Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renewal of the digestive mucosa is the most efficient process assuming the maintenance of the gastrointestinal barrier. The mucous and absorptive cells, born in the proliferative zone, are migrating to the surface and they extrude duirng meals, living 4 to 6 days. Hyperphagia, pregnancy, lactation and intestinal resection induce a hypertrophic state. Fasting, ageing, germ free status provoke a hypoplasia. The ulcerogenic and antimitotic drugs decrease the proliferative activity. The gastrointestinal cell renewal is controlled by hormonal, vitaminic and nervous agents. Gastrin and growth hormone are the major trophic factors, secretom amd cprtocpsteroids act as antitrophic agents. The vitamins A, D and B12, and the nervous transmittors participate in the feed back control assuming a steady state between proliferation and extrusion. Chalones and immunologic factors are probably the most important but unknown inhibitors. The pathological events concerned with abnormal renewal are peptic ulcer, atrophic gastritis, intestinal villous atrophy and digestive cancer.
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PMID:[Regulation of cell renewal in the gastrointestinal mucosa (author's transl)]. 32 43

Many gastrointestinal structural and functional properties are known to be altered in diabetes. In this study, we investigated whether serum and tissue gastrin levels are abnormally altered in a strain of genetically diabetic mice (C57BL/KSJ). Both serum and antral gastrin concentration were found to be significantly increased 3.4- and 2-fold above normal values in diabetic mice fed ad libitum. The increase in tissue gastrin concentration is most probably due to an increase in both cellular gastrin content and G-cell number, since the latter property is increased 130% in diabetic animals. Pair feeding studies demonstrated that diabetes associated hyperphagia is not a major factor in inducing these endocrine changes, since antral and serum gastrin are still significantly elevated above normal in diabetic animals fed a restricted diet. G-cell number, however, is not significantly increased above normal values in pair fed diabetic mice. The peak serum gastrin concentration after a meal and the duration of postprandial hypergastrinemia are also significantly increased above normal in diabetic animals. Gel filtration chromatography studies indicate that the antral nucosae of normal and diabetic mice have identical molecular forms of the hormone. It is therefore concluded that antral and serum gastrin concentration are increased in genetically diabetic mice due to both dietary alterations and other, as yet undefined, factors specific for the disease, and that the resultant hypergastrinemia may contribute to some of the gastrointestinal alterations seen in diabetes.
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PMID:Alterations in serum and antral gastrin levels in genetically diabetic mice. 49 15

Somatostatin, gastrin-releasing peptide (GRP) and gastrin were measured in the stomach of rats with streptozotocin-induced diabetes, insulinoma-bearing rats and their respective controls. Rats injected with streptozotocin exhibited hyperphagia, insulinopenia and severe hyperglycemia. Stomach weights, and the concentrations and total amounts of GRP and gastrin in the stomach, were similar to nondiabetic control rats. The concentration of somatostatin in the stomach of diabetic rats was 25% greater, but the total stomach content of somatostatin was similar to that of control rats. Insulinoma-bearing rats exhibited hyperphagia, hyperinsulinemia and hypoglycemia. Concentrations of GRP and gastrin in the stomach were 72% and 19% lower, respectively, than in control rats. Despite 45% greater stomach weight, the total stomach content of GRP was 61% lower. Stomach concentrations of somatostatin, and total stomach contents of somatostatin and gastrin, were similar in insulinoma-bearing and control rats. The results demonstrate abnormalities in the stomach concentrations of regulatory peptides in rats with diabetes and insulinoma. These abnormalities are not attributable to changes in food intake alone, suggesting specific effects of these metabolic diseases on gastric regulatory peptides and gastric function.
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PMID:Somatostatin, gastrin-releasing peptide and gastrin in the stomach of rats with streptozotocin-induced diabetes and insulinoma. 167 27

It has been hypothesized that G-cell hyperplasia secondary to increased food consumption in the obese Zucker rat was responsible for the hypergastrinemia observed in vivo and from the isolated perfused stomach preparation. This possibility was investigated in pair-feeding experiments wherein the food intake of obese animals was restricted to match that of lean littermates from 5 to 8 weeks of age. Dietary restriction reduced the antral G-cell population of the obese rat to a similar level as that seen in lean animals, supporting the view that hyperphagia is the trigger for G-cell hyperplasia. However, basal gastrin levels measured in vivo and in vitro from the stomach preparation of the pair-fed obese animals were not significantly lower than those of obese animals fed ad libitum. Thus, abnormal feeding behavior in the obese phenotype cannot be directly related to gastrin hypersecretion and G-cell hyperplasia is not the primary cause of hypergastrinemia.
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PMID:The effect of dietary restriction on gastrin secretion in the obese Zucker rat. 222 4

1. In the absence of intraluminal inducers, low "basal" levels of cytochrome P-450 and its dependent MFO activities are detected in the rat intestinal mucosa, and may be regulated by endogenous hormones. 2. Rats were nutritionally maintained by either short term (48 hr) intravenous glucose infusion or chronic (8 days) intravenous hyperalimentation, and were treated with various doses of pentagastrin in the infusate. 3. Regardless of the dose (6-90 micrograms/kg/hr) or duration of infusion (2-8 days), pentagastrin had no effect on small intestinal cytochrome P-450, its dependent MFO activity, or the activity of delta-aminolevulinic acid synthetase. 4. The intestinal trophic peptide hormone, gastrin, apparently does not regulate the cytochrome P-450-dependent MFO system of the small intestine.
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PMID:Role of gastrin/pentagastrin in regulation of intestinal cytochrome P-450. 290 72

