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

Recent studies have established the existence of substrate cycles in humans, but factors regulating the rate of cycling have not been identified. We have therefore investigated the acute response of glucose/glucose-6P-glucose (glucose) and triglyceride/fatty acid (TG/FA) substrate cycling to the infusion of epinephrine (0.03 microgram/kg.min) and glucagon. The response to a high dose glucagon infusion (2 micrograms/kg.min) was tested, as well as the response to a low dose infusion (5 ng/kg.min), with and without the simultaneous infusion of somatostatin (0.1 microgram/kg.min) and insulin (0.1 mU/kg.min). Additionally, the response to chronic prednisone (50 mg/d) was evaluated, both alone and during glucagon (low dose) and epinephrine infusion. Finally, the response to hyperglycemia, with insulin and glucagon held constant by somatostatin infusion and constant replacement of glucagon and insulin at basal rates, was investigated. Glucose cycling was calculated as the difference between the rate of appearance (Ra) of glucose as determined using 2-d1- and 6,6-d2-glucose as tracers. TG/FA cycling was calculated by first determining the Ra glycerol with d5-glycerol and the Ra FFA with [1-13C]palmitate, then subtracting Ra FFA from three times Ra glycerol. The results indicate that glucagon stimulates glucose cycling, and this stimulatory effect is augmented when the insulin response to glucagon infusion is blocked. Glucagon had minimal effect on TG/FA cycling. In contrast, epinephrine stimulated TG/FA cycling, but affected glucose cycling minimally. Prednisone had no direct effect on either glucose or TG/FA cycling, but blunted the stimulatory effect of glucagon on glucose cycling. Hyperglycemia, per se, had no direct effect on glucose or TG/FA cycling. Calculations revealed that stimulation of TG/FA cycling theoretically amplified the sensitivity of control of fatty acid flux, but no such amplification was evident as a result of the stimulation of glucose cycling by glucagon.
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PMID:Hormonal control of substrate cycling in humans. 328 15

The brain is an important target organ for both endogenous and synthetic corticosteroid hormones, but the nature of steroid action there is complex. We review a series of studies that was designed to elucidate possible relationships between the behavioral and biological effects of exogenous corticosteroids. In these studies, corticosteroids were administered to intact animals or to currently healthy volunteers, and behavioral and biological indices of corticosteroid effects were jointly assessed. In the first study, chronic corticosterone administration to intact rats resulted in increased locomotor activity (consistent with increased caudate or nucleus accumbens dopamine activity) and increased caudate homovanillic acid (HVA) levels. In the second study, acute dexamethasone administration to healthy human volunteers resulted in increased plasma HVA levels. These findings in animals and humans may help explain vulnerability factors for experiencing psychotic reactions during chronic corticosteroid treatment. To more closely mimic clinical conditions in which "steroid psychoses" develop, we administered a higher dose and more chronic corticosteroid medication (prednisone, 80 mg/day for 5 days) in a double-blind manner to healthy volunteers. Consistent with prior clinical observations, behavioral changes were variable across subjects. Seventy-five percent of the individual volunteers developed mild behavioral side effects during prednisone administration; in addition, significant, specific deterioration in cognitive performance was observed. Prednisone administration was also associated with significant decreases in plasma levels of adrenocorticotropic hormone (ACTH), cortisol, and 3-methoxy,4-hydroxyphenyl glycol (MHPG) and in cerebrospinal fluid (CSF) levels of ACTH, beta-endorphin (BE), beta-lipotropin (BLPH), somatostatin-like immunoreactivity (SLI), and norepinephrine (NE). It was also associated with significant slowing of brain wave electrical activity (viz., an increase in theta wave activity) on quantitative electroencephalography. Several behavioral changes, particularly those relating to mood or cognition, were related to changes in CSF levels of NE, MHPG, ACTH, BE, BLPH, and SLI and to the slowing of brain wave activity. Our preliminary data raise the possibility that the behavioral effects of exogenous corticosteroids have specific neural concomitants and that the pattern of biological changes produced contributes to the behavioral variability observed. Steroid effects on levels of biogenic amines, pro-opiomelanocortin (POMC)-related peptides and somatostatin, among others, as well as on brain electrophysiology, may be behaviorally relevant and are highlighted as being worthy of further investigation.
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PMID:Prospective controlled studies of the behavioral and biological effects of exogenous corticosteroids. 751 7

Elevated levels of circulating corticosteroids are frequently associated with behavioral alterations in man, although the mechanisms by which corticosteroids may affect behavior are poorly understood. To evaluate possible effects of exogenous corticosteroids on brain electrophysiological functioning and the relationship of such effects to behavioral and biochemical changes, we administered prednisone (80 mg p.o. daily for 5 days) in a double-blind manner to 11 medically healthy volunteers. Quantitative electroencephalogram analysis was performed following 4 days of prednisone administration and during the preceding and ensuing placebo administration periods. Central theta wave brain electrical activity significantly increased following prednisone administration and returned to baseline following prednisone withdrawal. This effect was directly correlated with prednisone-induced increases in subjective sadness ratings and with decreases in self-rated energy and well-being. Prednisone-induced reductions in peak alpha wave activity were also directly correlated with increases in subjective sadness and Symptom Checklist-90 ratings and with decreases in self-rated 'hypomanic' symptoms. Further, prednisone-induced increases in theta activity were significantly correlated with prednisone-induced decreases in CSF levels of somatostatin-like immunoreactivity, and prednisone-induced decreases in peak alpha activity were significantly correlated with decreases in CSF levels of norepinephrine and with relative increases (or lesser decreases) in CSF levels of beta-endorphin and beta-lipotropic hormone. This preliminary report of the concomitant development of prednisone-induced changes in brain electrical activity, neurochemistry and behavior highlights areas for future exploration in the study of corticosteroid effects on behavior in man.
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PMID:Quantitative electroencephalographic correlates of steroid administration in man. 823 43

We make a retrospective evaluation of clinical and radiologic features, treatment, and outcome of Erdheim-Chester disease, a rare non-Langerhans cell histiocytosis. We report a case of Erdheim-Chester disease and review 60 cases from the literature. These cases are consider to have Erdheim-Chester disease when they have either typical bone radiographs (symmetrical long bones osteosclerosis) and/or histologic criteria disclosing histiocytic infiltration with distinctive immunohistochemical phenotype of the non-Langerhans cell histiocytes with positive staining for CD68 and negative staining for S-100 protein and CD1a. Our patient undergoes chemiotherapy according to the LCH-II stratification and therapy plan (Vinblastine, Etoposide and Prednisone) and thereafter receives Carboplatin and Etoposide, and Somatostatin. She is alive and clinically well 33 months after onset of symptoms and the lesions don't appear to progress at imaging examinations. In conclusion, Erdheim-Chester disease may be confused with Langerhans cell histiocytosis as it sometimes shares the same clinical (exophthalmos, diabetes insipidus) or radiologic (osteolytic lesions) findings. However, the characteristics radiological pattern of Erdheim-Chester disease together the immunohistochemical phenotype of hystiocytic infiltration supports the theory that Erdheim-Chester disease is a unique disease entity distinct.
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PMID:[Erdheim-Chester disease: a non-Langerhans cell histiocytosis. A clinical-case and review of the literature]. 1534 69