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Biomedical subjects

H Watanobe

Publications and source records attributed to H Watanobe.

At least 37 records · Page 2Linked to original sources
PubMed2000

Downregulation of melanocortin receptors in brain areas involved in food intake and reward mechanisms in obese (OLETF) rats.

The melanocortin (MC)4 receptor is important for food intake and weight homeostasis as it mediates the orexigenic and anorexigenic effects of the MCs. OLETF (Otsuka-Long-Evans-Tokushima-Fatty) rats are a selective inbred strain of polygenic variant rats which overeat and develop obesity with elevated leptin levels. We investigated by autoradiography if the expression of MC receptors were altered in ovariectomized estradiol-replaced female OLETF rats compared to their controls (Long-Evans-Tokushima-Otsuka (LETO) rats). We found that OLETF rats show a reduction in total [125I]NDP-MSH MC receptor binding in the ventromedial hypothalamic nucleus, perhaps reflecting an increased release of MC peptides in this region. The levels of MC receptors in the arcuate nucleus and the paraventricular hypothalamic nucleus were not changed. Interestingly, the OLETF rats also showed reduced MC-receptor binding in areas such as the nucleus accumbens shell, and the ventral tegmental area, both of which are believed to be involved in reward systems. Similarities in the changes of MC receptor expression in obese animals and in animals treated with opiates may suggest a neurobiological link between food intake mediated through the MC receptors and reward.

Animals↗
PubMed1999

Evidence that physiological levels of circulating leptin exert a stimulatory effect on luteinizing hormone and prolactin surges in rats.

Increasing evidence suggests that leptin, an adipocyte-derived hormone, may positively regulate the reproductive axis, and serve as a critical metabolic signal linking nutrition and the reproductive function. However, along this line there remains an as-of-yet unresolved important issue whether physiological levels of circulating leptin exert a stimulatory effect on the reproductive axis. It is also unknown whether hyperleptinemia affects the reproductive function. In this study, we attempted to examine these unexplored issues, employing as an indicator the estradiol/progesterone-induced luteinizing hormone (LH) and prolactin (PRL) surges in ovariectomized female rats. Experiments were performed on normally fed, 3-day starved, 3-day starved + murine leptin (100 microg/kg/day), and normally fed + murine leptin (300 microg/kg/day) groups. Leptin was administered utilizing osmotic minipumps during 3 days immediately before experimentation. From 11:00 to 18:00 h, blood was collected every 30 min to measure LH and PRL. The 3-day starvation completely abolished both LH and PRL surges, but 3-day starved + leptin (100 microg/kg/day) group, whose plasma leptin levels (3.7 +/- 0.4 ng/ml) were similar to those in normally fed group (3.4 +/- 0.5 ng/ml), showed a significant recovery of the hormonal surges. On the other hand, the magnitudes of LH and PRL surges in normally fed + leptin (300 microg/kg/day) group, whose leptin levels were 10.8 +/- 1.5 ng/ml, were statistically the same as those in normally fed group. These results indicate for the first time that physiological concentrations of circulating leptin exert a stimulatory effect on the steroid-induced LH and PRL surges in the rat. It was also suggested that mild hyperleptinemia of 3 days' duration may not significantly affect the hormonal surges.

Animals↗
PubMed1999

A detailed study on the role of sex steroid milieu in determining plasma leptin concentrations in adult male and female rats.

We examined the effects of sex steroid milieu on plasma leptin levels in adult male and female rats. Since the body weight is known to influence leptin concentrations, the hormone was measured in rats with a very similar body weight (about 250 g) throughout this study. Plasma leptin levels were significantly higher in female than in male rats. Orchidectomy (ODX) caused a significant rise in leptin, and replacement of a physiological dose of testosterone (T) completely abolished the effect of ODX. Since the effect of tamoxifen (estrogen antagonist) coadministered with T on leptin levels in ODX rats was the same as that of T alone, it was suggested that the suppressive effect of T on leptin may be mediated by the androgenic potency of T, but not by its aromatized product, estradiol. In female rats, plasma leptin concentrations did not change significantly during the estrous cycle. Furthermore, leptin levels were not affected either by ovariectomy alone or by the administration after ovariectomy of physiological doses of estradiol, progesterone, or both. This is the first study to demonstrate in rats with a very similar body weight the existence of a clear sexual difference in plasma leptin levels, and also a suppressive action of T on the adipocyte hormone concentrations.

