ENZYMATIC AND METABOLIC ADAPTATIONS: II. CHANGES IN ADRENALECTOMIZED RATS SUBJECTED TO DIETARY MODIFICATIONS

1962 ◽  
Vol 40 (1) ◽  
pp. 961-972 ◽  
Author(s):  
J. S. Willmer ◽  
T. S. Foster

Changes in the activity of five liver enzymes in adrenalectomized rats were observed during adaptation to three experimental diets. Considerable differences were observed between these results and those obtained from intact rats, some of the changes being attributable to limitations of caloric intake. Differences between adrenalectomized and unoperated animals were also demonstrated in the rates of oxidation of glucose-1-C14 and glucose-6-C14.Partial restoration of normal adaptive enzyme patterns was accomplished by treatment with individual adrenal cortical steroids. Hydrocortisone was found to be the most effective steroid used in this respect.

1962 ◽  
Vol 40 (7) ◽  
pp. 961-972 ◽  
Author(s):  
J. S. Willmer ◽  
T. S. Foster

Changes in the activity of five liver enzymes in adrenalectomized rats were observed during adaptation to three experimental diets. Considerable differences were observed between these results and those obtained from intact rats, some of the changes being attributable to limitations of caloric intake. Differences between adrenalectomized and unoperated animals were also demonstrated in the rates of oxidation of glucose-1-C14 and glucose-6-C14.Partial restoration of normal adaptive enzyme patterns was accomplished by treatment with individual adrenal cortical steroids. Hydrocortisone was found to be the most effective steroid used in this respect.


1962 ◽  
Vol 40 (1) ◽  
pp. 953-960 ◽  
Author(s):  
J. S. Willmer ◽  
T. S. Foster

A study of hepatic enzymes concerned in glucose metabolism was made after transfer of rats from a standard laboratory ration to three experimental diets. The change to two high-carbohydrate diets resulted in elevated levels of enzymes of the hexosemonophosphate shunt. Glucose-6-phosphatase, phosphoglucomu-tase, and phosphoglucoseisomerase exhibited an initial transitory decrease in activity, succeeded by restoration to normal or above-normal levels. Animals fed a low-glucose diet showed a tendency towards decreased activity of all enzymes except glucose-6-phosphatase. Hepatic oxidation of glucose-1-C14and glucose-6-C14and liver glycogen levels were also measured. These results are discussed in relation to the observed enzyme changes.


1962 ◽  
Vol 40 (7) ◽  
pp. 953-960 ◽  
Author(s):  
J. S. Willmer ◽  
T. S. Foster

A study of hepatic enzymes concerned in glucose metabolism was made after transfer of rats from a standard laboratory ration to three experimental diets. The change to two high-carbohydrate diets resulted in elevated levels of enzymes of the hexosemonophosphate shunt. Glucose-6-phosphatase, phosphoglucomu-tase, and phosphoglucoseisomerase exhibited an initial transitory decrease in activity, succeeded by restoration to normal or above-normal levels. Animals fed a low-glucose diet showed a tendency towards decreased activity of all enzymes except glucose-6-phosphatase. Hepatic oxidation of glucose-1-C14and glucose-6-C14and liver glycogen levels were also measured. These results are discussed in relation to the observed enzyme changes.


1980 ◽  
Vol 87 (1) ◽  
pp. 65-71 ◽  
Author(s):  
MASAYOSHI KUMEGAWA ◽  
NORIHIKO MAEDA ◽  
TOSHIHIKO YAJIMA ◽  
TAISHIN TAKUMA ◽  
EIKO IKEDA ◽  
...  

The effects of cortisol (10 μg/g body weight) and l-thyroxine (T4; 0·2 μg/g body weight) on the activity of parotid gland amylase in young rats were investigated. Administration of cortisol or T4 for 5 consecutive days from day 5 after birth caused the precocious appearance of amylase, T4 having almost twice the effect of cortisol. Cortisol and T4 did not have synergistic effects. In thyroidectomized-adrenalectomized rats, T4 increased amylase activity but cortisol did not. The increase in enzyme activity after day 20 was much less in rats thyroidectomized on day 10 than in rats adrenalectomized on day 10. These results suggest that T4 has a direct effect on the early increase of amylase activity (days 15–25) and that the action of glucocorticoid requires the presence of endogenous thyroid hormones. The hormone-induced level of amylase in intact rats was less than that of normal adult rats. Forced weaning of intact rats resulted in a further increase in amylase activity, suggesting that further amylase accumulation (after day 25) may be due to dietary factors.


