Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of age at diabetes onset and of capillary microangiopathy on the severity and evolution of hypothalamo-pituitary-gonadal changes was studied morphologically and morphometrically in male rats 4 and 8 months after streptozotocin injection. At each time period we studied 2 groups of rats, one made diabetic before (age 1 month), the other after puberty (age 3 months), and compared them with corresponding controls. The size of hypothalamic axons, numerical density and size of pituitary gonadotrophs, size of testicular tubules, and basement membrane thickness of retinal capillaries were measured. Major differences were found at 8 months. Changes of pituitary glands (i.e. small and numerous gonadotrophs) and testes (i.e. small tubular size) were more important in pre- than in postpubertal diabetic rats. This was a consequence of the aggravating prepubertal diabetes between 4 and 8 months. On the contrary, these changes partially regressed in postpubertal diabetic animals. Pituitary and testicular changes were correlated. Other lesions, such as swollen axonal processes in the hypothalamus, increased thickness of seminiferous epithelium and of capillary basement membranes, though very evident in diabetics, were independent from age at induction. Neither microangiopathy nor glycemia were correlated with any other change which confirmed their secondary role in diabetic neuroendocrine disorders. Thus, two types of diabetic disorders of the hypothalamo-pituitary-gonadal axis could be distinguished: 1) those with irreversible effects on immature yet partially reversible effects on mature structures; and 2) those independent from age at induction.
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PMID:The changes in the hypothalamo-pituitary-gonadal axis of streptozotocin-treated male rats depend from age at diabetes onset. 311 85

We studied serum TSH, pituitary TSH and alpha and beta-subunits of TSH and their messenger ribonucleic acids (mRNAs) in three models of nonthyroidal illness (NTI) in the rat, ie diabetes mellitus (1 wk after 65 micrograms streptozotocin/g BW IP), turpentine oil-injection (8 to 48 hours after after a dose of 5 microliter/g bw SC), and complete fasting for 72 hours. Euthyroid, hypothyroid (two months after thyroidectomy) and hyperthyroid rats (30 micrograms T4/d X 7, SC) were also studied for comparison. Pituitary TSH, alpha and beta subunits and serum TSH, T4, and T3 were measured by RIA. Pituitary mRNAs coding for common delta and TSH-beta subunits were determined by cytoplasmic dot hybridization technique using specific [32P]-cDNA probes. In all NTI models there were significant decreases in serum levels of TSH, T4, and T3, but no significant changes were observed in the pituitary content of TSH, and alpha and TSH-beta subunits. Hypothyroid rats had an increase in serum TSH, pituitary TSH, and pituitary TSH-beta subunit and a decrease in pituitary alpha subunit. On the other hand, hyperthyroid rats showed a decrease in serum TSH, pituitary TSH, and pituitary TSH-beta subunit, while there was no change in the alpha subunit. A significant reduction in the pituitary TSH-beta mRNA levels was observed in all NTI models and hyperthyroidism, while TSH-beta mRNA was increased in thyroidectomized rats. alpha-mRNA was increased only in the pituitary of hypothyroid rats; there was no appreciable change in the pituitary alpha-mRNA in the various other pituitary groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A study of pituitary thyrotropin, its subunits, and messenger ribonucleic acids in nonthyroidal illness. 335 21

Previous studies of the relationship of gonadal function to impotence in men with diabetes mellitus have yielded conflicting results. Pituitary-testicular function was studied in 28 impotent diabetic men and 15 normal men. Impotence was documented by clinical history and subdivided into categories of primary organic (n = 16), primary psychogenic (n = 7), and unclassified (n = 5) on the basis of nocturnal penile tumescence (NPT) testing, psychological testing, and penile vascular studies. All NPT parameters were diminished (P less than or equal to 0.001) in the impotent diabetic men compared to values in the normal men. Endocrine studies revealed increased urinary LH (P less than or equal to 0.05) and diminished serum free testosterone levels in the diabetic men with primary organic impotence. These changes were not found in normal men or diabetic men with primary psychogenic impotence. Six months of treatment in a home blood glucose-monitoring program resulted in significant improvement in metabolic control but no improvement in pituitary-testicular function, NPT, or sexual performance in the primary organic impotent group. Eight patients with primary organic impotence and no evidence of penile vascular disease had significant improvement (P less than or equal to 0.01) in NPT results as well as subjective improvement in sexual function after 6 months of parenteral testosterone administration. These studies suggest that primary gonadal dysfunction may be related to organic impotence in diabetes, and improvement in selected patients can occur with androgen therapy.
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PMID:Gonadal dysfunction in diabetic men with organic impotence. 358 93

