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)

This study aimed at identifying factors influencing aortic valve calcification in old age. Echocardiographic and Doppler characteristics of the aortic valve were compared with possible clinical and biochemical predictors in 501 people aged 75-86 years and in 76 aged 55-71. Slight calcification was seen in 222 people (40%) and severe calcification in 72 (13%); 21 people had moderate or severe aortic stenosis. Age (P = 0.000) and serum parathyroid hormone (P = 0.015) were higher and body mass index lower (P = 0.002) in the presence of aortic valve calcification. In multivariate analysis, age (P = 0.000), hypertension (P = 0.005) and body mass index (P = 0.005) were independent predictors of aortic valve calcification, and age (P = 0.022) and serum ionized calcium (P = 0.037) of valve stenosis. The odds ratio (95% confidence interval) for valve calcification was 1.89 (1.42-2.50) for a 10-year increase in age, 1.74 (1.19-2.55) in the presence of hypertension, and 1.39 (1.10-1.76) for a 5 kg.m-2 decrease in body mass index. Sex, smoking, diabetes, serum lipids and insulin were unrelated to valvular calcification. These data suggest that leanness and a history of hypertension increase the likelihood of senile aortic valve calcification. Calcium metabolism may also be of significance. The mechanisms of these associations deserve further study.
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PMID:Factors associated with calcific aortic valve degeneration in the elderly. 792 4

A 50-year-old man was admitted to our hospital for the evaluation of hypocalcemia and the treatment of diabetes mellitus. Seven months before admission, he sometimes felt thirst and polyuria, and 4 months before admission, he went to a doctor to check his blood glucose and was diagnosed as having diabetes mellitus which had suddenly developed. At that time he was treated with sulfonylurea, but his diabetic control was very poor. At the time of admission to our hospital, the patient's serum calcium (Ca) level was 5.7 mg/dl, phosphorus (P) 5.0 mg/dl, and fasting blood glucose 308 mg/dl, but urinary ketone bodies were not detected. High sensitive assay of parathyroid hormone (HS-PTH), intact PTH and C-terminus PTH concentrations were under the level of detection. TSH level was slightly high (6.1 mu U/ml) with positive antimicrosomal and antithyroglobulin antibodies but thyroid hormone levels were within normal limits. TRH test showed over-response of TSH. Based on Ellsworth-Howard test, we made the diagnosis of idiopathic hypoparathyroidism associated with primary hypothyroidism and diabetes mellitus. He was treated with insulin twice a day and reached good control, and he was also administered 1 alpha-OH-D3 and calcium lactate resulting in an increase of serum Ca level after 2 weeks. These findings suggest that this case may be a polyglandular autoimmune (PGA) syndrome type 1 reported by Neufeld, which is very rare in Japan. The type of diabetes mellitus of this case is controversial. It is, however, necessary to pay attention to the decrease of the patient's insulin-secreting activity because autoimmune disorders are accompanied by this case.
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PMID:[A case of idiopathic hypoparathyroidism associated with primary hypothyroidism and diabetes mellitus]. 795 10

Glucose metabolism was studied in a patient with vitamin D deficiency during its treatment with small doses of vitamin D. A continuous infusion of glucose test was performed to assess glucose tolerance and insulin sensitivity and beta-cell function were derived by mathematical modelling. Fasting glucose was 5.6 mmol/l and achieved glucose after the infusion was 10.4 mmol/l confirming diabetes. The test was repeated 0.5, 1, 3 and 5 months after starting treatment. Serum calcium increased glucose intolerance from 1.76 to 2.0, 2.08, 1.96 and 2.0 mmol/l, respectively; vitamin D reached supraphysiological levels initially and returned to normal levels, and parathyroid hormone levels were normalized. Her weight did not change during treatment. Glucose tolerance improved during treatment and achieved glucose was 9.4, 8.6, 9.2 and 9.0 mmol/l at 0.5, 1, 3 and 5 months, respectively; insulin sensitivity did not change. Beta-cell function improved from 101% at diagnosis to 126%, 147%, 173% and 198% at 0.5, 1, 3 and 5 months, respectively. Improvement in beta-cell function and consequently in glucose tolerance is likely to have been due to correction of hypocalcaemia, vitamin D deficiency and secondary hyperparathyroidism.
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PMID:Improvement in glucose tolerance and beta-cell function in a patient with vitamin D deficiency during treatment with vitamin D. 802 65

