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PubMed2000

Hypophysectomy results in a loss of connexin gap junction protein from the adrenal cortex.

To test the hypothesis that gap junctions are dependent on the tropic state of the adrenal gland, the effect of hypophysectomy on connexin 43 (alpha1-Cx43) gap junction protein occurrence and distribution was examined in mice. Gap junction protein occurrence was assessed with immunohistochemical techniques. In the adrenal gland from intact animals, alpha1-Cx43 gap junction protein was detected in the zonae fasciculata(ZF) and reticularis (ZR) while only a few alpha1-Cx43 gap junction plaques were found connecting zona glomerulosa(ZG) cells. Hypophysectomy led to a profound atrophy of the cortex which was more marked in the inner zones (zonae fasciculata and reticularis) than in the zona glomerulosa. There was a time dependent loss of alpha1-Cx43 gap junction protein in the adrenal cortex after hypophysectomy. At 33 day following hypophysectomy there was a two fold decrease in gap junctions in the zona fasciculata while the average gap junction plaque size was not different than the size seen in control animal adrenal glands.. ACTH (1U/gm body weight) treatment in hypophysectomized animals increased the number of gap junction plaques in the zona fasciculata. Hypophysectomy led to diminished alpha1-Cx43 gap junction expression in the zona fasciculata which could be restored by ACTH treatment. Because altering the tropic state of the adrenal glands via hypophysectomy leads to a reduction in gap junction number, it can be suggested that control of gap junction expression in the adrenal gland is hormone dependent and linked to adrenal gland function.

Adrenal Cortex↗
PubMed1992

The effect of hypophysectomy on proluminal movement of 3H-androgens across the epididymal epithelium in the rat.

The effect of hypophysectomy on transepithelial movement of 3H-androgen in the rat epididymis was examined by using in vivo microperifusion of 3H-testosterone followed by in vivo micropuncture to obtain peritubular and intraluminal fluids. Experiments were performed on animals without hypophysectomy or on animals 5-6 days after hypophysectomy and 9-10 days after hypophysectomy. Tubules were perifused with Minimum Essential Medium containing 3H-testosterone. 14C-polyethyleneglycol was included in the perifusion fluid as a marker for contamination of the intraluminal fluid by peritubular fluid. Radioactivity of isotopes in the interstitial and intraluminal fluid was determined at 1 and 2 hours after perifusion and the percentage of peritubular isotopes appearing in the intraluminal fluid was determined. A sperm concentration microassay was performed on micropuncture samples from the epididymal tubules to assess testicular contribution to the lumen content. Proluminal movement of 3H-androgen and intratubular sperm concentrations in the caput epididymal tubules of rats 9-10 days after hypophysectomy were significantly decreased. Proluminal movement of 3H-androgen and intratubular sperm concentrations in the cauda epididymal tubules of rats 9-10 days after hypophysectomy were significantly increased. These results suggest that proluminal androgen movement is controlled by the presence of some testicular product in the epididymal lumen.

Androgens↗
PubMed1990

Study of long-term survival after transsphenoidal hypophysectomy in clinically normal dogs.

Experimental hypophysectomies were performed in 7 clinically normal dogs, using a new modification of the transsphenoidal approach. This approach facilitated centering of the sphenoid bone trephination and allowed safe exposure of the hypophysis regardless of the size or shape of a dog's skull. Complications did not occur during surgery and all dogs recovered well from surgery. Growth hormone secretory capacity was measured over a 3-month period to assess completeness of hypophysectomies. One dog was euthanatized 2 months after surgery, 4 dogs were euthanatized at 3 months after surgery, and 2 dogs were allowed to survive and their progress was followed for 2.5 years. Soft palate dehiscence and keratoconjunctivitis sicca developed in 2 of the dogs. The technical deficiencies responsible for these complications were corrected shortly after the beginning of the study. In 4 of the 5 necropsied dogs, minute remnants of adenohypophyseal tissue were found in the sellae turcica. Measurement of in vivo growth hormone secretory capacity revealed that these remnants had an altered stage of functional activity. Although complete hypophysectomy was not achieved consistently, the main technical obstacle of hypophysectomy, the reliable identification and the avoidance of the vascular structures surrounding the hypophysis, has seemingly been overcome. The surgical technique proved to enhance the safety of hypophysectomy, and the procedure can be recommended to treat clinical cases of canine pituitary-dependent hyperadrenocorticism. The clinical significance of potential subtotal hypophysectomy remains yet to be evaluated.