1958 ◽  
Vol 195 (1) ◽  
pp. 142-146 ◽  
Author(s):  
Joseph H. Perlmutt ◽  
Donald A. Olewine

The increased urinary Na+ output induced by Diamox in water-loaded adrenalectomized rats was partially antagonized by the mineralocorticoid, desoxycorticosterone glucoside (DCG), the increased K+ excretion was augmented and urine volume was not affected. Intact rats subjected to the same treatment showed only a small, but significant, rise in K+ excretion. Under the same conditions, the glucocorticoid, hydrocortisone hemisuccinate (compound FH), significantly elevated Na+, K+ and H2O excretion in adrenalectomized rats receiving Diamox; intact rats showed an increase in Na+ and H2O excretion with no significant change in K+ output. Of particular interest is the finding that 2.5 mg compound FH alone increased H2O excretion in adrenalectomized rats to a slightly greater extent than Diamox alone with considerably less Na+ loss.


1963 ◽  
Vol 41 (10) ◽  
pp. 2189-2195 ◽  
Author(s):  
Rosemary D. Hawkins ◽  
R. E. Haist

In the rat, the magnitude of the hypoglycaemic response to a dose of tolbutamide (50 mg/kg per os) which does not depress blood glucose levels to the point where adrenal compensatory mechanisms are stimulated is unaffected by adrenalectomy. On the other hand, when a dose is given which induces a greater hypoglycaemia (100 mg/kg per os) a very significant difference between adrenalectomized and sham-operated animals is observed, the adrenalectomized rats displaying a far greater sensitivity to the hypoglycaemic action of this compound. In intact rats, the hypoglycaemia induced by tolbutamide (100 mg/kg per os) is lessened by pretreatment of the animals with Dibenzyline (4 mg/kg) but enhanced by the prior injection of dihydroergotamine (2 mg/kg). Larger doses of dihydroergotamine alone cause a reduction in glucose levels of tail blood which is greater than that found in carotid blood samples withdrawn at the same times.


1991 ◽  
Vol 261 (3) ◽  
pp. E325-E331 ◽  
Author(s):  
Y. Hamatani ◽  
M. Inoue ◽  
K. Kimura ◽  
M. Shiota ◽  
M. Ohta ◽  
...  

The effects of calmodulin antagonists on the capacity of hydrogen-translocating shuttles were studied in the perfused rat liver. The capacity was estimated by measuring the changes in the rate of production of glucose from sorbitol during the oxidation of ethanol [T. Sugano, T. Ohta, A. Tarui, and Y. Miyamae. Am. J. Physiol. 251 (Endocrinol. Metab. 14): E385-E392, 1986]. Thyroxine given to intact rats increased the activity of alpha-glycerophosphate dehydrogenase (alpha-GPD). Glucocorticoid replacement in adrenalectomized rats decreased the activity of the alpha-GPD to values obtained after treatment with PTU. In either thyroxine-treated or steroid-replaced rats, the capacity of hydrogen-translocating shuttles increased markedly. However, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), trifluoperazine, and chlorpromazine inhibited the increased capacity in steroid-replaced rats and had no effect on the increased capacity in thyroxine-treated rats. W-7 inhibited the stimulatory effects of norepinephrine on the capacity of the malate-aspartate shuttle without inhibition of efflux of intracellular Ca2+. The stimulatory effects of vasopressin on the malate-aspartate shuttle were also inhibited by W-7, trifluoperazine, and chlorpromazine. The results suggest that the malate-aspartate shuttle may be regulated by Ca(2+)-calmodulin.


