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Hypophysectomy depresses immune functions in rainbow trout.

As the immune system is known to be influenced by the endocrine system, the effects of hypophysectomy on immune functions were examined in the rainbow trout (Oncorhynchus mykiss). Superoxide anion (O2-) production, accompanied by phagocytosis, was significantly decreased in leucocytes isolated from the head kidney 7 days after hypophysectomy. Significant reduction was also observed in plasma immunoglobulin (Ig) M levels, whereas no change was observed in plasma lysozyme activity. The number of Ig-secreting leucocytes in peripheral blood had decreased after hypophysectomy, although total leucocyte number was not affected. The percentage of Ig-producing leucocytes as assessed by flow cytometry using a monoclonal antibody to trout IgM showed significant reduction in the head kidney. However, hypophysectomy did not affect the number of Ig-producing leucocytes in spleen, thymus or peripheral blood. By RT-PCR, expression of two growth hormones (GH I and II) and prolactin (PRL) mRNA was detected in lymphoid tissues, such as head kidney, spleen, thymus and intestine, as well as in leucocytes from blood and head kidney, indicating the local production of these hormones. These results indicate important roles of hypophyseal hormones produced not only in the pituitary, but also in the lymphoid tissues, in the maintenance of the immune functions in trout.

Analysis of Variance↗

The effect of hypophysectomy and subsequent replacement therapy with sheep prolactin or bovine growth hormone on the lactose synthetase activity of rabbit mammary gland.

1. The effects of hypophysectomy and replacement therapy with sheep prolactin and bovine growth hormone on the lactose synthetase activity of the mammary glands of lactating rabbits were studied. 2. There was an approximately fourfold decline in the lactose synthetase activity of homogenates calculated on a DNA basis within 6-7 days of hypophysectomy. Prolactin reversed this decline but growth hormone had no effect. 3. Changes in the properties of a particulate fraction isolated from the glands indicated that a decline in the effective concentration of alpha-lactalbumin was one factor contributing to the decreased lactose synthetase activity after hypophysectomy. 4. As the changes in lactose output produced by hypophysectomy and prolactin therapy are much greater than the changes in total lactose synthetase activity it is concluded that the activity of this enzyme is not the main factor controlling lactose output under these conditions.

Animals↗

Endocrinologically incomplete transethmoidal trans-sphenoidal hypophysectomy with relief of bone pain in breast cancer.

To assess endocrinologic completeness of transethmoidal trans-sphenoidal hypophysectomy and the relation between postoperative pituitary hormone levels and relief of bone pain, we tested pituitary reserve by measuring base-line values of follicle-stimulating hormone and luteinizing hormone, thyrotropin-relasing-factor-stimulated thyrotropin and prolactin, and levodopa-stimulated growth hormone after hypophysectomy in 15 menopausal women with metastatic breast cancer. In all 15 bone pain diminished or disappeared within 24 hours of operation. Pituitary-function testing identified only one patient as having had an endocrinologically complete hypophysectomy. Base-line gonadotropin levels and thyrotropin-releasing-factor-stimulated prolactin were the most reliable measures of residual pituitary function. We conclude that transethmoidal trans-sphenoidal hypophysectomy may not totally ablate pituitary endocrine function; effective relief of bone pain in patients with metastic breast cancer can follow this procedure despite residual pituitary function and the lack of objective tumor remission.

Bone Neoplasms↗

Hypophysectomy enhances interleukin-1beta, tumor necrosis factor-alpha, and interleukin-10 mRNA expression in the rat brain.

Although the effects of various cytokines as regulators of hormone synthesis and production are well documented, the role for pituitary hormones as modulators of cytokine synthesis is not fully understood. In this study, we investigated the effect of pituitary hormones' depletion on cytokine synthesis after short- (21 days) and long- (35 days) term hypophysectomy (ST-HX and LT-HX, respectively). The expresssion of the proinflammatory cytokine interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) and the anti-inflammatory cytokines IL-10 and transforming growth factor-beta (TGF-beta) in the rat brain was studied using in situ hybridization. Our results indicate that IL-1beta mRNA-expressing cells were significantly upregulated at day 21 in hypophysectomized rats compared to sham-operated controls. This enhanced expression was also detected later at day 35 post hypophysectomy. However, TNF-alpha mRNA expression was significantly increased only at the later sampling interval. IL-10 mRNA-expressing cells were increased after long-term hypophysectomy compared to controls. TGF-beta mRNA-expressing cells were not increased after hypophysectomy. In conclusion, these results suggest a role for pituitary hormones in IL-1beta, TNF-alpha, and IL-10 synthesis.

