growth. These studies were designed to examine effects of chronic administration of bethanechol and cholecystokinin-pancreozymin (CCK-PZ) on the pancreas. Male albino rats were given saline, bethanechol, 6 mg/kg, or CCK-PZ, 20 U/kg, intraperitoneally twice daily and killed after 5 days. The following changes were studied; pancreatic weight; RNA, DNA, and protein content; and [(14)C]thymidine incorporation into DNA. Bethanechol administration was associated with a 20% increase in pancreatic weight and a 33% increase in mg protein/100 mug DNA. In bethanechol-treated groups, amounts of DNA/gram body weight and incorporation of [(14)C]thymidine into DNA were similar to controls. CCK-PZ administration was associated with a 71% increase in pancreatic weight and a 38% increase in mg protein/100 mug DNA. In CCK-PZ-treated groups, amounts of DNA/gram body weight were increased by 42% and [(14)C]thymidine incorporation into DNA was increased by 185%. These studies indicate that bethanechol administration was associated with increases in pancreatic cell mass (hypertrophy). CCK-PZ administration was associated with increases in cell mass and cell numbers (hypertrophy and hyperplasia). This information suggests the importance of CCK-PZ in maintaining pancreatic functional integrity. Although bethanechol and CCK-PZ elicit similar secretory responses, their mode of action on the cell, at least as far as growth influences are concerned, appears to be different.

Animals↗
PubMed1990

Treatment of patients with metastatic pancreatic and gastrointestinal tumours with the somatostatin analogue Sandostatin: a phase II study including endocrine effects.

Somatostatin analogues can suppress the secretion of some gastrointestinal hormones and growth factors involved in the growth regulation of gastrointestinal cancers and can inhibit the growth of experimental pancreatic tumours. Therefore, in a phase II study 34 patients with metastatic pancreatic (n = 14), colorectal (n = 16) and gastric cancer (n = 4) were treated with three daily subcutaneous injections of 100-200 micrograms of the somatostatin analogue Sandostatin (SMS 201-995). All patients had an extensive tumour load and 13 were pretreated with chemotherapy. Before Sandostatin treatment the patients with pancreatic cancer showed a higher mean plasma concentration of GH (P less than 0.05) and a lower concentration of 'total' somatomedin-C (P less than 0.005) compared with patients with colorectal cancer; there was no significant difference between these two groups in plasma levels of directly assayable somatomedin-C, EGF/TGF-alpha, insulin and prolactin. Within 3 days after start of treatment, somatomedin-C levels initially decreased (without a change in basal plasma GH levels), but returned to pretreatment levels within 4-13 weeks. Plasma insulin levels also were suppressed but only during the first 3-5 days of treatment. Plasma EGF-TGF-alpha levels increased significantly at day 5 of treatment only in the pancreatic cancer patients. Twenty-seven per cent of the patients showed stable disease for 3-9 months, but most patients experienced subjective improvement in the absence of serious side-effects. However, the overall survival remained disappointing, emphasising the need for better treatment regimens.

Adult↗
PubMed2006

The entero-insular axis and adipose tissue-related factors in the prediction of weight gain in humans.

Obesity has now reached epidemic proportions. Epidemiological studies in the past decades have shown that adults gain weight and adiposity from the early twenties until their sixties. In the paediatric population, growing numbers of children and adolescents put on unhealthy weight. Many environmental, socio-economical and biological determinants that predispose to weight gain have been identified thus far. The aim of the present review is to summarize the current knowledge on the role of the circulating levels of adipokines and other entero-insular hormones and biological markers of obesity to predict weight gain in humans. The review focuses on relationship between hormonal and biochemical markers (insulin, insulin-like growth factors, gastrointestinal hormones, leptin, adiponectin, resistin, inflammatory proteins and cytokines) and weight gain in prospective studies. The complex relationships displayed by these hormonal factors with future weight gain in humans are critically reviewed and integrative models are proposed. Overall, most of the studies reported to date made adjustments for baseline body mass index but failed to consider dietary intake and physical activity as confounding factors. Outstanding questions are raised and new directions for future prospective studies are proposed in order to improve our understanding of the role of biological determinants of energy balance and development of obesity in humans.

Adipokines↗
PubMed1996

Octreotide in malignant intestinal obstruction.

Octreotide has proved an effective agent in the palliation of refractory malignant intestinal obstruction. This may be achieved through a pro-absorptive effect on the small bowel mucosa, an effect on improving gastrointestinal motility, by a reduction in gastrointestinal hormone levels and by a direct anti-neoplastic effect on the obstructing tumour. The simple route of administration of octreotide and the paucity of side effects reported in two recent studies should make the physician consider its use in this particularly distressing complication of advanced cancer.

Animals↗
PubMed1991

Neuromuscular disease of the gastrointestinal tract.

