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 proestrus preovulatory luteinizing hormone (LH) surge was absent or delayed in more than 56% of untreated streptozotocin-diabetic rats. Absence of LH surge was associated with anovulation. Insulin treatment for 10-14 days restored the diminished surge and ovulation frequency. Pituitary LH release in response to exogenous gonadotropin-releasing hormone administration in diabetic rats was not different from controls. Impaired hypothalamic function may comprise the basis for the increased incidence of infertility in diabetes mellitus.
Diabetes 1984 Apr
PMID:Absent or delayed preovulatory luteinizing hormone surge in experimental diabetes mellitus. 636 91

Three women with insulin-dependent diabetes mellitus (IDDM) from childhood and early development of diabetic retinopathy are described. Insulin requirement was reduced to 5-12 IU daily in all three after relatively uncomplicated births and all had very brittle diabetes on this dosage. At re-examination 16-22 years after these births and after 34-42 years of IDDM, regression of retinopathy was observed in two patients, while the third had a light retinopathy at the same level as initially. Other diabetic complications were few and none of the patients had nephropathy. Pituitary examination revealed incomplete hypopituitarism in all cases, human growth hormone (HGH) being the sole common factor lacking. These findings and a review of four similar cases reported previously lend some support to the hypothesis of HGH as a possible pathogenetic co-determinant in the development of diabetic retinopathy.
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PMID:Long-term insulin-dependent diabetes mellitus with secondary pituitary insufficiency and regression of retinopathy. 666 30

To evaluate GH pituitary responsivity to nonphysiological stimuli in insulin-dependent (type I) diabetes, a TRH test (200-micrograms iv bolus) was carried out in 31 type I diabetics (16 females and 15 males). TRH was capable of inducing GH responses in most of the studied patients, with a striking difference between the sexes; responses were documented in 7 of 15 males and in 13 of 16 females. Linear regression analyses of the results showed a positive correlation between basal values and peak levels of GH and a negative correlation between GH peaks and the ages of the patients. No correlation was found between GH values (basal and peak levels) and blood glucose levels or duration of disease. In conclusion, our results support the observation that GH secretion in diabetes is abnormal. TRH induces GH secretory responses, especially when GH basal values are elevated and in female patients. Pituitary GH responsiveness to TRH shows a progressive decline with advancing age unrelated to the duration of the disease or the presence of retinopathy.
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PMID:Nonspecific growth hormone responses to thyrotropin-releasing hormone in insulin-dependent diabetes: sex- and age-related pituitary responsiveness. 680 82

Pituitary-gonadal function was studied in 50 male diabetic patients under 53 years of age. Forty-three had normal sexual activity and 7 were impotent. Plasma testosterone levels and urinary 17 ketosteroids, androsterone and dehydroepiandosterone levels were measured. LH and FSH levels before and after LHRH, and prolactin levels before and after TRH were also measured in plasma. No significant changes in pituitary-gonadal function were detected, irrespective of the patient's sexual activity. Neither the type and degree of control of diabetes nor the presence of absence of microangiopathy had any influence on the results. Basal LH and FSH levels were slightly higher in older patients. Prolactin levels after TRH were significantly higher in the later stages of the test in patients with microangiopathy.
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PMID:[Pituitary-gonadal function in male diabetic patients (author's transl)]. 707 53

Pituitary glands from 500 consecutive autopsies were reviewed and the findings correlated with clinical symptomatology. Occult pituitary adenomas were identified in 42 pituitary glands (8.5%). In only one case was a pituitary lesion clinically questioned, but specific hypophyseal function studies were not performed. These tumors occurred most frequently in the sixth and seventh decade of life, without obvious sex predominance. Of these patients, 48% were obese, 57% were hypertensive, and diabetes mellitus was noted in 11. The tumor size ranged from 1 to 15 mm, but was greater than 1 cm in only one case. In 34 cases, the tumor was located along the periphery of the gland. Even though the etiological and functional significance of these tumors is unclear, the clinical course appears to be relatively benign.
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PMID:Incidental pituitary adenomas. 745 37

Pituitary abscess is relatively rare. Only about 80 cases have been reported. Preexisting lesions in pituitary fossa, such as pituitary adenoma, craniopharyngioma and Rathke's cleft cyst, are inclined to be complicated by infection more than the normal pituitary glands are. We reported a case of pituitary abscess caused by infection of Rathke's cleft cyst. A 67-year-old male had general fatigue and loss of appetite 4 months before admission. On admission he was found to have diabetes mellitus, diabetes insipidus, and hypernatremia. These defects were controlled by medication but he gradually became comatose and febrile. CT and MRI revealed an intrasellar lesion with ring enhancement. Lumbar puncture demonstrated an increase of mononuclear cells and protein. Blood chemistry revealed a marked increase of CRP. He was operated on via the transsphenoidal approach, which revealed sphenoid sinusitis and abscess formation in the pituitary gland. Histological examination of the surgical specimen revealed infection of Rathke's cleft cyst but the fluid in the cyst was sterile. By the drainage of the cyst and the use of antibiotics the patient became alert and signs of infection disappeared. He was discharged with a slight hypopituitarism and returned to normal life. Mortality rate of pituitary abscess is decreasing but is still high because of hypopituitarism and severe infection. Accurate diagnosis and operation are necessary. Transsphenoidal surgery is preferable for postoperative drainage of the abscess.
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PMID:[A case of pituitary abscess caused by infection of Rathke's cleft cyst]. 747 22