Animals↗
PubMed1977

[The morphogenic effect of gonadotropic hormones on the Leydig cells of the boar testis. II. Effects of administration of chorionic gonadotropin after hypophysectomy. Effects in vivo and in organ culture].

The longer ago the hypophysectomy has been performed, the more marked is Leydig cell atrophy in the testis. The effects of HCG on cellular morphology have been observed in vivo and in organ culture; qualitative quantitative and ultrastructural aspects were studied. In vivo, the effects of a daily injection of gonadotropin on the testis of 2 boars hypophysectomized 3 1/2 months ago are shown. Markedly atrophied cells are strongly stimulated by HCG during the 15 first days (the cell and nucleus recover nearly to standard size, with the typical histological and ultrastructural appearance with all the cell organelles which characterize a functional steroid cell). Then after 1 1/2 month injection it decreases again to the initial state (very small size cytoplasm strongly reduced with very low organelle content). The number of the Leydig cells is maintained during the first 15 days, then it progressively decreases. The effects of HCG on the testicular tissue of 4 boars were studied in organ culture. Interstitial tissue with a greater or lesser degree of atrophy was examined experimentally (1 month, 3 months and 4 months after hypophysectomy) in order to prove a possible irreversibility of the effects of hypophysectomy. In each case, cell changes were studied according to the duration of the culture. Control cultures without HCG in the medium were set up simultaneously. 1 month and/or 3 months after hypophysectomy, the Leydig cells in culture progressively recover the size and the histological and ultrastructural appearances of a typical Leydig cell. After 16 days of culture, the stimulation is highest, as in vivo. The number of Leydig cells is maintained. From the 17th day stimulation decreases and the cell enters a new atrophy phase. In the anhormonal control medium the atrophy continues as long as the culture is maintained, and the number of Leydig cells decreases. 4 months after hypophysectomy, stimulation in culture is still possible during the first 10 days (proved by the same tests); however the size of the cell remains small compared to the normal; then it atrophies again quickly. In this case the hormone does not maintain the number of the Leydig cells. In the control cultures, slight response of the cell is observed, but this effect is limited and disappears a few days later; the number of the cells rapidly decreases. It has been shown that markedly atrophied Leydig cells can highly be stimulated during the first 2 weeks under the influence of HCG as well in vivo as in organ culture. The lability of the effect is not yet explained. 4 months after hypophysectomy, stimulation is not so effective.

Animals↗
PubMed1982

Effects of hypophysectomy and dexamethasone administration on central and peripheral S-adenosylmethionine levels.

The effects of hypophysectomy and dexamethasone administration on S-adenosylmethionine (SAM) levels in the adrenal, liver, pineal, and various brain regions were examined to determine the central and peripheral relationships between SAM and glucocorticoids in vivo. A simple and sensitive radioenzymatic assay was developed to measure tissue SAM concentrations following removal of its demethylated metabolite, S-adenosylhomocysteine (SAH), whose presence precludes accurate SAM determinations. Three patterns of SAM control emerged. In the adrenal, pineal, striatum, and midbrain, SAM levels fell after hypophysectomy and were restored by dexamethasone administration. In the thalamus, hypothalamus, hippocampus, and cerebellum, SAM levels increased after hypophysectomy and were not altered further by dexamethasone administration. In the liver, cortex, septum, and pons-medulla, SAM levels were not affected by either hypophysectomy or dexamethasone administration. These results suggest that multiple controls regulate SAM levels in vivo. The control factors are both highly tissue and region specific. While glucocorticoids are an important regulatory factor of SAM in some peripheral and CNS tissues, they are not the sole regulatory factor. In CNS regions where hypophysectomy increases SAM levels but glucocorticoid administration does not reverse the effects, other hypothalamic hormones, pituitary hormones, or neural factors may be involved in SAM regulation. Likewise, in regions where neither hypophysectomy nor glucocorticoid administration affects SAM levels, hypothalamic or neural factors may be involved even though pituitary factors do not appear to be important.

Adrenal Glands↗
PubMed1993

Brain death-induced cardiac contractile dysfunction and long-term cardiac preservation. Rat heart studies of the effects of hypophysectomy.

