Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormal growth hormone (GH) and adrenocorticotropic hormone (ACTH)/cortisol secretory patterns in response to a glucose load have been observed in underweight anorectic women. The present study was performed in an attempt to establish whether changes in the hypothalamic/pituitary sensitivity to hyperglycemia occur in bulimia in the absence of weight disturbance. Therefore, serum GH, plasma cortisol, and plasma insulin concentrations were measured in eight women with normal weight bulimia and in eight normal women during an intravenous glucose (0.33 g/kg as an IV bolus) tolerance test (IGTT). In addition, since abnormal pituitary hormone responses to a glucose load might reflect alterations in somatostatin (SRIH) release, TSH secretion also was measured, in view of its sensitivity to SRIH inhibition. Both GH and cortisol levels progressively and significantly declined during IGTT in the normal subjects. In the bulimic women, cortisol levels remained unchanged, whereas GH concentrations rose significantly after glucose injection. Plasma cortisol and serum GH levels were significantly higher in the bulimic than in the control subjects. No significant differences between groups were observed in hyperglycemia-induced insulin increments or in TSH decrements. These data indicate that an altered sensitivity to hyperglycemia affects the hypothalamic/pituitary centers controlling the secretion of the counterregulatory hormones GH and ACTH/cortisol in bulimia nervosa. The lack of a simultaneous change in the TSH secretory pattern argues against a possible involvement of SRIH in the pathophysiology of this disorder.
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PMID:Abnormal growth hormone and cortisol, but not thyroid-stimulating hormone, responses to an intravenous glucose tolerance test in normal-weight, bulimic women. 136 37

The eating disorders, anorexia nervosa and normal weight bulimia, are associated with disturbances of hypothalamic-pituitary-adrenal cortical (HPA) and growth hormone function. Because somatostatin (SRIF) is one of the neuropeptides known to modulate feeding behavior and neuroendocrine systems, we measured cerebrospinal fluid (CSF) concentrations of this peptide in patients with eating disorders. CSF SRIF concentrations in patients with anorexia nervosa, both at low weight and after weight recovery, were similar to those in controls. When normal weight bulimic women stopped binging, they had a modest but significant increase in CSF SRIF. CSF SRIF was not related to plasma growth hormone concentrations but did show relationships to HPA axis hormones. Healthy volunteer women had a significant positive relationship between CSF SRIF and CSF corticotropin releasing hormone (CRH). In underweight anorectics, CSF SRIF was negatively related to both 24-hr urinary free cortisol and plasma cortisol concentrations after dexamethasone, but it was not significantly related to CSF CRH. These relationships more closely resembled those of healthy controls after weight correction. In bulimics, CSF SRIF was positively related to CSF CRH and negatively related to plasma cortisol. Our findings support a previously described relationship between CSF SRIF and HPA axis activity. The differences in SRIF-HPA relationships in anorectics and bulimics may constitute or reflect pathophysiological distinctions between these disorders.
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PMID:CSF somatostatin in anorexia nervosa and bulimia: relationship to the hypothalamic pituitary-adrenal cortical axis. 290 May 33

In the past 10 years, numerous gut peptides have been tested for their satiating effect on food intake. Cholecystokinin (CCK), bombesin, pancreatic glucagon, and somatostatin have the best supporting evidence for such a specific behavioral effect. The satiety effect of CCK, somatostatin, and glucagon is abolished or markedly reduced by abdominal vagotomy, but the satiety effect of bombesin is not. The effect of vagotomy has been interpreted as the result of the loss of vagal afferent fibers that are necessary for carrying information about visceral effects of these peptides to the brain. This hypothesis is under active investigation. There are three reports that CCK decreases the size of a test meal in lean and obese humans. This suggests that CCK or the other peptides may be useful in treating human obesity and bulimia.
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PMID:Gut peptides and postprandial satiety. 614 53

Bulimia nervosa is an eating disorder characterised by recurrent episodes of binge eating and associated efforts to purge the ingested calories through self-induced vomiting, laxative or diuretic abuse, fasting or intensive exercise. The aetiopathogenesis and pathophysiology of the disorder are currently unclear. Biological bases have been proposed repeatedly, based on several lines of evidence: hunger, satiety and food choice are regulated by neurotransmitters and neuropeptides, and impairment of eating habits may be related to alterations in the secretion of these chemicals; genetic studies suggest that these neurotransmitter systems are dysfunctional in individuals with bulimia nervosa; and the frequent comorbidity of bulimia nervosa with major depressive and obsessive-compulsive disorders, conditions in which multiple alterations of brain biochemical functions have been demonstrated. Data in the literature suggest that levels of noradrenaline (norepinephrine) and serotonin (5-hydroxytryptamine; 5-HT) are lower in individuals with bulimia nervosa than in healthy controls. Levels of dopamine are similar to, or lower than, those in controls. After remission of the disorder, noradrenergic function returns to that seen in controls, whereas dopaminergic and serotonergic function rebound to levels higher than in controls. Among the neuropeptides, alterations in the levels of neuropeptide Y, peptide YY, beta-endorphin, corticotrophin-releasing hormone, somatostatin, cholecystokinin and vasopressin have been found in the symptomatic phase of bulimia nervosa, with a return to levels seen in controls after remission. Pharmacological treatment of bulimia nervosa that is directed at correction of the neurochemical alterations observed is difficult because of the complexity of the impairments. However, such treatment is necessary and should be continued long after symptomatic remission to ensure reinstitution of cerebral biochemical homeostasis.
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PMID:Aetiopathogenesis and pathophysiology of bulimia nervosa: biological bases and implications for treatment. 1146 Aug 90