The five somatostatin receptor mRNAs are expressed with distinct though overlapping patterns of distribution in the CNS and peripheral tissues. All receptor types are expressed in the anterior pituitary and hypothalamus and could therefore be modulated in states of growth hormone (GH) dysregulation. Metabolic perturbations such as food deprivation and diabetes mellitus lead to suppression of GH levels in the rat, in part due to increased somatostatin tone. In rats deprived of food, pituitary sstr1, 2 and 3 mRNAs were reduced by 80% compared to fed controls; sstr4 and sstr5 mRNAs were unchanged. Hypothalamic sstr mRNA expression was unaltered. In diabetic rats pituitary sstr1, 2 and 3 mRNAs were reduced by 50-80% with sstr1 mRNA restored in part by insulin therapy. Pituitary sstr4 mRNA and hypothalamic expression of these four types was unaffected. sstr5 mRNA is reduced by 70% in the pituitary and by 30% in the hypothalamus with restoration of both by insulin treatment. Altered pituitary sstr expression in food deprivation and diabetes could result from chronic exposure to increased plasma somatostatin. In rat GH3 pituitary tumour cells exposed to 1 microM somatostatin for up to 48 h, sstr1, 3, 4 and 5 mRNA increased dramatically while sstr2 mRNA exhibited a biphasic response. We observed a net increase in receptor binding associated with increased sstr mRNA. Somatostatin receptor expression is regulated in a tissue- and type-specific manner, adding further complexity to the action of the multifaceted peptide somatostatin.
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PMID:Regulation of somatostatin receptor mRNA expression. 758 42

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

To examine the molecular basis for the decreased pituitary growth hormone (GH) and thyrotropin (TSH) content during restricted feeding, fasting and diabetes, we measured steady-state levels of mRNA for TSH-alpha, TSH-beta and GH in the pituitary from normal rats either fed ad libitum (C), limited to 75%, 50% and 25% (FR75, FR50, FR25, respectively) of ad libitum intake, or deprived of food for 2 and 4 days (F2 and F4, respectively), and also in streptozotocin-diabetic (D) and D insulin-treated animals. The results from these experimental groups were compared with those in thyroidectomized (Tx) rats. Pituitary mRNA was quantified by Northern blot hybridization with cDNA probes specific for rat TSH-alpha, TSH-beta and GH. Although changes in the pituitary GH mRNA during restricted feeding, fasting and diabetes were similar qualitatively to those induced by hypothyroidism, GH mRNA levels in Tx rats (> 10% of C values) were less than in the other experimental groups (p < 0.001). Pituitaries from FR50, FR25 and D rats also contained less GH mRNA than F2 and F4 animals (p < 0.05). Thyroidectomy resulted in a marked increase in both TSH-beta and TSH-alpha mRNAs, the changes in TSH-beta mRNA being greater than those in TSH-alpha mRNA. In contrast, FR50, FR25, F2, F4 and D rats exhibited a decrease in pituitary TSH-beta mRNA (60%, 50%, 35%, 36% and 33%, respectively, of C values; p < 0.01-0.05) and in TSH-alpha mRNA levels (81%, 64%, 46%, 43% and 36%, respectively, of normal values; p < 0.02-0.05), TSH-beta mRNA showing the greater changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of food restriction, fasting, diabetes and thyroidectomy on growth hormone and thyrotropin gene expression in the rat pituitary. 762 31

To elucidate the roles of the hypothalamic peptides, GH-releasing hormone (GRH) and somatostatin (SRIH), potentially responsible for altered GH dynamics in diabetes, we studied the time courses of their changes in level associated with altered GH secretion in streptozotocin (STZ)-induced diabetic mice. Diabetic mice were used at 4, 7, and 14 days after STZ injection for analyses of 1) GH secretion in vivo, 2) hypothalamic GRH and SRIH messenger RNA (mRNA) levels, 3) pituitary GH mRNA and protein contents, and 4) pituitary GH response to GRH in vitro. GH secretion was completely suppressed 7 and 14 days after STZ injection. The hypothalamic GRH mRNA level was reduced to 59.8%, 61.2%, and 48.5% of control values at 4, 7, and 14 days, respectively. In contrast, the hypothalamic SRIH mRNA level was not altered at all of these time points. Pituitary GH mRNA and protein contents were significantly reduced to 70.2% and 61.5% of those in controls, respectively, only at 14 days. Pituitary GH responses to GRH at three doses (10, 50, and 250 nM) in vitro were remarkably increased at 4, 7, and 14 days. These findings indicate that the diabetic state rapidly and primarily inhibits hypothalamic GRH gene expression without affecting SRIH. A persistent decrease in hypothalamic GRH tone has been suggested to result in inhibition of GH synthesis in the pituitary. Enhancement of GH responsiveness to GRH may be due to the up-regulation of GRH receptors in the pituitary.
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PMID:Suppression of episodic growth hormone secretion in streptozotocin-induced diabetic mice: time-course studies on the hypothalamic pituitary axis. 766 70


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