Analysis of Variance↗

Inhibition of metastatic behavior of murine osteosarcoma by hypophysectomy.

BACKGROUND: We recently reported that human osteogenic sarcoma cells are mitogenically responsive in tissue culture to insulin-like growth factor I (IGF-I), a mitogen important in the regulation of cellular proliferation of many tissues, including bone. PURPOSE: The present study was designed to determine whether these in vitro observations could be extended to an in vivo experimental system and whether reduction of IGF-I levels by hypophysectomy could inhibit the aggressive metastatic behavior of osteosarcoma. METHODS: We used standard competitive binding and affinity-labeling techniques to characterize the IGF-I-binding sites of MGH-OGS, a model of human osteosarcoma. Radioimmunoassay of serum, preprocessed to remove IGF-binding proteins, was used to quantitate IGF-I levels. In vitro proliferative response of MGH-OGS cells to IGF-I and other pituitary-dependent factors was determined by thymidine-incorporation experiments. In vivo growth of the neoplasm in 12 hypophysectomized C3H mice and in 14 control C3H mice was determined by serial measurements of implanted tumors and by gross and microscopic examination of the lungs for metastases. RESULTS: MGH-OGS exhibited specific binding sites for 1.39 pmol IGF-I per milligram MGH-OGS cellular membrane protein, a concentration similar to that which we previously reported for human osteosarcoma. In tissue culture, MGH-OGS exhibited mitogenic response to IGF-I (P less than .01) but not to other pituitary-dependent factors. Hypophysectomy reduced levels of circulating IGF-I to 15% of control, significantly inhibited local growth of MGH-OGS tumors (increased time for growth to 1 cm3 from 49 to 84 days, P less than .001), and profoundly inhibited metastatic behavior (decrease in mean number of metastases per host from 16 to less than one; P less than .001). CONCLUSIONS: This study is the first to document the profound inhibitory effect of hypophysectomy on the metastatic behavior of an experimental sarcoma. We conclude that the metastatic behavior exhibited by MGH-OGS osteosarcoma is dependent on pituitary factors, and we suggest that the inhibitory effects of hypophysectomy are related, at least in part, to the reduction of IGF-I levels.

Animals↗

Vasoconstrictor function of the rat isolated perfused mesenteric arterial bed seven days after hypophysectomy.

The effect of removal of the pituitary on mesenteric arterial function was examined in adult male rats that had undergone hypophysectomy 7 days earlier. Sham-operated rats and weight-matched rats served as controls. The body weight of hypophysectomized rats decreased from 220.75 +/- 0.48 g to 188.03 +/- 2.53 g (n = 7). Sham-operated controls gained weight, from 223 +/- 1.47 to 275.85 +/- 3.45 g (n = 8). Frequency-dependent vasoconstriction to electrical field stimulation (2-32 Hz, 90 V, 1 ms, 30 s) was significantly augmented after hypophysectomy. The maximal constrictor response of hypophysectomized preparations, 215.5 +/- 14.9 mm Hg (n = 6), was approximately twice that of the sham-operated controls, 100 +/- 6.1 mm Hg (n = 7) and weight-matched controls 109.8 +/- 5.8 mm Hg (n = 8). Norepinephrine (NE) (0.05-1,500 nmol) elicited dose-dependent vasoconstriction; the maximal response was significantly augmented after hypophysectomy, 221.71 +/- 15.9 (n = 7) as compared with 148.0 +/- 16.0 mm Hg (n = 8) in sham-operated controls and 146.3 +/- 8.7 mm Hg (n = 7) in weight-matched controls. Dose-dependent vasoconstrictor responses to ATP, 5-hydroxytryptamine, vasopressin, and endothelin were similar between the groups. High-performance liquid chromatography analysis showed no difference in NE content of the superior mesenteric artery from hypophysectomized and sham-operated controls. Hypophysectomy of rats caused an increase in sympathetic constrictor function of the mesenteric arterial vasculature that appeared to involve postjunctional adrenoceptors rather than prejunctional mechanisms and was not due to arrested growth or the smaller size of the mesenteric preparations.

Animals↗

Effects of hypophysectomy on purinergic and noradrenergic contractility of the rat vas deferens.