Animals↗
PubMed1999

The melanocortin 4 receptor mediates leptin stimulation of luteinizing hormone and prolactin surges in steroid-primed ovariectomized rats.

We have previously reported that leptin, the product of the obese (ob) gene, may play a physiologically relevant role in the generation of estradiol/progesterone-induced luteinizing hormone (LH) and prolactin (PRL) surges in female rats. In the present study, we examined whether the stimulatory effect of leptin on the hormonal surges is mediated through the melanocortin (MC) 4 receptor in the brain, as is leptin's effect on feeding behavior. We also explored whether the MC4 receptor participates in tonic stimulation of steroid-induced LH and PRL surges. Experiments were performed on both normally fed and 3-day starved rats, which were ovariectomized and primed with estradiol and progesterone. At 11:00 h on the day of the experiments, the normally fed rats received an intracerebroventricular administration of artificial cerebrospinal fluid (vehicle), SHU 9119 (a nonselective MC3/MC4 receptor antagonist, 1.0 nmol), or HS014 (a selective MC4 receptor antagonist, 1.0 nmol). The 3-day starved rats were given vehicle, recombinant mouse leptin (0.3 nmol), leptin (0.3 nmol) + SHU9119 (1.0 nmol), or leptin (0.3 nmol) + HS014 (1.0 nmol). From 11:00 to 18:00 h, blood was collected every 30 min to measure LH and PRL. The 3-day starvation completely abolished both LH and PRL surges, but leptin significantly reinstated these hormonal surges. Both SHU9119 and HS014 significantly decreased the magnitude of LH and PRL surges in normally fed rats and also significantly blocked the leptin stimulation of the hormonal surges in starved rats. These results suggest that the MC4 receptor may be the pivotal subtype of MC receptors mediating the leptin stimulation of LH and PRL surges. The data also suggest that endogenous MC(s) may tonically stimulate the hormonal surges in normally fed rats via the MC4 receptor. This is the first report describing a physiological role of a specific MC receptor in regulating the reproductive axis.

Animals↗
PubMed1999

A significant role of leptin in the generation of steroid-induced luteinizing hormone and prolactin surges in female rats.

Recent evidence suggests that leptin, the product of obese (ob) gene, may play an important role in the regulation of reproductive function. However, a possible role of leptin in the preovulatory surges of luteinizing hormone (LH) and prolactin (PRL) in rodents has yet to be explored, and thus examined in this study. Experiments were performed on both normally fed and 3-day starved rats, which were ovariectomized and primed with estradiol and progesterone. At 11:00 h on the day of the experiments, normally fed rats received an intracerebroventricular injection of artificial cerebrospinal fluid, anti-leptin serum, or normal rabbit serum. Three-day starved rats were given artificial cerebrospinal fluid or recombinant human leptin (2.5 microgram) via the same route. From 11:00 to 18:00 h, blood was collected every 30 min to measure LH and PRL. The 3-day starvation completely abolished both LH and PRL surges, but leptin resumed these hormonal surges to the levels of normally fed rats. In addition, anti-leptin serum given to normally fed rats significantly depressed LH surge and delayed the onset of PRL surge. This study is the first to demonstrate that leptin plays a physiologically important role in the generation of steroid-induced LH and PRL surges in female rats.

Animals↗
PubMed1999

A comparative study of the effects of nitric oxide and carbon monoxide on the in vivo release of gonadotropin-releasing hormone and neuropeptide Y from rat hypothalamus during the estradiol-induced luteinizing hormone surge: estimation by push-pull perfusion.