BACKGROUND: Ischemic brain death induces cardiac contractile dysfunction, which may exclude the heart as a donor organ for transplantation; the mechanism is unknown. Since cerebral ischemia might alter pituitary function, we investigated the influence of hypophysectomy on basal contractile function, brain death-induced contractile malfunction, and the tolerance of the heart to hypothermic ischemic storage. METHODS AND RESULTS: Rats were hypophysectomized and maintained for 5 days; during this time, left ventricular developed pressure (LVDP) fell to 70% of its control value (92 +/- 8 versus 132 +/- 6 mm Hg, P < .05). Diastolic function of isolated blood-perfused hearts 5 days after hypophysectomy was severely impaired (left ventricular volume at 12 mm Hg of end-diastolic pressure was 141 +/- 20 versus 250 +/- 30 microL in sham-operated control rats; P < .05). Brain death in nonhypophysectomized rats resulted in a transient increase in mean arterial pressure (from 112 +/- 4 to 180 +/- 7 mm Hg within the first 30 seconds) followed by a rapid decline to less than 50% of the control value (54 +/- 3 mm Hg after 5 minutes, P < .05). Changes in cardiac function were comparable (cardiac index fell from 34 +/- 2 to 17 +/- 1 mL/min per 100 g body weight, and stroke volume index fell from 82 +/- 5 to 41 +/- 4 microL per beat per 100 g body weight within 10 minutes; P < .05). Brain death in hypophysectomized rats resulted in a similar (but attenuated) biphasic response with arterial pressure (already reduced to 82 +/- 9 mm Hg as a consequence of hypophysectomy) transiently increasing to 144 +/- 9 mm Hg after 30 seconds and then falling to 52 +/- 5 mm Hg by 5 minutes. Finally, we assessed the effects of coincident hypophysectomy and brain death on the ability of the heart to recover from 6 hours of hypothermic (4 degrees C) ischemic storage. Brain death alone had no effect on the postischemic recovery of LVDP (133 +/- 14 versus 129 +/- 12 mm Hg at 8 mm Hg of end-diastolic pressure in the non-brain death group). LVDP in hearts from hypophysectomized rats with brain death recovered to only 84 +/- 13 mm Hg; however, this was virtually identical to the LVDP in hearts from hypophysectomized rats that had not been subjected to brain death (83 +/- 5 mm Hg) or had not even been exposed to hypothermic ischemia (83 +/- 10 mm Hg). CONCLUSIONS: Hypophysectomy induces a deterioration of cardiac function that becomes apparent after 2 days. However, it does not exacerbate the cardiac dysfunction induced by brain death. Hearts from hypophysectomized animals, with or without brain death, recovered less well after prolonged hypothermic storage; nevertheless, the hearts recovered to preischemic levels, indicating that, although hypophysectomy impairs cardiac contractile function, it does not adversely influence the tolerance of the heart to hypothermic ischemia. Pituitary function may be an important factor in determining cardiac function without influencing resistance to ischemia or responses to brain injury.

Animals↗
PubMedDate not supplied

cAMP response of cultured Sertoli cells from immature and adult hamsters. Effect of hypophysectomy and cryptorchidism.

The ability of FSH to stimulate cAMP accumulation in Sertoli cells cultured from either hamsters or rats declines with the age of the animal. Hypophysectomy or bilateral cryptorchidism of immature rats prevents this normal age-related decline in Sertoli cell response to FSH. However, neither hypophysectomy nor cryptorchidism of adult rats can restore the Sertoli cell response to that of the immature animal. In contrast, the Sertoli cell response to FSH in the adult golden hamster, a photoperiodic animal, can be restored to that of an immature animal during short photoperiod-induced testicular regression. Thus, the purpose of these experiments was to determine if the Sertoli cell response to FSH would also be restored to that of an immature animal when testicular regression was induced by other means, namely, hypophysectomy or bilateral cryptorchidism. As in the rat, hypophysectomy or cryptorchidy of immature hamsters resulted in decreased testicular growth and a cAMP response to FSH in cultured Sertoli cells, which remained at the high level of an immature animal. However, in contrast to the rat, hypophysectomy or bilateral cryptorchidism of the adult hamster resulted in not only testicular regression, but also a restored ability of FSH to stimulate cAMP accumulation in Sertoli cells cultured from these animals. Indeed, the magnitude and specificity of the Sertoli cell cAMP response to agents was the same in Sertoli cells cultured from testes undergoing testicular regression induced by either short photoperiod (ie, natural means), hypophysectomy, or cryptorchidy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1979

A comparative trial of transsphenoidal hypophysectomy and estrogen suppression with aminoglutethimide in advanced breast cancer.