Elevations in serum gastrin concentration of six to seven times were found in postabsorptive 5- and 10-wk-old, but not 30- and 40-wk-old, obese mice in comparison with the appropriate lean controls. At 10 wk of age a fourfold hypergastrinemia was also evident in (ob/ob) mice denied food for 48 h. In 10-wk-old (ob/ob) mice that had eaten the same amount of food as lean mice from weaning, serum gastrin was six times that of lean controls. Antral gastrin concentration was 54% higher in fed 10-wk-old (ob/ob) mice than in lean mice. No relationship was found between alterations in serum gastrin and measures of gastrointestinal size or proliferative status. Maximal gastric acid output, expressed with respect to oxyntic mucosal dry weight, was reduced by 52% in 10-wk-old (ob/ob) mice compared with lean controls. It is concluded that the hypergastrinemia of 10-wk-old (ob/ob) mice is not caused by hyperphagia, but may be a consequence of reduced acid inhibition of gastrin release.
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PMID:Elevated serum and antral gastrin in obese (ob/ob) mice. 397 34

Basal plasma gastrin levels were significantly higher in obese rats induced by ventromedial hypothalamic lesions (VMH rats) than in sham-operated controls. Gastrin secretion in response to insulin hypoglycemia and a liquid diet load was higher in VMH rats than in controls. The antral gastrin concentration was also elevated in VMH rats. Pair-fed rats with VMH lesions showed increased gastrin secretion as did the non-pair-fed group. These results show that gastrointestinal hormone secretions as well as pancreatic endocrine function are abnormal in obese rats with VMH lesions. Increased gastrin secretion is probably induced by factors other then hyperphagia, such as disturbance of the autonomic nervous system due to the VMH lesions.
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PMID:Alterations of gastrin secretion in obese rats with ventromedial hypothalamic lesions. 636 Sep 24

Acute and chronic experiments in adult mongrel dogs were performed to investigate the influences of a low residue diet (Group I) and an elemental diet (Group II) on pancreatic function. 1) In the acute experiment, intraduodenal administration of the low residue diet produced a significant increase in amylase output in pancreatic juice, while the elemental diet die not. 2) Intragastric administration of the low residue diet or elemental diet to conscious dogs showed little difference between the two groups regarding secretin and gastrin release, at the same pH. 3) Long term enteral hyperalimentation showed that it is the low residue diets which enhance pancreatic secretions. 4) In both groups, carbohydrate metabolism, liver function and electrolyte balance were satisfactorily maintained during long term enteral hyperalimentation and morphologic changes of the liver, pancreas and small intestine were not evident. 5) From the viewpoint of nutritional management, low residue diets should be prescribed in some cases of alimentary surgery.
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PMID:Effects of long term enteral hyperalimentation on pancreatic secretion in dogs. 677 30

Luminal nutrition is known to have a trophic effect on small bowel mucosa after intestinal resection. Humoral agents, however, may also contribute to this process. Two of the proposed humoral agents, enteroglucagon and gastrin, were therefore investigated after intestinal resection and transection in the rat, and changes in their concentration in the plasma were related to cellular proliferation. Forty-eight male Wistar rats had either 75 per cent proximal small bowel resection or jejunal transection. The animals were further divided into three groups, each with a different nutritional intake. The first group were allowed food ad libitum. The second group were kept under hypothermic conditions which resulted in hyperphagia, while the last group were nourished intravenously. A further 8 animals had a laparotomy only (sham operation). All animals were killed 12 days after operation, plasma enteroglucagon and gastrin were measured, while determination of the crypt cell production rate (CCPR) was used to denote cellular proliferation. In each group resected rats had significantly higher crypt cell production rates and greater enteroglucagon levels compared with transected animals. However, only in the normally fed group was plasma gastrin increased in resected animals, there being no significant difference in the plasma concentration of this peptide in transected compared with resected rats, in both the intravenously fed and hyperphagic groups. In the models studied enteroglucagon appears to be a more likely candidate for a humoral trophic agent than gastrin in intestinal adaptation.
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PMID:The effect of altered luminal nutrition on cellular proliferation and plasma concentrations of enteroglucagon and gastrin after small bowel resection in the rat. 705 95

People with anorexia (AN) and bulimia nervosa (BN) have altered patterns of eating. It is possible that alterations of the neuropeptide gastrin releasing peptide (GRP), a bombesin (BBS) -like peptide with potent central anorexigenic activity, could contribute to disturbed eating behavior. To avoid the confounding effects of pathologic eating behavior, we measured cerebrospinal fluid (CSF) GRP concentrations in women who were long-term recovered (>1 year, normal weight, and regular menstrual cycles, no binging or purging) from AN (REC AN, N=12) or BN (REC BN, N=21) compared to healthy control women (NC, N=15). CSF GRP was significantly lower (chi(2)=9.41(3), p<0.01) in REC BN (9.6+/-3.1 pg/ml) compared to NC (13.4+/-5.5 pg/ml) and REC AN (11.6+/-2.9 pg/ml). Persistent GRP abnormalities after recovery from BN raise the possibility that this alteration might be trait-related and contribute to episodic hyperphagia in BN.
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PMID:Reduced gastrin releasing peptide in cerebrospinal fluid after recovery from bulimia nervosa. 1156 53


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