Recent evidence suggests that nitric oxide (NO), a free radical gas, plays an important role in regulating the function of a variety of neuroendocrine systems. With respect to the hypothalamo-pituitary-gonadal axis, a stimulatory effect of NO on the release of gonadotropin-releasing hormone (GnRH) from rat hypothalamus has been demonstrated in vitro. However, no previous study has reported NO-stimulated secretion of GnRH from in vivo hypothalamus, and also the precise cellular site of action of NO within the GnRH neuronal system remains to be elucidated. In the present study, utilizing the push-pull perfusion technique of rat hypothalamus, we examined the effect of L-arginine (L-Arg), an NO donor, on the release of GnRH, neuropeptide Y and cyclic GMP (c-GMP), which is a pivotal second messenger molecule of the NO system. For comparison, we also examined the effect of carbon monoxide (CO), another putative gaseous neurotransmitter, using hematin, a CO donor. During the period of 11.00-18.00 h, we collected blood and hypothalamic perfusates from ovariectomized adult rats that had been implanted with an estradiol capsule 2 days before. During the entire period of observation, L-Arg (1.0 or 10 mM), hematin (10 or 100 microM) or artificial cerebrospinal fluid alone (as the control) was infused into the medial preoptic area (MPOA) where there are cell bodies of GnRH neurons, or the median eminence-arcuate nucleus complex (ME-ARC) where axon terminals of GnRH neurons are localized. Although 10 mM of L-Arg significantly stimulated GnRH and c-GMP, but not neuropeptide Y, levels in both the MPOA and ME-ARC, GnRH and c-GMP in the ME-ARC were already increased by 1.0 mM of L-Arg. By contrast, both concentrations of hematin were without effect at either site of the hypothalamus. This study is the first to demonstrate that NO is capable of stimulating GnRH release from rat hypothalamus in vivo. Our data also suggests that both cell bodies and axon terminals of GnRH neurons may be sites of action of NO. Our data do not support a previous study by other investigators that reported a stimulatory effect of CO on the GnRH release.

Animals↗
PubMed1999

A case of acromegaly accompanied by adrenal preclinical Cushing's syndrome.

We encountered a 58-year-old woman with acromegaly accompanied by a cortisol-secreting adrenal tumor without clinical features of hypercortisolism. The simultaneous occurrence of these two endocrinopathies in one individual is extremely rare. She was diagnosed as having diabetes mellitus 8 years ago. Afterwards, in spite of insulin therapy, her hyperglycemia could not be well controlled. Her acromegaly and preclinical Cushing's syndrome were histopathologically proven to be due to a pituitary adenoma and an adrenocortical adenoma, respectively. Successful treatment for these endocrinopathies resulted in greatly improved blood sugar control because of a reduction in insulin resistance. In this case of preclinical Cushing's syndrome, replacement therapy with glucocorticoid was able to be discontinued at only 8 weeks after adrenalectomy, so that the period of necessary replacement was much shorter than that for overt Cushing's syndrome. This is the first report describing insulin resistance before and after treatment in a case of acromegaly accompanied by adrenal preclinical Cushing's syndrome.

Acromegaly↗
PubMed1999

A case of amyloid goiter secondary to Crohn's disease.

We herewith report a case of amyloid goiter secondary to Crohn's disease. The patient had been diagnosed as having Crohn's disease at the age of 15, and underwent right hemicolectomy at age 20. When he was 26 years old he complained of swelling of the anterior neck. Both TSH and thyroid hormones were within the normal range, and anti-thyroglobulin and anti-microsomal antibodies were negative. Only thyroglobulin was noticeably above the normal range. During the next year his goiter enlarged further and because he had a feeling of pressure he underwent total thyroidectomy. The presence of amyloid A protein in his surgical specimen led to the diagnosis of amyloid goiter. Although most cases of secondary amyloidosis are known to develop in neoplasms or chronic inflammatory diseases, our patient had no illness other than Crohn's disease. Perusal of literature revealed that Crohn's disease is rarely a cause of amyloid goiter.

Adult↗
PubMed1999

Temporal profiles of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in the plasma and hypothalamic paraventricular nucleus after intravenous or intraperitoneal administration of lipopolysaccharide in the rat: estimation by push-pull perfusion.

