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

Sixteen women volunteers with menstrual irregularities were studied with an intravenous injection of 100 microgram of gonadotropin-releasing hormone (GNRH). Serial blood samples were obtained for 2 hours after the injection and assayed for their concentration of glucose, insulin, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). There was a significant increase in the levels of both gonadotropins following the injection, with the peak for LH occurring at 30 minutes and the peak for FSH occurring at 90 minutes. There was a slight decrease in the glucose level at 45 minutes and in the insulin levels at 60 and 120 minutes. Because GNRH causes only minor changes in these parameters of carbohydrate metabolism, it would appear to be safe to use in women with ovulatory abnormalities secondary to diabetes mellitus.
 ...
PMID:The effect of gonadotropin-releasing hormone on blood glucose insulin, luteinizing hormone, and follicle-stimulating hormone levels. 32 82

Insulin-deficient states are associated with an impaired function of the hypothalamic-pituitary-gonadal axis, but the mechanisms underlying hypothalamic alterations in experimental diabetes are still unknown. We investigated the effect of glucose concentrations, in the presence and absence of insulin, on LHRH release from perifused hypothalamic fragments from female adult ovariectomized rats. Glucose and insulin were added to the perifusion medium (Earle's, pH 7.4, gassed with 95% O2/5% CO2, flow rate 50 microliters/min). When glucose was absent (in the presence of insulin 10 mU/l), LHRH release was reduced, peak levels being < 5 pg/100 microliters. The addition of glucose (100 and 300 mg/dl), in the absence of insulin, resulted in peak LHRH levels fluctuating around 35 pg/100 microliters (p < 0.05 vs. glucose 0 mg/dl). When glucose (100 or 300 mg/dl) and insulin (10 mU/l) were combined, an eightfold increase in peak LHRH values was observed, and peak levels reached 300 pg/100 microliters (p < 0.05 vs. glucose 100 and 300 mg/dl alone). In conclusion, LHRH release by perifused hypothalamic fragments is dramatically increased by low concentrations of insulin; this occurs only when glucose is available. Acutely elevated glucose levels (from 100 to 300 mg/dl) do not affect LHRH release.
 ...
PMID:Effect of insulin on LHRH release by perifused hypothalamic fragments. 143 80

A 27-year-old woman with type 1 diabetes mellitus was admitted to the Shimane Medical University Hospital because of secondary amenorrhea. She had been treated with insulin since July, 1986. Fasting plasma glucose and HbA1c levels were controlled within normal limits. However, body weight gradually decreased and amenorrhea started in 1988. Physical examination revealed emaciation with BMI of 17.3. Basal levels of plasma T3, somatomedin C, LH, FSH and estradiol levels were low, whereas HGH levels were slightly elevated. Plasma LH markedly increased in response to LHRH administration. She was diagnosed as having weight loss-related hypothalamic amenorrhea. Induction of ovulation was not obtained with clomiphene citrate. Treatment with subcutaneous pulsatile administration of LHRH (20 micrograms every 120 min) resulted in an increase in plasma levels of LH, FSH and estradiol, which was accompanied by ovulation and corpus luteum formation. Further treatment with pulsatile LHRH administration was followed by conception. Two gestational sacs were detected by ultrasonography. One of them was absorbed at the early stage of pregnancy. She was delivered of one healthy female infant without complications. These findings suggest that it is important not only to control plasma glucose levels but to keep the appropriate weight and support the psychological aspects of the subject in the treatment of diabetes mellitus. Subcutaneous pulsatile LHRH therapy may be effective for the induction of ovulation in clomiphene-resistant hypothalamic amenorrhea; however, it will be necessary to solve the problem of dosage and the interval of LHRH administration in the future.
 ...
PMID:[A case of type 1 diabetes mellitus with hypothalamic amenorrhea: successful pregnancy following subcutaneous pulsatile administration of LHRH]. 158 22