The effects of insulin deprivation on the growth rate, plasma and pituitary growth hormone (GH) and GH synthesis were investigated in male Wistar rats. Diabetes was induced by administration of streptozotocin (STZ), 7 mg/100 g bw, and plasma and pituitary GH levels were measured by means of a specific radioimmunoassay. GH synthesis was determined in pituitaries by the in vitro incorporation of [3H] leucine into specific immunoprecipitates. The body weight and the pituitary GH content of normally developing rats showed an almost linear increase throughout the observation period, whereas diabetic rats stopped growing immediately after receiving STZ, and remained smaller than age-paired controls. Pituitary GH content remained within the control range through the 5 days following STZ administration and thereafter decreased reaching 10% of control values by the 30th day. Furthermore, pituitaries from diabetic rats incorporated [3H] leucine into r-GH at a greatly reduced rate, which could explain the diminished r-GH storage in pituitaries of diabetic rats. Plasma GH concentrations remained within the normal range for 10 days after STZ, thereafter plasma GH were markedly reduced. Insulin treatment prevented the metabolic changes, and restored normal levels of plasma and pituitary GH in diabetic rats. These findings indicate that diabetes, in rat, is characterized by an inhibitory effect on GH secretion, probably via a diminished GH synthesis by the pituitary gland.
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PMID:Effect of streptozotocin diabetes and insulin replacement on growth hormone in rats. 388 72

GH secretion is stimulated by hypothalamic GH-releasing factor (GHRH) and inhibited by somatostatin. Since GH induces the production of insulin-like growth factors (IGF) in liver and other tissues, it is of interest to learn whether IGF alters GH release through long loop feedback inhibition. Pituitary adenomas which had been removed from six acromegalic patients were processed for dispersed cell cultures and/or cell membrane preparations. Binding studies using 125I-labeled IGF-I, IGF-II, and insulin revealed specific hormone binding for each ligand to cell membranes derived from four somatotropinomas. A partially purified somatomedin preparation inhibited basal and/or GHRH-stimulated GH release from cultured pituitary cells derived from three of four adenomas; there was no effect of somatomedin in one tumor. In a single tumor, insulin also partially inhibited GHRH-stimulated GH release. Additionally, in one nonadenomatous pituitary removed from a patient with diabetes mellitus, insulin and somatomedin inhibited GHRH-stimulated GH release, and insulin inhibited basal GH secretion. These results indicate that specific cell membrane receptors for somatomedin peptides and insulin may be found on cell membranes from GH-secreting tumors, and that somatomedins and insulin can inhibit GH release in cultured human somatotropinoma cells. Thus, these data suggest that somatomedins may exert feedback inhibition of GH secretion in some patients with acromegaly.
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PMID:Regulation of growth hormone release from cultured human pituitary adenomas by somatomedins and insulin. 388 29

LHRH (median eminence) and LH (pituitary and plasma) from male and female Sprague-Dawley rats were assayed 1 month after streptozotocin injection and compared with values in controls either fed ad libitum or offered a restricted diet. Plasma LH was also assayed after stimulation with exogenous LHRH or naloxone. In diabetic males, the median eminence LHRH content and the plasma LH response to exogenous LHRH were unaltered, pituitary LH was increased, and plasma LH was decreased under basal conditions and after naloxone treatment. In diabetic females, while the median eminence LHRH content and the plasma LH response to exogenous LHRH or naloxone were reduced, pituitary and plasma LH levels were not different. Measurements made in undernourished rats excluded the possibility that the alterations found in diabetic animals were nutrition dependent. In parallel experiments, hypothalami and pituitaries were examined morphologically. In diabetic animals, degenerate axons, mainly of the LHRH type, were found in the arcuate nucleus and median eminence, and LH gonadotrophs were altered and more numerous. Strong differences between control males and females were revealed by morphometry; moreover, diabetic females had higher brain weights and fewer LH gonadotroph changes than diabetic males. These studies indicate that 1) the hypothalamo-pituitary changes that occur early in our streptozotocin-treated rats are unrelated to undernourishment and are possibly caused by insulin deficiency; 2) the LHRH axonal lesions might play a primary pathogenic role in the hypothalamo-pituitary disorder; 3) some anatomical data indicate that the brain and pituitary are less severely affected by diabetes in female than in male animals; and 4) differences between control males and females may account for some of the dissimilarities between the sexes observed under diabetic conditions.
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PMID:One month of streptozotocin-diabetes induces different neuroendocrine and morphological alterations in the hypothalamo-pituitary axis of male and female rats. 389 14

An immunofluorescence study using unfixed cryostat sections of human pituitary glands was carried out on sera from patients with type-Ia (juvenile-onset) diabetes (61 recent onset, 48 longstanding). 63 of their selected high-risk first-degree relatives and 117 patients with type-Ib ("polyendocrine") diabetes were tested for comparison. Healthy controls included 48 sera from laboratory staff and students. Pituitary-cell antibodies were found in none of the controls, in 2% of patients with longstanding diabetes, in 16.6% of patients with diabetes of recent onset, and in 36.6% of genetically predisposed relatives with islet-cell antibodies in their sera (of whom 7 became diabetic during a 3-year follow-up period, 4 of them reacting with pituitary cells for 1-3 years before the onset of diabetes). Thus pituitary antibodies tended to disappear after onset of symptoms. Many of the sera reacted with multiple anterior-pituitary cell types. These findings suggest a wider involvement of the endocrine-organ system in the pathogenesis of insulin-dependent diabetes and are in accordance with clinical observations showing excess growth in prepubertal boys at onset of diabetic symptoms and with the results of experiments on virus-induced diabetes in mice. The connection of these pituitary antibodies with autoimmune lymphocytic hypophysitis is at present unknown.
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PMID:Autoimmunity to anterior pituitary cells and the pathogenesis of insulin-dependent diabetes mellitus. 612 Dec 22