1. The effects of removal of the pituitary on vas deferens contractile function were examined in young adult male rats having undergone hypophysectomy 7 days previously. Sham-operated age-matched rats served as controls. Responses to electrical field stimulation (EFS), and exogenous noradrenaline (NA) and beta, gamma-methylene ATP (beta, gamma-meATP) were tested. 2. Hypophysectomized rats lost weight over the 7 days. Body weights were 267.2 +/- 3.9 g (n = 7) in controls and 195.3 +/- 1.56 g (n = 5) with hypophysectomy. The wet weight of the vas deferens from rats with hypophysectomy, 22.8 +/- 1.8 mg (n = 5) was approximately half that of the controls, 41.3 +/- 1.2 mg (n = 7). The contractile response to KCl was smaller in hypophysectomized preparations (0.97 +/- 0.9 g, n = 5) than in controls (2.91 +/- 0.2 g, n = 7). 3. The alpha 1-adrenoceptor antagonist prazosin (1 microM) was more effective as an inhibitor of the tonic than of the twitch component of the contractile response, indicating a dominant adrenergic component. However, alpha, beta-methylene ATP was also effective at inhibiting the tonic component, indicating that ATP is also released secondarily to NA. 4. Absolute contractions to EFS of vas deferens from hypophysectomized rats were smaller than those of the controls; however, when corrected for the difference in smooth muscle function (expressed as a percentage of the contraction to 120 mM KCl), the twitch response was significantly greater than in the controls at frequencies of up to 16 Hz, maximal responses being unaffected. In contrast, the tonic response was not significantly different between the two groups. 5. The sensitivity of contractions evoked by NA (1-300 microM) was less in vas deferens from hypophysectomized rats than in the controls. 6. Contractions of the vas deferens to beta, gamma-meATP (1-300 microM) were greater in hypophysectomized rats than in the controls. 7. In conclusion, the present results indicate that hypophysectomy of rats causes an increase in the twitch, but not the tonic component of the vas deferens contractile response to EFS. This appears to be due to an increase in the number or sensitivity of postjunctional P2X-purinoceptors, there being a reduction in sensitivity to NA.

Adenosine Triphosphate↗

Atrial natriuretic peptide (ANP): response to NaCl is attenuated in rat atria in vitro after hypophysectomy.

The present study documents the effects of hypophysectomy on the NaCl-stimulated release and on the basal secretion rates of ANP from rat atria in vitro. Three weeks before the experiments rats were subjected to hypophysectomy or to a corresponding sham operation. Atria were excised and superfused in an organ bath with a physiological buffer solution (PBS, 294 mosmol kg-1). After a control period of 5 min, superfusion was made with hyperosmotic NaCl (330 mosmol kg-1) for 10 min, and then again with PBS, but now for 15 min. Atria were paced with field stimulation (4 Hz, 20 V, 1 ms) and the resting tension was kept at 5 mN. The sham-operated animals responded with a significant increase (P less than 0.05) in the secretion rate of ANP (from 137 +/- 13 pg ml-1 [n = 35] to 235 +/- 24 [n = 34], means +/- SE) to the NaCl stimulus. The hypophysectomy blunted the ANP response to hyperosmotic NaCl. In addition, basal secretion rate was significantly (P less than 0.001) lower in the hypophysectomized than in the sham-operated animals during the whole experiment. Gel filtrations revealed that, during the hyperosmotic NaCl, both groups secreted exclusively ANP 1-28. We conclude that hypophysectomy blunts the basal as well as stimulus-induced in-vitro release of ANP from rat atria.

Animals↗

Adrenal cortex of fetal lamb: changes after hypophysectomy and effects of Synacthen on cytoarchitecture and secretory activity.

The effects of hypophysectomy on the cell population of the adrenal cortex has been examined with light and electron microscopy. The sensitivity of the adrenal cortical cells to exogenous ACTH in both normal and hypophysectomized fetuses has been investigated by comparing plasma cortisol concentrations with structural changes in the adrenal cortex. Hypophysectomy was carried out at about 100 d and the subsequent analysis was made at about 135 d on fetuses catheterized at least 6 d earlier. The zona fasciculata of intact fetuses contained about 25% mature and 75% immature cells at 130-136 d. After hypophysectomy this zone contained a uniform population of immature cells and no mature cells; there was a significant reduction in both adrenal weight and cortical thickness. The zona glomerulosa was unaffected by hypophysectomy. The infusion of Synacthen 0 . 25 mg/d I.V. for 48 h did not affect the zona glomerulosa but resulted in a 2-fold increase in the thickness of the zona fasciculata in hypophysectomized and intact fetuses. This cortical growth was due to both hypertrophy and hyperplasia. All the cells in the zona fasciculata were mature following Synacthen treatment in both groups. The most striking difference between the secretory response of the adrenal cortex to Synacthen in the two groups was found within 3-6 h of the onset of infusion. Within this period there was a significant increment in the plasma cortisol concentration in the intact fetuses while no response was observed in the hypophysectomized animals. After 12 h infusion by contrast, a steadily rising response was observed in both groups. There was a significant correlation between the final plasma cortisol concentration and both the adrenal weight and cortical thickness after 48 h treatment. The increased sensitivity of the adrenal cortex to exogenous ACTH as term approaches in the sheep is considered to be dependent upon the increasing proportion of mature zona fasciculata cells within the adrenal cortex.

