gamma-Aminobutyric acid (GABA; 50 or 500 microgram/10 microliter) was injected into the right lateral ventricle of urethane- or pentobarbital-anesthetized male rats. The animals were decapitated 15 min after injection. Serum GH and hypothalamic somatostatin (SRIF) concentration were measured by specific RIAs. Intraventricular GABA caused a dose-related increase in GH and SRIF. In another study, aminooxyacetic acid (5 or 20 mg) was injected ip into urethane-anesthetized rats. Aminooxyacetic acid at 20 mg produced a significant increase in both serum GH and hypothalamic SRIF. Furthermore, 12.5 mg gamma-hydroxybutyric acid (GHB) injected ip into urethane- or pentobarbital-anesthetized rats elicited a significant increase in both serum GH and hypothalamic SRIF. Pretreatment with 20 mg L-dopa produced decreases in the GHB-induced serum GH increase and in hypothalamic SRIF in pentobarbital-anesthetized rats. These results show that GABA and GHB stimulated GH secretion, which was accompanied by increased hypothalamic SRIF. Thus, the GH release induced by GABA or GHB may be partly involved in inhibiting the release of hypothalamic SRIF. As the GHB-induced GH release was inhibited by L-dopa, the stimulatory effect of GHB on GH secretion might be mediated by inhibition of the dopaminergic mechanism.
Several procedures have been reported for the assay of corticotrophine-releasing factor (CRF), each having its advantages and disadvantages. This report deals with an in vitro assay of ACTH releasing activity utilizing pituitary incubation combined with ACTH radioimmunoassay. Rat half pituitary was preincubated in 2 ml Krebs Ringer bicarbonate buffer containing 0.2% glucose and 0.25 % BSA (KRBG-BSA) for 1.5 hr (45 min X 2). The medium was replaced by 1 ml KRBG-BSA and incubated for 30 min. Then the medium was again replaced by 1 ml KRBG-BSA or KRBG-BSA containing test materials and incubated for another 30 min. The amount of ACTH assayed by radioimmunoassay in the 2nd 30 min incubation was compared with in the 1st 30 min incubation and expressed as percentage. In ACTH radioimmunoassay, anti-ACTH serum was diluted to 1 : 1,500-3,000. The 125I-alpha 1-24ACTH-antibody system was not affected by lysine-vasopressin (LVP), arginine-vasopressin (AVP), rat's pituitary LH, GH and prolactin. Human 1-39ACTH was used as ACTH standard, and the dilution curve of incubation medium was paralleled with the standard curve. Repeatability of immunoassayable ACTH within-assay was 174 +/- 5.0 pg/tube (CV = 2.9%). A log dose-relationship was observed between the amounts of stalk median eminence extracts (SME ; NIAMDD) added to the incubation medium and its ACTH releasing activities. The sensitivity of this assay method was at least 0.1 SME or 10 mU of LVP and AVP. Using this method, it found that LVP, AVP, norepinephrine (100 ng/ml200 ng/ml) and 5-hydroxytryptophane (1 mug/ml) had ACTH releasing activities but LH-RH, TRH, glucagon, dopamine, phentolamine, propranolol, haloperidol, prostaglandin E1 and indomethacin did not affect the release of ACTH.
Healthy male volunteers injected subcutaneously with 200 mg L-GABOB showed no significant changes in plasma GH, prolactin and cortisol levels. On the other hand, an intrathecal injection of 300 mg D, L-GABOB to cerebrovascular patients caused significant increases in plasma GH, prolactin and cortisol levels at 60 min after injection. These results indicate that GABOB may elicit the secretion of GH, prolactin and ACTH via the central nervous system.
Hypothalamic pituitary adrenal function was studied in 14 patients with anorexia nervosa. Although basal plasma cortisol levels in the morning were elevated in most cases, basal plasma ACTH levels were not suppressed. Oral administration of 1 mg dexamethasone 10 hr before blood sampling failed to suppress plasma ACTH and cortisol levels in most patients with anorexia nervosa. Apparent biological half-life of exogenous cortisol was prolonged in all 4 patients with anorexia nervosa tested. The cortisol response to insulin-induced hypoglycemia and exogenous ACTH appeared to be blunted in these patients. It is concluded that anorexia nervosa has dysfunctions of hypothalamic pituitary adrenal axis, especially an abnormal feedback mechanism on ACTH secretion.
Wereport a case of non-insulin-dependent diabetes mellitus (NIDDM)complicated with idiopathic hypoparathyroidism. A 74-year-old male was hospitalized because of diplopia. He was revealed to have NIDDM.The levels of serum Ca and intact-PTH were 6.3 mg/dl and <5 pg/ml, respectively. Brain computed tomography revealed abnormal calcification in the cerebral basal ganglia and the cerebellum. After recovery from hypocalcemia, the endogenous insulin secretion was normalized. It is suggested that the pathogenesis of NIDDMin this patient may have been related to an insulin secretory defect as a result of hypocalcemia in addition to the hereditary risk. (Internal Medicine 34: 904-907, 1995)
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