Lipopolysaccharide (LPS) is known to stimulate the synthesis and secretion of various proinflammatory cytokines in both the peripheral immune cells and the brain. Yet, the relative contribution of peripheral and central cytokines to the LPS-induced activation of the hypothalamo-pituitary-adrenal axis is still poorly understood. In this study, utilizing the push-pull perfusion technique of the rat brain, we attempted to characterize in detail the temporal profiles of interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha after intravenous (i.v.) or intraperitoneal (i.p.) administration of LPS in both the general circulation and the hypothalamic paraventricular nucleus (PVN), which is the primary source of corticotropin releasing hormone (CRH). Temporal changes in plasma adrenocorticotropic hormone (ACTH) and CRH levels in the PVN were also monitored. We collected blood and perfusates every 30 min from 11:00 to 17:00 h. At 12:00 h, 1.0 or 2.5 mg/kg body weight of LPS was given via an i.v. or i.p. route, respectively. Peak ACTH response occurred 30 min after i.v. LPS and 1.5 h after ip LPS. Of the three cytokines measured in the plasma, TNF-alpha showed the fastest rise in synchrony with peak ACTH secretion after both i.v. and i.p. LPS. Although plasma IL-6 also showed a robust rise, its peak level occurred later than the ACTH peak. Elevation of plasma IL-1beta was the smallest among the three cytokines. CRH levels in the PVN reached their peaks 1 and 2.5 h after the ACTH peak following i.p. and i.v. LPS, respectively. Irrespective of the route of LPS administration, IL-6 and TNF-alpha levels in the PVN showed significant rises 1-2 h after the ACTH peak, but IL-1beta in the PVN did not significantly change during the entire period of observation. The results of the present study suggest that circulating TNF-alpha may play the most important role in triggering the early, peak phase of ACTH secretion after both i.v. and i.p. LPS. Although it is possible that brain TNF-alpha, IL-6, and circulating IL-6, may be involved in the later, protracted phase of ACTH secretion induced by LPS, IL-1beta in both the brain and peripheral circulation seems to play the smallest role in ACTH secretion. This is the first study to characterize the LPS-induced temporal changes in IL-1beta, IL-6, and TNF-alpha in both plasma and PVN simultaneously in conscious, freely moving rats.

Adrenocorticotropic Hormone↗
PubMed1998

Serotonin stimulates corticotropin-releasing factor gene expression in the hypothalamic paraventricular nucleus of conscious rats.

To examine the direct effects of serotonin (5-HT) on the release and synthesis of corticotropin-releasing factor (CRF) in the hypothalamic paraventricular nucleus (PVN), 5-HT was microinjected just onto the bilateral PVN of conscious rats. Plasma adrenocorticotropic hormone (ACTH) levels peaked at 30 min and returned to the basal levels in 90 min. Northern blot analysis revealed that the CRF messenger RNA (mRNA) level in the PVN as well as the proopiomelanocortin mRNA level in the anterior pituitary significantly increased 120 min after the 5-HT injections (50-250 nmol/side). Pretreatment with intracerebroventricular (i.c.v.) injection of pindobind 5-HT1A (5 nmol) or LY-278584 (500 nmol) completely abolished the 5-HT-induced ACTH response, whereas LY-53857 (100 nmol) was without effect. These results suggest that 5-HT stimulates CRF release, which has interactions with 5-HT1A and 5-HT3 receptors on CRF neurons in the PVN, and activates CRF synthesis in conscious rats.

Adrenocorticotropic Hormone↗
PubMed1998

Evidence that a fast, rate-sensitive negative feedback effect of corticosterone is not a principal mechanism underlying the indomethacin inhibition of interleukin-1 beta-induced adrenocorticotropin secretion in the rat.

A number of previous studies have concluded that prostaglandins (PGs) play a crucial role in mediating the corticotropin-releasing hormone and adrenocorticotropin (ACTH) secretion induced by interleukin (IL) 1 beta in the rat. This is mainly based on a significant inhibitory effect of indomethacin, a cyclooxygenase inhibitor, on the hormonal response. However, there is one previous study which reported that such an inhibitory action of indomethacin on ACTH secretion is mediated principally by a fast, rate-sensitive negative feedback effect of corticosterone which increases after indomethacin injection, rather than by a decrease in PG production. In order to have a better understanding of this unresolved issue, in the present study the authors compared the effects of two different time intervals (10 or 20 min) between the intravenous injections of indomethacin (10 mg/kg body weight) and of recombinant human IL-1 beta (3 micrograms/kg body weight) on the cytokine-induced ACTH secretion in male rats. Although IL-1 beta-induced ACTH response was significantly suppressed by indomethacin given either 10 or 20 min before, the latter protocol led to a significantly greater inhibition of the hormonal response than the former. However, between the two groups, the rising slope of corticosterone from -20 or -10 min to time zero and that from time zero to 10 min after IL-1 beta injection were statistically indistinguishable. There results strongly suggest that the fast, rate-sensitive negative feedback effect of corticosterone may not be a principal mechanism whereby indomethacin inhibits IL-1 beta-induced ACTH secretion in the rat. It was concluded that such an action of indomethacin is primarily mediated by its inherent pharmacological action, i.e. the inhibition of endogenous PG production.