We compared two treatment regimens, transsphenoidal hypophysectomy and estrogen suppression with aminoglutethimide in women with metastatic breast carcinoma. Three of fourteen patients experienced partial objective tumor regression with a median duration of 4.6 months following hypophysectomy, whereas 10 of 21 women receiving aminoglutethimide responded (2 complete, 8 partial) with a median duration of 11.5 months. Side effects in the medical group were minimal while surgical complications included 2 cases of CSF rhinorrhea, one leading to meningitis and death. In patients receiving aminoglutethimide, urinary free cortisol and plasma dehydroepiandrosterone sulfate fell significantly as did plasma estrone and estradiol. In the hypophysectomy group, anterior-pituitary function testing postoperatively revealed adequate suppression of gonadotropin and prolactin secretion but incomplete inhibition of the ACTH-cortisol axis in 4 of 7 surgical patients studied. Five patients initially treated with hypophysectomy experienced a further reduction of plasma (and urinary) estrone and estradiol levels when given aminoglutethimide. We conclude that estrogen suppression therapy with aminoglutethimide is a feasible alternative to surgical hypophysectomy in providing endocrine suppression and palliation in advanced breast carcinoma.

Adult↗
PubMed1979

Transsphenoidal hypophysectomy in breast cancer: evidence for an individual role of pituitary and gonadal hormones in supporting tumor growth.

Transsphenoidal hypophysectomy was performed in 212 consecutive patients with metastatic breast cancer: 11 died within 30 days, two of surgical complications and nine of advanced metastatic disease. Two patients were unevaluable because of inadequate follow-up in one and simultaneous radiation treatment in the other. Of 199 evaluable patients 42% had an objective remission. Duration of remission averaged 18+ months with 10 out of 84 patients still in remission. Presence of estrogen receptors in the tumor significantly predicted response to hypophysectomy. Of 156 patients in whom completeness of hypophysectomy was assessed, 128 were thought to have a complete removal as shown by the fact that their growth hormone and prolactin were undetectable after stimulation with arginine or chlorpromazine, respectively. Of 26 patients in whom TRH test was performed, TSH and prolactin were undetectable in 20. Of 23 patients where autopsy was performed only six had microscopic pituitary tissue remaining. Hypophysectomy induced remission in eight of 15 patients who had previously responded and then relapsed to the antiestrogen Tamoxifen and in four of 17 who had failed. Conversely, antiestrogen therapy induced remission in six of 26 patients who had previously responded to hypophysectomy and in whom serum estrogens were present in small amount. These data indicate that both gonadal and pituitary hormones play a role in the growth of some human breast cancers.

Adult↗
PubMed1994

Effect of hypophysectomy on corticotropin-releasing hormone and adrenocorticotropin immunoreactivities in the rat adrenal gland.

It has previously been shown that rat adrenal zona medullaris possesses an interleukin-1 beta (IL-1 beta)-responsive peripheral branch of the CRH/ACTH system that duplicates the hypothalamopituitary central one (Mazzocchi et al., Mol. Cell. Neurosci. 4: 267, 1993). The intraadrenal content of corticotropin-releasing hormone (CRH) and adrenocorticotropin (ACTH) immunoreactivities (ir), as well as IL-1 beta-stimulated release of CRH-ir and ACTH-ir, increased in relation to the number of days elapsed from hypophysectomy; the effect of hypophysectomy required at least 48 h to become significant and reached its maximum after 72 h. The action of IL-1 beta on ACTH-ir release was annulled by simultaneous exposure to alpha-helical-CRH, an antagonist of CRH. ACTH infusion, at a rate restoring a normal blood level of the hormone, prevented the effect of hypophysectomy on intraadrenal concentrations of both CRH-ir and ACTH-ir; similarly, the hypophysectomy-evoked rise in intraadrenal ACTH-ir content was completely annulled by treating hypophysectomized rats with CRH or dexamethasone. Taken together our findings suggest that the elimination of the central branch of CRH/ACTH system induces a marked increase in the activity of the intraadrenal peripheral one. The hypothesis is advanced that the hypophysectomy-induced lowering of circulating ACTH and the consequent drop in the production of adrenal glucocorticoids enhances, via a classic negative feedback mechanism, gene expression of CRH and ACTH in adrenal medullary chromaffin cells.