Gastrointestinal motility is the function of gastrointestinal smooth muscle. It is controlled by both the intrinsic and extrinsic nerves of the gastrointestinal tract and, to a lesser degree, the gastrointestinal hormones. Therefore, any abnormality of the above factors, theoretically, can cause gastrointestinal dysmotility. In a clinical situation, commonly seen is gastrointestinal dysmotility caused by either smooth muscle or intrinsic and extrinsic nerves dysfunction. Diseases that cause smooth muscle dysfunction include familial visceral myopathies, nonfamilial visceral myopathies, collagen disease, muscular dystrophies, amyloidosis, thyroid disease, and so on. Diseases that cause enteric nerve dysfunction include familial visceral neuropathies, nonfamilial visceral neuropathies, diabetes mellitus, Chagas' disease, ganglioneuromatosis of the intestine, visceral neuropathy of carcinomatosis, Parkinson's disease, and so on. The patients with neuromuscular disease of the gastrointestinal tract have a wide range of clinical manifestations regardless of the underlying cause. At one end of the spectrum, the patients may be asymptomatic, and at the other end of the spectrum, the patients may have functional obstruction of the gastrointestinal tract. Plain abdominal x-rays, upper gastrointestinal (UGI) and small bowel x-rays, enteroclysis, barium enema, and manometric studies are useful for the work-up of these patients. Enteroclysis is especially helpful in ruling out mechanical obstruction of the small intestine in patients with chronic intestinal pseudo-obstruction. Treatment is mainly symptomatic and supportive. There is no effective drug to improve gastrointestinal motility. Surgery may be helpful in selected cases of severe gastrointestinal dysmotility.

Gastrointestinal Diseases↗
PubMed1993

Inhibition of growth of a transplanted rat pancreatic acinar carcinoma with CCK-8.

Gastrointestinal hormones and neuropeptides are known to regulate growth of various normal gastrointestinal tissues and many cancers. Since cholecystokinin (CCK) is considered the most potent trophic factor for the exocrine pancreas, we studied its effect on growth of an acinar cell tumor, initially induced by azaserine and transplanted to the rat, in comparison with the normal pancreas. When tumors became palpable, rats were treated three times daily for 12 or 14 days with CCK-8 or NaCl 0.9% (controls) alone or in combination with the CCK receptor antagonist CR1409 (10 mg/kg) administered subcutaneously twice daily. Then tumors and pancreata were analyzed for their size, composition, and CCK receptors. Tumor volume, weight, and protein content, RNA, DNA, and enzymes decreased after CCK-8 treatment in a dose-dependent manner, the maximal effect being observed with 4-micrograms/kg treatment. This inhibitory effect was partially suppressed by CR1409, which by itself also reduced tumor growth, but to a lesser degree. CCK-8 exerted a stimulating effect on growth of the normal pancreas with low doses (1 and 2 micrograms/kg) and an inhibitory effect or no effect with a higher dose (4 micrograms/kg). CR1409 prevented this latter effect, but did not affect by itself the normal pancreas. These findings suggest that CCK-8 inhibits growth of an acinar cell tumor grafted to the rat; this effect is mediated by the occupation of specific CCK receptors present in high density on these cells. In contrast, CCK-8 exerts a biphasic effect on the normal pancreas as a function of its dose.

Animals↗
PubMed1979

[The effect of atropine on the pancreas].

The literature relating to the effect of atropine on exocrine pancreatic secretion in man and animals is critically reviewed. In most species basal secretion of volume, bicarbonate, and enzyme secretion are reduced by atropine, thus indicating some neural control of basal pancreatic secretion. The literature is replete with conflicting findings on the effect of atropine on pancreatic response to exogenous hormones. In well controlled studies atropine had no effect on the action of cholecystokinin-pancreozymin (CCK) or caerulein on the pancreas. Atropine either moderately depressed or did not alter the volume and bicarbonate response to secretin but constantly reduced enzyme secretion. With respect to pancreatic response to a meal, and to intestinal instillation of aminoacids, fat or HCL, all studies agree that pancreatic secretion is depressed by atropine. The recent finding that atropine did not alter the response of a transplanted denervated pancreas to intestinal stimulants suggests that atropine acts on the pancreas by interrupting an enteropancreatic vago-vagal reflex and not by blocking the action of hormones on the pancreas or by interfering with cholinergic facilitation of gastrointestinal hormone release.

Anesthesia↗
PubMed1983

Regulation of the mucosal gastrin receptor.

The gastrin receptor in rat oxyntic gland mucosa is highly regulated. This regulation has so far only been found to be directed at the total numbers of receptors present. The affinity of the receptor is not altered significantly by agents which affect receptor numbers. Homospecific regulation occurs in that gastrin upregulates its receptor over long periods of time. Upregulation, however, appears to be preceded by a brief period of downregulation. During development corticosterone triggers the synthesis, or at least the appearance of gastrin receptors. Receptor development is maintained by solid food and presumably the gastrin it releases, but the change in diet which occurs at weaning does not in itself induce development. In female rats, estrogens prevent the increase of gastrin receptor levels to those found in males. These results with the gastrin receptor emphasize the importance of studying receptor concentrations as well as hormone levels to the total understanding of an endocrine response. They also suggest that the receptors of the other gastrointestinal hormones are likely to be regulated and that this regulation will probably be important in understanding some of the diseases of the gastrointestinal tract.

Adrenal Cortex Hormones↗