Endocrine functions were examined in 21 patients with mitochondrial myopathies presenting with chronic progressive external ophthalmoplegia and other additional neurological and multisystemic symptoms. Ten patients had the features of the Kearns-Sayre syndrome. Deletions of the mitochondrial DNA were found in 4 out of 5 patients examined. Fourteen patients, including 3 with deletions of the mitochondrial DNA, had various and often multiple endocrine abnormalities: 6 patients were of short stature, 3 had irregular menstrual cycles, 3 had undersized testicles, 5 showed an insufficient rise of growth hormone following the administration of growth-hormone-releasing hormone, 4 showed an insufficient rise in FSH after administration of gonadotropin-releasing hormone, 5 had manifest diabetes mellitus, 3 showed an impaired glucose tolerance, and 2 patients had subnormal serum levels of parathormone in combination with hypocalcaemia. One patient additionally had Klinefelter's syndrome with a kariotype 47, XXY and increased levels of FSH and LH, subnormal levels of testosterone and subnormal testicular volume. The occurrence of endocrine defects correlated with the duration of disease. The data demonstrate that endocrine abnormalities are frequently associated with mitochondrial myopathy, indicating that this multisystemic disease also involves various endocrine tissues.
 ...
PMID:Endocrine abnormalities in mitochondrial myopathy with external ophthalmoplegia. 160 Mar 49

Luteinizing hormone (LH) responses to gonadotropin-releasing hormone (GnRH) (100 micrograms injected intravenously (IV)) or naloxone (4 mg injected plus 8 mg infused in 2 hours IV) were evaluated in 29 women with insulin-dependent diabetes mellitus (IDDM) (duration, group I (n = 15): less than 10 years, range 3 to 9 years; group II (n = 14): greater than 10 years, range 11 to 20 years) and in 15 normal controls, on the 22nd days of normal menstrual cycles. Both GnRH- and naloxone-induced LH responses were similar in group I diabetics and normal controls, whereas they were significantly lower in group II than in group I diabetics or normal controls. Positive correlations were found between LH responses to GnRH and naloxone, whereas negative correlations were observed between maximal LH peaks in response to GnRH or naloxone and duration of diabetes. These data indicate that a hypothalamic pituitary disorder affects LH secretion with time after the onset of IDDM.
 ...
PMID:Luteinizing hormone responses to gonadotropin-releasing hormone and naloxone in menstruating women with type I diabetes of different duration. 200 95

Diabetes interferes with reproductive function in laboratory animals. Previous studies in female diabetic rats have not resolved if the reproductive abnormalities observed are at the hypothalamic, pituitary and/or ovarian level. The interaction of the gonadal and adrenal axes has not been studied in the diabetic female rat. The purpose of this study is twofold: first, to determine the level of dysfunction in the hypothalamic-pituitary axis caused by diabetes in the adult female rat controlling for stage of the estrous cycle, and, second, to evaluate basal corticosterone secretion in female diabetic rats. Sixty cycling 40-day-old female rats were randomly assigned to 3 groups; control (n = 32), diabetic (n = 14), and diabetic insulin-replaced animals (n = 14). The level of hyperglycemia in each group was documented by glycosylated hemoglobin levels and biweekly blood glucoses. Three weeks after induction of diabetes, pituitary luteinizing hormone (LH) responsiveness following an i.v. injection of gonadotropin-releasing hormone (GnRH) was assessed in representative diestrous rats from each group. All animals were sacrificed in either diestrus or proestrus for determination of GnRH concentration in the hypothalamus, LH and follicle-stimulating hormone (FSH) content in pituitary and LH, FSH, estradiol and corticosterone in serum. Uterine weight to body weight ratios (a bioassay for estrogen) were also calculated. Hypothalamic GnRH concentration was significantly lower in diabetic versus control diestrous rats. Basal pituitary and serum gonadotropin levels were not different between any groups. GnRH-stimulated serum LH levels were higher in diabetic vs. control and diabetic insulin-treated animals. LH surges occurred in the control and diabetic insulin-replaced but not the diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Diabetes-induced alterations of reproductive and adrenal function in the female rat. 211 87

Diabetes mellitus is commonly associated with reproductive neuroendocrinopathy in both humans and animal models for the disease. Diabetes-associated reproductive failure in the male is a result of multilevel dysfunction within the hypothalamo-pituitary-testicular axis. In view of the known effects of diabetes on hypothalamic gonadotropin-releasing hormone (GnRH) and gonadotropins in chemically-induced animal models for diabetes, we examined hypothalamic aminergic activities (important to the regulation of GnRH release), circulating gonadotropin levels and testicular morphology in the infertile, genetically diabetic (C57BL/KsJ-db/db) male mouse. Groups of 2-5 month old (average age: 3.4 months) and 6-11 month old (average age: 8.8 months) diabetic mice were compared with age-matched non-diabetic (C57BL/KsL(-)+/?) male mice. Diabetic mice in both age groups were markedly obese and hyperglycemic. Hypothalamic serotonin synthesis was inhibited in the preoptic area-anterior hypothalamus (POA-AH) in both 2-5 month old and 6-11 month old diabetic mice as well as in the mediobasal hypothalamus-median eminence (MBH-ME) of 6-11 month old diabetic mice. Catecholamine synthesis (norepinephrine and dopamine) was reduced in the POA-AH of 2-5 month old diabetic mice and in the MBH-ME of 6-11 month old mice. These aminergic changes were associated in 2-5 month old diabetic mice with reduced circulating levels of LH and in 6-11 month old diabetic mice, of both LH and FSH. In 6-11 month old diabetic mice, testes were characterized by a thickened tunica albuginea, numerous Sertoli cells and the near absence of any spermatogenic cells. The epididymis from these diabetic mice was devoid of spermatozoa.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Reduced aminergic synthesis in the hypothalamus of the infertile, genetically diabetic (C57BL/KsJ-db/db) male mouse. 212 14