1968 ◽  
Vol 42 (2) ◽  
pp. 253-260 ◽  
Author(s):  
C. W. OGLE ◽  
MARY F. LOCKETT

SUMMARY Repeated exposures of intact rats, neurohypophysectomized rats and rats with denervated kidneys to high-pitched sound (20 kcyc./sec.) for 2 sec. with an intensity of 98–100 decibels caused diuresis, natriuresis and kaluresis: the rate of urinary excretion of adrenaline rose very significantly. Adrenal demedullation abolished the natriuresis and kaluresis in response to 20 kcyc./sec. and converted the diuresis to an antidiuresis. The renal response of normal rats to 20 kcyc./sec. was therefore attributed to the release of adrenaline from the adrenal medulla in amounts sufficient to prevent an emotional release of antidiuretic hormone from the neurohypophysis. Since 20 kcyc./sec. caused a significant increase in the urinary output of vasopressin by adrenalectomized rats, an emotional release of vasopressin is assumed to have proceeded, uninhibited, in adrenal-de-medullated rats exposed to 20 kcyc./sec., and to have caused the observed antidiuresis. The diuresis, natriuresis and kaluresis caused by 150 cyc./sec. mimicked by s.c. injection of 4 m-u. oxytocin, was unaffected by demedullation of the adrenals and was not accompanied by increase in urinary adrenaline.


2005 ◽  
Vol 288 (2) ◽  
pp. E342-E346 ◽  
Author(s):  
Elise P. Gomez-Sanchez ◽  
Naveed Ahmad ◽  
Damian G. Romero ◽  
Celso E. Gomez-Sanchez

Very small amounts of adrenocorticosteroids are synthesized by brain tissue in vitro. While there is evidence suggesting that the synthesis of aldosterone in the brain may have a role in the hypertension of the Dahl salt-sensitive rat, the de novo synthesis of aldosterone or corticosterone within the brain of a living animal has not been demonstrated. We have used sensitive ELISAs to measure aldosterone and corticosterone in the plasma and whole brains of intact rats receiving a normal-, low-, or high-salt diet to alter adrenal aldosterone production and of adrenalectomized rats provided sodium replacement, some of which received aldosterone, corticosterone, or DOC replacement. The results of several experiments were consistent. In intact rats, the brain concentration of aldosterone and corticosterone reflected that in the plasma. However, whereas aldosterone and corticosterone were undetectable or barely undetectable in the plasma of adrenalectomized animals, as was the corticosterone in their brains, aldosterone was consistently found in the brains of adrenalectomized rats, ranging from a mean of 6.6–41 pg/g, depending on the experiment. Provision of DOC as substrate for the endogenous aldosterone synthase and 11β-hydroxylase did not significantly increase brain aldosterone or corticosterone content. It is postulated that the small amounts of aldosterone synthesized in the brain could provide a local ligand for autocrine or paracrine activation of the mineralocorticoid receptor.


1991 ◽  
Vol 260 (1) ◽  
pp. R73-R81 ◽  
Author(s):  
L. Devenport ◽  
A. Knehans ◽  
T. Thomas ◽  
A. Sundstrom

Corticosterone-free (adrenalectomized, ADX) and intact rats were offered experimentally compounded diets in which 65% of available calories were supplied by a single macronutrient (single-diet study). ADX impaired the intake, weight gain (especially as body fat), and efficient utilization of high-protein and high-fat diets. In contrast, no behavioral, metabolic, or compositional changes could be found among ADX rats maintained on a diet high in carbohydrates. When ADX rats were given separate sources of macronutrients (self-selection study) they did not self-select a high-carbohydrate diet. Instead, they displayed a strong fat avoidance and a relative increase in protein intake, the macronutrient they utilize least efficiently. Separate groups of ADX animals were continuously infused with 25 or 125 micrograms.kg-1.day-1 aldosterone, a specific type I adrenocorticoid receptor agonist. Type I receptor stimulation eliminated all ADX-related deficiencies found in the single-diet and self-selection studies: caloric intake, feeding efficiency, carcass composition, and macronutrient preferences were restored to or beyond the corresponding values of adrenal-intact rats. The normal rat's ability to ingest and utilize macronutrients optimally is dependent on corticosterone's stimulation of type I receptors.


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