The effects of streptozotocin-induced diabetes on pituitary growth hormone (GH) content and release from incubated pituitaries were investigated. Male rats were made diabetic by a single injection of streptozotocin (65 mg/kg) and sacrificed by decapitation 15 days later. Pituitary GH concentration was significantly reduced in streptozotocin diabetic rats as compared to that observed in control animals. The amount of GH released from hemipituitaries was also lower in diabetic rats than in controls. Kinetic characteristics of somatostatin (SRIF) inhibition of GH release were not affected by the treatment. These results suggest that the decrease in plasma GH observed by some investigators in streptozotocin diabetic rats is probably due to a deficiency in GH storage and/or synthesis rather than a change in the responsiveness of pituitary GH cells to SRIF.
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PMID:Influence of streptozotocin-induced diabetes on growth hormone secretion in the rat. 613 72

Studies of the hypothalamic-pituitary-thyroid axis have been performed in streptozotocin (STZ)-diabetic Wistar rats and their controls. Plasma PBI concentration, plasma and pituitary TSH, contents, and hypothalamic TRH content were measured by RIA in basal and stimulated conditions. Compared to controls, rats made diabetic by 6.0 or 7.5 mg STZ/100 g BW showed decreased plasma PBI and TSH and diminished pituitary TSH content, with greater alterations in rats receiving the highest STZ dose. Both diabetic groups showed an almost 50% reduction of hypothalamic TRH content in comparison with the mean control value. After thyroidectomy, pituitary TSH secretion increased in diabetic, ad libitum fed, and semistarved animals, but it was lower in the diabetic group in which the reduction in plasma PBI was similar or greater. To evaluate pituitary sensitivity to the inhibitory action of L-T4 on TSH secretion in diabetes, thyroidectomized control (Thx-C), thyroidectomized diabetic (Thx-D), and thyroidectomized semistarved (Thx-S) rats were injected twice daily for 7 days with either saline or a fractional L-T4 dose of 0.25, 0.50, or 1.00 microgram/100 microgram/100 g BW. In Thx-D rats, a daily dose of 1.00 microgram L-T4 was sufficient to normalize pituitary TSH secretion, while a dose of 2.00 microgram was required to induce a similar effect in the Thx-C and Thx-S animals. Pituitary TSH content was increased in the Thx-C group with increasing T4 doses. No modification in this parameter was seen in the Thx-D and Thx-S animals. The fact that diabetes caused a reduction in the hypothalamic TRH content indicates that the primary cause of pituitary-thyroid alterations in STZ-diabetic rats lies in the hypothalamus, although the metabolic imbalance induced by diabetes and, in less degree, by undernutrition could also be partly responsible for some of the described modifications.
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PMID:Effect of streptozotocin diabetes on the hypothalamic-pituitary-thyroid axis in the rat. 615 7

The effect of experimental diabetes on T4 to T3 conversion, T3-deiodination, and the pituitary response to a dose of T4 and T3 was studied. Pituitary GH and plasma TSH were determined as a measure of the biological response to thyroid hormones. Thyroidectomized rats, 5 days after injection with saline or streptozotocin (thyroidectomized-control (Th.C) and thyroidectomized-diabetic (Th.D) rats, respectively) received an ip dose of T4 + [125I]T4 or T3 + [125I]T3. Rats from each group were sacrificed at varying intervals after thyroid hormone injection. Th.D rats had hyperglycaemia, glycosuria, and a body weight of about 80% of that of Th.C rats. The concentrations of [125I]T4 and [125I]T3 were measured in several tissues after ethanol extraction, separation by thin-layer chromatography, and identification with markers. Plasma TSH and pituitary GH were measured by specific RIAs. Diabetes decreased the conversion of T4 to T3 in several tissues, including the pituitary, but did not affect the deiodination of T3. The decrease in pituitary T3 content after a dose of T4 was accompanied by a diminution of the biological effect of the T4 dose on pituitary GH. Since diabetes also interferes with this biological response to a T3 dose, it seems likely that the reduced biological effect of thyroid hormones on pituitary GH may be related to an alteration in the somatotrophin T3 receptors, or in post-receptor events. Moreover, the data indicate that although T3 generation in the pituitary was reduced, the same dose of T4 had a greater inhibitory effect on TSH secretion in Th.D rats than in Th.C rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased T4 to T3 conversion in tissues of streptozotocin-diabetic rats. 632 20


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