The ability of testosterone to reverse the adverse effects of streptozotocin-induced (STZ) diabetes on male sexual function was tested in adult male rats. Treatment with STZ (50 mg/kg) led to a significant reduction of plasma testosterone (T) levels and in the number of rats exhibiting ejaculatory behavior in a 30-minute test period. A similar reduction in T levels and ejaculatory behavior was seen in rats subjected to caloric restriction to mimic the weight loss seen in the STZ-treated rats. T-replacement (200 micrograms/day) restored T levels to those seen in control animals, but did not reverse the adverse effects of STZ on copulatory behavior. STZ-induced changes in copulatory behavior were associated with changes in hypothalamic LHRH levels and catecholamine turnover. Caloric restriction also caused endocrine and neuroendocrine changes, but they were not similar to those seen in STZ rats suggesting that these two treatments affect copulatory behavior by different mechanisms.
 ...
PMID:Testosterone replacement fails to reverse the adverse effects of streptozotocin-induced diabetes on sexual behavior in the male rat. 214 Jan 95

Oral contraceptives are clearly contraindicated in patients with a history of thromboembolic disease, ischemic heart attack, or cerebral stroke. Patients requiring long-term anticoagulant treatment can be treated with gonadotropin-releasing hormone analogs to prevent ovulation, because ruptured follicles can cause massive intraperitoneal bleeding. Patients with essential hypertension and severe liver diseases should also discontinue treatment 4 weeks before major elective surgery. Migraine and diabetes mellitus are regarded as relative contraindications, depending on the individual situation. Long-term diseases, such as Crohn's disease, epilepsy, and sickle cell anemia, also require individualized consultation.
 ...
PMID:Oral contraception in disease states. 225 29

Numerous studies indicate that an impaired hypothalamopituitary axis plays an important role in reproductive and thyroid disorders in diabetic humans and animal models. Yet, several questions about the pathogenesis of these diabetic complications have not been answered. To evaluate the basal secretion of single gonadotrophs and thyrotrophs in vitro, uncultured pituitary cells from control rats and 1-mo streptozocin-induced diabetic (STZ-D) rats were studied with a reverse hemolytic plaque assay and morphometry. After light-microscopy immunocytochemistry for gonadotropin and thyrotropin (TSH), we recorded the ratio of plaque-forming to non-plaque-forming cells. The area of plaques produced by luteinizing hormone (LH), follicle-stimulating hormone (FSH), and TSH cells and the area of plaque-forming and non-plaque-forming cells were clearly smaller in diabetic than control rats. The plaque area, however, was more severely reduced than the cell area. The percentage of LH-, FSH-, and TSH-immunoreactive plaque-forming cells was greatly decreased in diabetic compared with control animals. In conclusion, our findings demonstrate that the LH-, FSH-, and TSH-secreting cells of diabetic rats released less hormone and were less numerous than the corresponding cells of control rats. Thus, several pathogenetic mechanisms might be involved in reduced gonadotropin and TSH release at the cellular level: 1) anatomical lesions of organelles involved in glycoprotein hormone synthesis and secretion, possibly due to insulin deficiency; 2) decreased gonadotropin-releasing hormone (GnRH) and thyrotropin-releasing hormone (TRH) receptors on pituitary cells; 3) inadequate GnRH and TRH stimulation; 4) high plasma corticosterone levels; or 5) a combination of points 1-4.
Diabetes 1989 Oct
PMID:Reverse hemolytic plaque assay study of luteinizing and follicle-stimulating hormone and thyrotropin secretion in diabetic rat pituitary glands. 250 79


1 2 3 4 5 6 7 8 9 10 Next >>