Adrenal Cortex↗

Androgens in male rat reproductive tract fluids: hypophysectomy and steroid replacement.

The control of androgen concentrations in the intraluminal fluids of the male reproductive tract is not well understood. The present experiments were performed to determine the effects of hypophysectomy, hypophysectomy plus testosterone (T), and hypophysectomy plus pregnenolone treatment on intraluminal androgen concentrations in the adult rat testis and epididymis. T and 5 alpha-dihydrotestosterone (DHT) concentrations were determined in the vascular, interstitial, and intraluminal compartments of the epididymis. Testicular and epididymal morphology also were examined under light microscopy. Hypophysectomy of at least 5 days duration significantly reduced T and DHT concentrations in serum, tissues, and intraluminal fluids of the reproductive tract. T replacement for 14 days, which produced peripheral T concentrations of 5 ng/ml, did not support intraluminal androgen concentrations in the seminiferous tubules equivalent to controls; rete testis androgen concentrations were similar to controls, however. Pregnenolone administration at 2 mg X rat-1 X day-1 for 14 days did not maintain spermatogenesis nor intraluminal T concentrations in the seminiferous tubules equivalent to controls; however, a low level of spermatogenesis continued when intraluminal and tissue androgen concentrations were maintained at 10-20% of controls by either the testosterone and pregnenolone treatments.

Androgens↗

Hypoprolactinemia induced by hypophysectomy and long-term bromocriptine treatment decreases tuberoinfundibular dopaminergic neuronal activity and the responsiveness of these neurons to prolactin.

The effect of long-term decreases in circulating concentrations of prolactin was determined on the responsiveness of tuberoinfundibular dopamine (DA) neurons to this hormone. The activity of these neurons in ovariectomized rats was estimated by measuring the rate of DA synthesis (DOPA accumulation after the administration of a decarboxylase inhibitor) in the median eminence at various times after serum concentrations of prolactin had been reduced by hypophysectomy or the chronic administration of a DA agonist (bromocriptine, 3 mg/kg/day). The concentration of DA in the median eminence, but not in striatum, declined progressively up to 12 days after hypophysectomy, but did not change at any time during bromocriptine treatment. On the other hand, norepinephrine concentrations in the median eminence were increased 12 days after both treatments. Within 24 h after hypophysectomy or the first injection of bromocriptine the rate of DA synthesis in the median eminence was decreased; this decrease was maintained for at least 12 days suggesting that tuberoinfundibular DA neuronal activity is normally maintained by endogenous prolactin. Intracerebroventricular (ICV) injections of prolactin (10 micrograms, 12 h prior to sacrifice) increased the rate of DA synthesis in the median eminence of control, 24-hour hypophysectomized and 24-hour bromocriptine-treated rats. After longer periods (6-12 days) of bromocriptine treatment or after hypophysectomy the responsiveness of tuberoinfundibular DA neurons to prolactin was reduced. Dose-response studies revealed that the sensitivity and magnitude of response to ICV prolactin was markedly reduced in 12-day hypophysectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Response of the hypothalamic neurosecretory system of the female catfish, Heteropneustes fossilis (Bloch), to hypophysectomy.

The effect of hypophysectomy on the hypothalamic neurosecretory system of the catfish, H. fossilis, was studied. Hypophysectomy resulted initially in an accumulation of NSM at the distal ends of the cut axons. The axons had grown and were reorganized into a neurohypophysis-like structure 3 weeks after hypophysectomy, and this persisted even more than 3 years post-hypophysectomy.

Animals↗

The effect of hypophysectomy on experimental endothelial cell regrowth and intimal thickening in the rat.