Adrenocorticotropic Hormone↗
PubMed1998

Different roles of brain interleukin 1 in the adrenocorticotropin response to central versus peripheral administration of lipopolysaccharide in the rat.

Although it is well established that peripheral administration of endotoxin activates the hypothalamic-pituitary-adrenal (HPA) axis, information is very limited regarding whether central administration of endotoxin can similarly stimulate the endocrine axis. Moreover, it is also unknown whether a difference exists in the mode of involvement of brain-derived cytokines in determining the HPA response to peripheral vs central administration of endotoxin. In the present study, the authors attempted to gain more knowledge on these issues focusing on interleukin (IL) 1 in the brain, one of key pro-inflammatory cytokines mediating the immuno-endocrine network. In male rats, both intravenous (i.v., 100 micrograms/kg body weight) and intracerebroventricular [i.c.v. (the 3rd ventricle), 10 micrograms] injections of Escherichia coli lipopolysaccharide (LPS) caused a significant elevation of adrenocorticotropin (ACTH) levels in plasma, even though peaked ACTH responses occurred earlier after the i.v. (60 min post-injection) than the i.c.v. (120 min post-injection) LPS. Although the ACTH response to i.c.v. LPS was significantly suppressed by a prior (5 min) i.c.v. administration of IL-1 receptor antagonist (IL-1Ra, 1 microgram), the hormonal response to i.v. LPS was not. That this dose of IL-1Ra was not biologically a small dose was indicated by another experiment that the same dose of i.c.v. IL-1Ra was able to significantly suppress the ACTH response to an i.c.v. injection of recombinant human IL-1 beta (50 ng). These results suggest that i.c.v. LPS, as i.v. LPS, can stimulate ACTH secretion in the rat, and this hormonal response may, at least in part, be mediated by brain-derived IL-1. Although there is one previous study reporting an important role of central IL-1 in mediating the HPA response to systemic LPS treatment, our present data suggest that such a mechanism may not operate before and during an early, peak phase of ACTH secretion after i.v. LPS.

Adrenocorticotropic Hormone↗
PubMed1998

Measurement of cytokines in the cavernous sinus plasma from patients with Cushing's disease.

In order to know more about the in vivo secretion of various cytokines from the human pituitary, this study measured the concentrations of interleukin (IL)-1alpha, IL-1beta, IL-2, IL-6, tumor necrosis factor-alpha and IL-1 receptor antagonist (ra) in both the peripheral blood and the cavernous sinus (CS) plasma from six patients with Cushing's disease before and after an intravenous bolus injection of human corticotropin-releasing hormone (CRH, 100 microg). As a routine procedure for the diagnosis of Cushing's disease, adrenocorticotropin (ACTH) levels were also determined in the same samples. In four of the six patients, unstimulated levels of IL-1ra in the CS ipsilateral to the ACTH-secreting adenoma were higher than those in the peripheral blood, with a ratio of > or = 1.5:1, even though CRH was without effect on the cytokine's concentration in the CS. In contrast, no consistent data were obtained for any of the remaining five cytokines. These results demonstrate for the first time that the in vivo release of IL-1ra is detectable in at least some corticotroph adenomas, and also suggest a possible role of the cytokine in physiological and pathophysiological processes occurring in the human pituitary.

Adolescent↗
PubMed1998

A hypopituitary patient who attained tall stature without growth hormone.

We describe an unusual patient with hypopituitarism who attained tall stature even without growth hormone (GH). A 37-year-old man was devoid of secondary sexual characteristics, but manifested tall stature with a eunuchoidal feature. Serum levels of GH, insulin-like growth factor-I, gonadotropins and testosterone were all below normal. GH secretion was not enhanced by any provocative stimulus. Adrenocorticotropic hormone increased after administration of corticotropin releasing hormone, but not after insulin-induced hypoglycemia. Thyrotropin increased in response to thyrotropin releasing hormone, but both free T3 and T4 did not rise. Magnetic resonance imaging disclosed a transected pituitary stalk. The present patient had hypopituitarism due to perinatal problems but had grown with the aid of non-GH growth-promoting factors, which suggests that man may be able to achieve statural growth even without GH.

