Selective reduction by dexamethasone of stress-related hyperphagias.
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Biomedical subjects
G K Yim
Publications and source records attributed to G K Yim.
Relationship between plasma concentrations of immunoreactive beta-endorphin and food intake in rats.
Periods of increased food intake in male rats were characterized by significant elevations in the plasma concentrations of immunoreactive beta-endorphin (beta-ep). Administration of 2-deoxy-D-glucose (400 mg/kg) produced rapid and concurrent increases in both food intake and plasma beta-ep. Administration of insulin (10 units/kg) produced large delayed increases in food intake but only modest delayed increases in plasma beta-ep. Spontaneous nocturnal feeding was associated with increased plasma beta-ep. Increases in daytime food intake in rats subjected to 24 hr of food deprivation were also characterized by elevated plasma beta-ep. In all cases examined, those feeding behaviors in male rats which were subject to inhibition by naloxone were characterized by elevated concentration of plasma beta-ep.
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CNS tissue levels of dynorphin-A immunoreactivity and the anorexia associated with sodium chloride imbibition in the rat.
Forced imbibition of increasing concentrations of sodium chloride (NaCl) in rats reduced daytime 2-deoxy-D-glucose (2-DG) induced feeding in a concentration dependent manner. Pituitary neurointermediate lobe (NIL) levels of immunoreactive (ir)-dynorphin-A 1-17 and 1-8 were also decreased by the NaCl regimen in a concentration dependent manner. However, there was no significant association between the reduction of NIL dynorphin levels and the suppression of 2-DG induced feeding on a within-animal basis. NaCl imbibition did not affect levels of either ir-dynorphin-A 1-17 or 1-8 in the hypothalamus, cerebral cortex, hippocampus, medulla/pons or anterior pituitary. Neither the acute changes following 2-DG administration, nor the comparison of ir-dynorphin-A 1-8/1-17 ratios appeared useful for the assessment of dynorphin-A turnover. Thus, the present results did not support the hypothesis that anorexia of NaCl treated animals results from the depletion of dynorphin-A.
Amino Acid Sequence↗
Experimental dissociation of food intake and plasma beta-endorphin following 2-deoxy-D-glucose in rats.
The present studies were undertaken to further assess the role of plasma beta-endorphin (beta-EP) in the hyperphagia induced by the glucose antimetabolite, 2-deoxy-D-glucose (2-DG). Plasma concentrations of immunoreactive beta-EP (ir-beta-EP) were measured at the end of the first hour of feeding in all animals treated with 400 mg/kg 2-DG. Previous studies had shown a consistent, positive association between 2-DG hyperphagia and plasma ir-beta-EP concentrations, but the present data revealed dissociations between hyperphagia and plasma ir-beta-EP. Dexamethasone administration blocked the 2-DG-induced rise in plasma ir-beta-EP, but had no effect on the 2-DG hyperphagia measured at 1 hour. Forced drinking of a 2% NaCl solution decreased 2-DG hyperphagia, but not the 2-DG induced rise in plasma ir-beta-EP. Thus, elevations in plasma ir-beta-EP are not necessary for the full expression of 2-DG-induced hyperphagia in dexamethasone-treated rats. Furthermore, decreased feeding responses to 2-DG could coexist with increased levels of plasma ir-beta-EP in NaCl-treated normal rats. Elevations in plasma ir-beta-EP do not appear to be the critical opiate link in 2-DG induced hyperphagia.
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A new view of the structural relationship between LSD and mescaline.
An examination of the effects of S-(-) and R-(+) 2-amino-1,2,3,4-tetrahydronaphthalene (2-AT) on mouse spontaneous activity and rabbit EEG has shown that the S-(-) enantiomer shows selective central effects similar to those of hallucinogens like mescaline. A stereochemical analysis of these results indicates that the structural relationship between mescaline, or other phenethylamine type hallucinogens, may involve correspondence between the aromatic ring of the phenethylamines and the pyrrole portion of the indole nucleus in LSD.
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Assessment of endogenous opioid mediation in stress-induced hypercholesterolemia in the rat.
Stressful stimuli are known to elevate total plasma cholesterol levels and activate endogenous opioid systems. In cholesterol-cholic, acid-fed female rats, a 5-day unpredictable immobilization stress paradigm increased levels of low plus very low density lipoprotein cholesterol and reduced levels of high density lipoprotein cholesterol. Pretreatment with the opiate antagonist, naltrexone (1.0 mg/kg, sc) prevented the stress-induced changes. Five-day morphine pellet implants (75 mg) duplicated the cholesterol alterations seen in immobilized rats. In addition, plasma triglyceride levels were elevated in morphine pelleted rats, but hepatic and aortic cholesterol levels were unchanged. Unchanged plasma sorbitol dehydrogenase activity and hepatic triglyceride levels indicated that both regimens were not hepatotoxic. These findings support the possible role for endogenous opioid systems in stress-induced hypercholesterolemia.
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