Adrenal Medulla↗
PubMed1995

Effects of hypophysectomy on soleus muscle fibers and spinal motoneurons in rats.

The fiber type distribution of the soleus muscle in male and female rats was investigated 4 weeks after hypophysectomy. Oxidative enzyme activity of the soleus motoneurons in the spinal cord was also examined by enzyme histochemical assay. In male rats, the total number of fibers in the soleus muscle was not changed after hypophysectomy, but the percentage of intermediate (INT) fibers (with intermediate adenosine triphosphatase activity following alkaline preincubation, and high succinate dehydrogenase and alpha-glycerophosphate dehydrogenase activities) was increased. All types of fibers in the soleus muscle of hypophysectomized rats showed high adenosine triphosphatase activity following acid preincubation. Oxidative enzyme activity of the motoneurons innervating the soleus muscle was not changed after hypophysectomy. Similar results were obtained in female rats. It is suggested that the increased percentage of INT fibers in the rat soleus muscle after hypophysectomy is due to a lack or reduced levels of growth hormones, and that the metabolic capacities of the muscle fibers and of the innervating motoneurons are affected independently by hypophysectomy.

Animals↗
PubMed1983

Effects of hypophysectomy on acetylcholinesterase and butyrylcholinesterase in the rat.

Acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities were examined in several tissues of normal and hypophysectomized male and female rats. Significant sex differences in the mean AChE activities of normal rats were observed in the superior cervical ganglion (three times more activity in males) and in serum (50% more activity in females). Sex differences in the BuChE activity of serum and liver were even larger (ten times more activity in females), but the activity of other tissues was similar in both sexes. Hypophysectomy had little effect on the mean activity of AChE but did alter BuChE activity in certain tissues. Most of the effects of hypophysectomy on mean BuChE activity were opposite in direction in the two sexes. For example, in males hypophysectomy caused increases in the BuChE activity of serum (300%) and liver (43%), while in females it caused decreases in both tissues (25 and 30% respectively). In rats of a given group, the AChE activity of each tissue appeared to be regulated independently of the activity in other tissues. By contrast, BuChE activity showed statistically significant correlations in more than half of the tissue-pairs examined in control rats of either sex. These correlations can be considered to reflect a tendency toward body-wide regulation. In female rats, the cross-tissue correlations were largely eliminated by hypophysectomy. This finding indicates that the regulation of BuChE may be strongly affected by hormones under the control of the pituitary gland. However, in male rats, only the correlations involving atria were altered by hypophysectomy. Therefore, the effects of hormones on BuChE are probably both sex and tissue dependent.

Acetylcholinesterase↗
PubMed1976

Effects of hypophysectomy on alloxan-diabetic, arteriosclerotic, breeder vs. non-arteriosclerotic, virgin rats.

A single s.c. injection (10 mg/100 g bw of alloxan) was given to nonarteriosclerotic, virgin, Sprague--Dawley rats and to breeder rats with preexisting arteriosclerosis, hyperlipidemia and hyperglycemia. All of the animals promptly developed severe diabetes with ketosis, hyperglycemia, and hyperlipidemia. Insulin therapy was deliberately withheld. Mortality was high. Seven days later one group was subjected to hypophysectomy and 30 days later, all of the animals were autopsied. The diabetes + hypophysectomy animals maintained their body weight better, did not have hypertrophied adrenal glands, showed the least elevation of serum enzymes, e.g., CPK, SGOT, SGPT and LDH, less hyperlipidemia and hyperglycemia and reduced corticosterone production than the animals with untreated severe diabetes. Despite the relative amelioration of metabolic derangements prognostic of cardiovascular degenerative changes, the diabetes + hypophysectomy animals manifested extensive renovascular damage and the breeder rats with pre-existing arteriosclerosis showed definite exacerbation of their arterial disease in response to the severe alloxan diabetes regardless of hypophysectomy. It is suggested that although hypophysectomy may alleviate certain metabolic derangements attributed to growth hormone, ACTH and adrenal steroids, the angiopathic damage proceeds inexorably.