We studied the influence of hypophysectomy on endothelial cell regrowth and intimal thickening following aortic endothelial removal. Modification of this influence by replacement doses of glucocorticoids, mineralocorticoids, thyroxin, and growth hormone also was investigated. Young adult male rats were used, and endothelial removal was achieved by the balloon catheter method. Percent endothelial regrowth and percent intimal thickening were quantified 1 or 2 weeks after injury (3 or 5 weeks after hypophysectomy). One week after injury, endothelial regrowth was 64% in hypophysectomized rats and only 54% in controls. At 2 weeks, values were 80% and 79% respectively. Intimal thickening (percent of wall thickness due to intima) at 1 week was 11% in hypophysectomized and 14% in control rats. At 2 weeks, values were 13% and 22%, respectively. All differences between hypophysectomized and control rats at 2 weeks were statistically significant. Neither endothelial regrowth nor intimal thickening in hypophysectomized rats was altered by hormone replacement. Comparison of areas in which endothelium had not regrown suggested that hypophysectomy had a direct effect on intimal smooth muscle cell proliferation. Thus, hypophysectomy suppresses intimal thickening and accelerates endothelial regrowth after wall injury. Neither effect depends on certain known hormones, and these effects are to some extent independent of one another. These findings are relevant to recent work on growth factors and atherogenesis.

Animals↗

Primate mammary development. Effects of hypophysectomy, prolactin inhibition, and growth hormone administration.

The pituitary gland has been found to be an important factor in mammary development in primates. Hypophysectomy in 12 sexually immature monkeys caused significant inhibition of estradiol (E2)-induced mammary growth and development. A histological index of mammary development in sexually immature hypophysectomized animals was lower (0.82) than in intact E2-treated controls (3.4; P less than 0.008). Hypophysectomy also inhibited growth of the mammary gland as judged by a size index. Despite the hypophysectomy, E2 stimulated some, albeit blunted, mammary growth and development, which may have been due to incomplete hypophysectomy. Selective inhibition of prolactin by ergot drugs in intact animals did not prevent full mammary development, suggesting that there may be pituitary mammogens other than prolactin, or that very low or unmeasurable concentrations of prolactin were sufficient to synergize with E2 to cause full acinar development. The mean histological index was 3.08 in E2-treated animals and 3.16 in animals treated with E2 plus pergolide. There was also no difference in the size of the glands. We evaluated the effect of growth hormone on mammary development by treating three hypophysectomized animals with pure 22,000 mol wt human growth hormone (hGH) (Genentech, Inc., South San Francisco, CA). We found that physiological or slightly supraphysiological concentrations of hGH in animals with unmeasurable prolactin were incapable of restoring the capacity of E2 to induce full mammary growth. These findings suggest that, if growth hormone is a mammary mitogen, that physiological concentrations are insufficient to synergize with E2 to induce full mammary growth or that other forms of hGH are mammogenic. Our studies suggest that the role of the pituitary gland in mammary mitogenesis in primates is more complicated than previously thought. They also raise the possibility that heretofore unidentified pituitary substances may be mammogenic.

Animals↗

Differential effect of hypophysectomy on the synthesis of beta-glucuronidase and other androgen-inducible enzymes in mouse kidney.

The levels of several androgen responsive enzymes including beta-glucuronidase, alcohol dehydrogenase, D-amino acid oxidase and arginase, were compared in kidneys of normal and hypophysectomized female mice after treatment with testosterone. While hypophysectomy did not alter the basal level of glucuronidase, the androgen-mediated accumulation of kidney beta-glucuronidase was greatly decreased in hypophysectomized mice. Measurements of the rate of synthesis of glucuronidase showed that after androgen treatment the enzyme was synthesized in kidney of hypophysectomized mice at only 5% the normal rate. Glucuronidase activity in seven other organs was not appreciably affected by treatment with androgens or by hypophysectomy. Unlike the effect of hypophysectomy on kidney glucuronidase, there was no reduction in the accumulation of alcohol dehydrogenase or D-amino acid oxidase in kidney of hypophysectomized mice after androgen treatment. Hypophysectomy caused a large reduction in kidney arginase activity. However, subsequent administration of testosterone restored much of this activity. It is concluded that there are at least two mechanisms by which androgens increase enzyme activity in kidney. The normal increase in activity or rate of synthesis of beta-glucuronidase following androgen administration requires pituitary hormones and/or products of these hormones, while the increase in activity of enzymes like alcohol dehydrogenase and D-amino acid oxidase does not require pituitary hormones.