Adult↗
PubMed1997

Pituitary apoplexy developed in a patient with androgen insensitivity syndrome.

At the age of 18, our patient was diagnosed as complete androgen insensitivity syndrome(AIS) based on androgen receptor studies in cultured genital skin fibroblasts. Compatible with this diagnosis, both testosterone and LH levels in her plasma were elevated as compared to levels in normal females. Later, the patient had been uneventful until she sought medical attention for headache at the age of 38. Magnetic resonance imaging (MRI) of the brain pointed to pituitary apoplexy. Since her symptoms were not alleviated by conservative therapy, neurosurgical decompression via a transsphenoidal approach was performed. A histopathological examination of a surgical specimen revealed that the pituitary hemorrhage occurred in an LH-producing adenoma. It is likely that the adenoma developed from gonadotroph hyperplasia which could exist in the AIS pituitary. It may be worth noting that this patient has never had a chance of receiving hormonal replacement therapy with estrogen and progesterone. Considering the fact that the majority of AIS patients are treated with gonadal steroids and such a treatment reestablishes an appropriate negative feedback on enhanced LH secretion, it is possible that the lack of hormonal therapy in our patient may have served as a precipitating factor for the apoplectic episode. Although we are not aware of any documented case report of pituitary apoplexy developed in AIS, such a pituitary emergency should be born in mind in the long-term follow-up of patients with AIS. In addition, it is also suggested that the hormonal replacement therapy with gonadal steroids may be recommended for AIS patients not only to endow them with physical characteristics as a woman but also to prevent the development of gonadotroph hyperplasia and possibly also of LH-producing adenoma in the pituitary.

Adenoma↗
PubMed1997

Painless thyroiditis developed in a patient with Sheehan's syndrome.

We experienced an unusual combination of painless thyroiditis and Sheehan's syndrome in a single patient. A 29-year-old postpartum woman was referred to us for suspected Sheehan's syndrome. Endocrine tests confirmed the diagnosis, but, unexpectedly, her thyroid hormone levels in the plasma were elevated. Based on the data from various examinations on her thyroid including an extremely low uptake of radioactive iodine and spontaneous alterations of the thyroid function without any therapy for the thyroid, we diagnosed the patient as suffering from Sheehan's syndrome and painless thyroiditis simultaneously. Underlying mechanism(s) whereby painless thyroiditis occurred in our patient may be an immunological rebound after parturition, an immunological alteration induced by secondary hypoadrenocorticism, or a combination of these. The simultaneous occurrence of Sheehan's syndrome and painless thyroiditis is rare, as evidenced by the existence of only one similar case report in the literature. However, since neither Sheehan's syndrome nor painless thyroiditis is a rare endocrine disorder, the thyroid function of patients with postpartum hypopituitarism and previously diagnosed chronic thyroiditis should be carefully evaluated.

Adrenal Insufficiency↗
PubMed1997

Stimulatory and inhibitory effects of neuropeptide Y on growth hormone secretion in acromegaly in vivo.

It has been reported that neuropeptide Y (NPY) affects growth hormone (GH) secretion in several animal species. With respect to the role of NPY in regulating GH release in humans, one previous study has reported that NPY inhibited GH secretion from cultured GH-secreting pituitary adenoma cells in vitro. However, since it has yet to be explored whether NPY affects GH secretion in acromegaly in vivo, in this study we attempted to examine the effect of intravenous (i.v.) bolus injection of 100 microg of human NPY on plasma GH levels in 15 patients with active acromegaly, trying to find a possible correlation among GH responses to NPY, thyrotropin-releasing hormone (TRH;500 microg, i.v.), luteinizing hormone-releasing hormone (LHRH;100 microg, i.v.), and bromocriptine (Br;2.5 mg, per os). NPY significantly increased GH secretion (more than twice the basal level) in 4 (27%) patients, and all of them were responsive to LHRH and non-responsive to Br. In contrast, 3 (20%) acromegalics showed a significant decrease in GH levels (less than half the baseline) after NPY, and all these patients were responsive to both TRH and Br. From these results, we hypothesize that the NPY-induced increase in GH release may be a feature of somatotroph-like pituitary adenoma causing acromegaly, whereas the NPY-induced decrease in GH secretion may be a feature of lactotroph-like adenoma.

Acromegaly↗