Adrenal Cortex Hormones↗
PubMed1978

Further characterization of the effects of hypophysectomy, FSH and estrogen on LH stimulation of testosterone production in Leydig cells isolated from immature rats.

Hypophysectomy of immature rats results after 5 days in a loss of LH responsiveness of Leydig cells. LH responsiveness can be partly maintained by treatment with FSH for 5 days. When estradiol benzoate was administered together with FSH to hypophysectomized rats the maintenance of LH responsiveness was not observed. The loss in LH responsiveness after hypophysectomy in terms of testosterone production could not be explained by either a change in the amount of Leydig cells present in the Leydig cell preparation or to a higher conversion of testosterone. The LH-stimulated cAMP production in cells from hypophysectomized rats was very low compared to cells from intact rats. There was no difference between cAMP production of Leydig cells from untreated, FSH-treated or FSH plus estradiol benzoate treated hypophysectomized rats. During the first 2 days after hypophysectomy LH responsiveness in both untreated and FSH-treated rats showed a comparable decrease. From day 2 after hypophysectomy LH responsiveness remained at a constant level in cells from rats treated with FSH, but declined further in cells from untreated rats. A single injection of estradiol benzoate to hypophysectomized rats treated with FSH counteracted the effect of FSH on LH responsiveness, but only when estradiol was administered at that time after hypophysectomy, when the effect of FSH on LH responsiveness was clear.

Animals↗
PubMed1983

Hypophysectomy-induced striatal hypersensitivity and mesolimbic hyposensitivity to apomorphine.

Seven days post-hypophysectomy female rats display a hyposensitivity to the locomotor effects of apomorphine and a hypersensitivity to the stereotypy effects of apomorphine, while at 28 days post-hypophysectomy they are hypersensitive to both the locomotor and stereotypy effects of apomorphine. The hyposensitivity to the locomotor effects, at 7 days post-hypophysectomy, was associated with a decrease in 3H-spiroperidol binding and an increase in tyrosine hydroxylase activity in the nucleus accumbens septi, whereas the hypersensitivity, at 28 days post-hypophysectomy, was associated with an increase in 3H-spiroperidol and a decrease in tyrosine hydroxylase activity in the n. accumbens septi. The increased apomorphine-induced stereotypy in both the 7 and 28 days post-hypophysectomized animals was related to an increased 3H-spiroperidol binding and a decreased tyrosine hydroxylase activity in the striatum. These behavioral and neurochemical data demonstrate that following hypophysectomy female rats will develop a transient decrease in dopamine receptor sensitivity in the n. accumbens septi, while the dopamine sensitivity in the striatum is increased. Thus the hypophysectomized female rat may prove to be a valuable model to study these two separate dopamine systems and their possible modulatory roles in the display of various behaviors.

Animals↗
PubMed2000

Role of glucose utilization in the restoration of hypophysectomy-induced hepatic cytochrome P450 2E1 by growth hormone in rats.

Growth hormone and insulin are the primary determinants for cytochrome P450 2E1 (CYP2E1) expression. The role of glucose on the induction of CYP2E1 by hypophysectomy and on the restorative effect by growth hormone was investigated in the rat liver. Western and Northern blot analyses revealed that hypophysectomy induced CYP2E1 by 5-fold at 1-4 weeks, relative to control, with a concomitant increase in CYP2E1 mRNA. Hypophysectomized rats (HXR) showed a 20% reduction in the plasma glucose level. Hypophysectomy-induced increase in the CYP2E1 mRNA was completely abolished by glucose feeding in drinking water (10%) for 7 days. Treatment of HXR with hGH (2 I.U./kg, twice a day, for 7 days) inhibited the increases in CYP2E1 protein and mRNA levels with restoration of the plasma glucose level. In contrast to the effect of human growth hormone (hGH) on CYP2E1 in HXR with free access to foods, CYP2E1 expression failed to be restored by hGH in starving HXR. However, glucose feeding of starving HXR abolished the induction of CYP2E1. Effects of hypophysectomy and hGH treatment were studied in streptozotocin-induced diabetic rats. Insulin, but not hGH, prevented an increase in CYP2E1 mRNA in diabetic rats. The hepatic CYP2E1 induction in hypophysectomized diabetic rats was inhibited by hGH treatment, indicating that the hGH effect on CYP2E1 expression did not involve insulin production. These results provide evidence that the induction of hepatic CYP2E1 by hypophysectomy may result from reduced glucose utilization, and that the effect of hGH on CYP2E1 expression may be mediated with enhanced glucose utilization, but not with insulin production.