Adrenalectomy↗

Hypophysectomy and growth hormone receptors in liver membranes of male rats.

The effects of hypophysectomy on GH binding were studied in liver membranes of male rats. Ten days after surgery, the specific binding of [125I]iodobovine GH and of [125I] iodohuman GH was 2- to 3-fold higher in microsomal membranes of hypophysectomized rats than in membranes of control male animals. The number of receptors rather than the affinity of the binding was affected. A nonspecific membrane effect due to hypophysectomy is unlikely since membrane markers such as 5' nucleotidase, galactosyl transferase, and insulin binding were not different in liver membranes of hypophysectomized and control rats. The somatogenic specificity and the subcellular distribution of the binding sites were not altered by hypophysectomy; the number of the GH binding sites were increased in plasma membranes as well as in Golgi fractions. Hypophysectomy in male rats creates a situation where growth failure, absence of circulating GH, and lack of plasma somatomedin activity are associated with increased concentration of liver somatogenic receptors. The latter finding could explain why livers of hypophysectomized rats are more sensitive to GH than those of normal rats.

5'-Nucleotidase↗

Effect of hypophysectomy and 1,25-dihydroxyvitamin D on duodenal calcium absorption.

Intestinal active and passive transport of calcium were studied in hypophysectomized (HX) and intact rats using the in vivo duodenal loop technique. In the vitamin D-supplemented condition, hypophysectomy resulted in a decrease in serum 1,25-dihydroxyvitamin D [1,25-(OH)2D]. Hypophysectomy prevented a gain in body weight and decreased intestinal mucosal weight and total calcium absorption. When the data were expressed per unit mucosal wet weight, duodenal active calcium transport was not different in the HX and intact groups, but passive transport was persistently decreased by hypophysectomy. Administration of bovine GH to the HX rats did not change the mucosal mass, but enhanced both active and passive duodenal transport to calcium. Vitamin D depletion for 6 weeks decreased serum 25-hydroxy-vitamin D and 1,25-(OH)2D levels in both intact and HX rats to about the same level. After bovine GH and 1,25-(OH)2D3 replacement, the calcium absorption studies suggest that 1) 1,25-(OH)2D3 enhances intestinal calcium passive transport as well as active transport in intact and HX rats; 2) GH enhances both active and passive transport of calcium in the presence of sufficient quantities of 1,25-(OH)2D; 3) this latter effect is independent of the metabolism of vitamin D; and 4) a decrease in mucosal mass is one of the factors that results in decreased calcium absorption after hypophysectomy.

Animals↗

Effects of hypophysectomy and cell isolation on the transport of L-arabinose by adipocytes.

Hypophysectomy decreased the basal rate of glucose metabolism in segments of epididymal fat studied in vitro and lowered their maximum capacity to use glucose. However, hypophysectomy changed neither the sensitivity to insulin nor the magnitude of the response when the results were expressed relative to the basal rate of glucose metabolism. Adipocytes isolated from both hypophysectomized and normal rats exhibited a higher basal rate of glucose metabolism than cells remaining in situ in the contralateral tissues, but this consequence of cell isolation was more pronounced for adipocytes of hypophysectomized than normal rats. Glucose metabolism could not be further increased by exposure of the adipocytes of hypophysectomized rats to insulin, whereas insulin produced a 3-to 5-fold stimulation of glucose oxidation in normal adipocytes. The effects of insulin and hypophysectomy on the transport of the nonmetabolizable sugar L-[1-14C]arabinose in tissue segments and isolated adipocytes were also studied. Uptake of L-arabinose was usually more rapid in segments of epididymal fat of normal rats than in segments of tissue obtained from hypophysectomized rats and was significantly accelerated by insulin in both groups. Uptake of L-arabinose was more rapid than normal in adipocytes isolated from hypophysectomized rats and, like glucose metabolism, could not be accelerated by insulin. The same concentration of insulin markedly promoted arabinose uptake in normal adipocytes. Efflux of L-arabinose from segments of tissue from hypophysectomized rats was twice as rapid as that from normal tissue and, in contrast with the rate of efflux from normal tissues, was not accelerated by insulin. The data suggest that in the absence of pituitary secretion, sugar transport in the adipocyte membrane may be asymmetrical. The data also support the view that hypophysectomy renders adipocytes more susceptible than normal to the cell isolation procedure which maximally accelerates glucose utilization and inward transport of arabinose in these cells.

Adipose Tissue↗