Animals↗
PubMed1985

Inducibility of the hepatic microsomal monooxygenase system experimentally reduced to a minimum amount/activity. Effect of hypophysectomy, partial hepatectomy and phenobarbital/toluene treatment on the hepatic polysubstrate monooxygenase system in rats.

Sham-operated, hypophysectomized, partially hepatectomized and hypophysectomized + partially hepatectomized groups of CFY rats were treated with phenobarbital (40 mg/kg/day) per os or physiological saline once a day, or toluene-vapour (inhalation: 4,000 mg/m3, 8 h/day), for 3 days. The polysubstrate monooxygenase (PSMO) system of the liver was induced by phenobarbital after all kinds of surgical interventions. Inducibility of the enzyme system was the highest in the group with combined hypophysectomy + partial hepatectomy and decreased in order in the groups with partial hepatectomy, hypophysectomy and sham-operation. The relative cytochrome P-450 content (quantity of cytochrome P-450/100 g b.w.) was the lowest after combined operation, higher in partially hepatectomized and hypophysectomized animals and it was the highest in the sham-operated group. Hypophysectomy after partial hepatectomy seems to inhibit hepatic regeneration and to increase the inducibility of the enzyme by phenobarbital, at the same time. Phenobarbital treatment brought about SER proliferation in a part of liver cells, in each group. In case of repeated liver damage due to the consequences of hypophysectomy, partial hepatectomy, phenobarbital administration, a group of the liver cells responds to the first, another to the second, but even after the third injury a group of the liver cells maintained its regular structure. The hypothetical hepatotoxic effect of toluene, a widely used industrial solvent, has been tested. Hepatotoxicity has been excluded. The minimum non-specific hepatotoxic effect of the solvent was not augmented by either partial hepatectomy or hypophysectomy, or by the combination of the two. In all the experimental groups toluene increased the hepatic cytochrome P-450 level and induced a moderate increase in SER. Inducibility of the enzyme system after toluene inhalation was similar to that of the enzyme system after phenobarbital treatment in each group.

Animals↗
PubMed1991

Effects of hypophysectomy on pro-thyrotropin-releasing hormone concentrations in rats.

The effects of hypophysectomy on pro-thyrotropin-releasing hormone (pro-TRH) and TRH concentrations in the rat hypothalamus, cerebrum, cerebellum and brain stem, stomach and eye were studied. The hypophysectomy was performed via ear route and the rats were used for experiments at seven days after the operation. The hypophysectomized rats were administered T4 (500 micrograms/kg), T3 (100 micrograms/kg), TRH (1.0 mg/kg), or bovine TSH (1.25 IU/kg) was injected ip, and five rats in each subgroup were decapitated at four hours after the injection. Pro-TRH, TRH, TSH and thyroid hormone were measured by their radioimmunoassays. Immunoreactive pro-TRH (ir-pro-TRH) concentrations in the hypothalamus increased significantly after hypophysectomy, while its concentrations in the other tissues showed no changes. The immunoreactive TRH (ir-TRH) concentrations in the hypothalamus decreased significantly after hypophysectomy, but its concentrations did not change in the other tissues. In the hypophysectomized rats, ir-pro-TRH concentrations in the hypothalamus decreased significantly after T4 or T3 injection and tended to decrease after TRH or TSH injection. The ir-TRH concentrations in the hypothalamus increased significantly after T4, T3, TSH or TRH injection in the hypophysectomized rats. However, ir-pro-TRH and ir-TRH concentrations in the other tissues did not change after these hormone injections. The findings suggest that hypophysectomy stimulates TRH synthesis and release in the hypothalamus, and that pro-TRH synthesis in the tissues except the hypothalamus may not be regulated with thyroid hormone.

Animals↗