Approximately 50% of the annual mortality in patients with end-stage renal disease (ESRD) is attributed to cardiovascular-related events. Multiple factors, including volume overload, hypertension, electrolyte abnormalities, and the presence of comorbid diseases, such as diabetes mellitus, may have an adverse effect on left ventricular function in ESRD. The purpose of this brief review is to advance the hypothesis that parathyroid hormone (PTH) is a cardiotoxin and a potential mediator of cardiac dysfunction in uremia. Recent studies have provided evidence that cardiocytes possess a distinct class of binding sites for PTH, and the PTH receptor has recently been cloned. Furthermore, the PTH receptor may be coupled to more than one effector pathway. Finally, the possibility that a PTH-related protein autocrine system may be present in cardiocytes and the implications of this signaling pathway on cardiocyte function are discussed.
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PMID:The cardiocyte as a target for parathyroid hormone in end-stage renal disease. 803 77

The authors evaluated the prevalence, magnitude, and contributing factors for osteopenia in insulin-dependent diabetes mellitus (IDDM). We measured bone mineral density (BMD) in the lumbar spine and femoral region in 90 patients aged 18-54 years with IDDM using dual-energy x-ray absorptiometry. The blood-glucose control, insulin dosage, duration of disease, and presence of chronic complications of diabetes were evaluated. Serum ionized calcium, magnesium, phosphorus, alkaline phosphatase (ALP), 25-hydroxycholecalciferol, immunoreactive parathyroid hormone (iPTH), and urinary calcium, phosphorus, and hydroxyproline were also analyzed. Thirty-one patients (34%) were classified as having a reduced BMD (less than 2 SD below the mean). The comparison between normal and low BMD patients showed that the osteopenics had a tendency to be younger (median, 28 years versus 32 years), showed a higher mean plasma glucose (15.5 +/- 5.0 mmol/L versus 12.9 +/- 3.8 mmol/L; p = 0.018), longer duration of disease (11.2 +/- 2.1 years versus 5.0 +/- 1.3 years; p = 0.004), and needed a higher insulin dosage (56 +/- 17 U/day versus 43 +/- 16 U/day; p < 0.001). There was a positive correlation between mean glucose levels, duration of disease, insulin dosage, and bone-mass decrease. A higher incidence of chronic complications, mainly retinopathy (58% versus 25%) and neuropathy (52% versus 22%) was found in the low BMD group. There was no alteration of serum calcium, phosphorus, iPTH, 25-hydroxycholecalciferol, and urinary calcium and phosphorus. The ALP levels were significantly higher in the osteopenic group, and magnesium and hydroxyproline levels were lower in the whole diabetic group, but these measurements did not correlate with BMD reduction.(ABSTRACT TRUNCATED AT 250 WORDS)
J Diabetes Complications
PMID:Prevalence and magnitude of osteopenia associated with insulin-dependent diabetes mellitus. 806 53

To clarify the role of serum vitamin D and bone remodeling markers in postmenopausal diabetic azotemics, we designed a study involving 3 different postmenopausal patient groups. Group I consisted of 20 diabetic women with renal insufficiency who were not yet on dialysis therapy. Group II consisted of 15 age-matched nondiabetic women with comparable degrees of renal insufficiency. Group III consisted of 20 age-matched women with normal renal function. We investigated the overnight fasting serum 25 (OH) vit-D, 1,25(OH)2 vit-D3, osteocalcin (OC), bone isoenzyme of alkaline phosphatase (ALK-PB) and intact parathyroid hormone (I-PTH) levels in these cases. The serum I-PTH and OC levels were statistically significantly higher, whereas 1,25(OH)2vit-D3 were significantly lower in Group I and Group II patients than in Group III patients. We found no significant correlation between elevation of I-PTH and reduced 1,25(OH)2 vit-D3 levels in Group I and Group II patients. I-PTH levels correlated positively with OC in Group I and Group II patients. There was no significant difference in serum 25(OH) vit-D among these 3 groups of patients. We conclude that (1) serum OC level may serve as a good parameter in evaluating secondary hyperparathyroidism in postmenopausal azotemics with or without diabetes, (2) even in the presence of menopause, renal failure per se is the main factor in determining serum 1,25(OH)2 vit-D3 levels in diabetic azotemics.
Diabetes Res 1993
PMID:Serum osteocalcin and vitamin D in postmenopausal diabetic azotemics. 807 46

Erythropoietin (EPO) given subcutaneously (SC) once per week has been successful in the treatment of anemia in continuous ambulatory peritoneal dialysis (CAPD) patients. We have identified a population of CAPD patients that requires EPO administration once per week or less often. To determine if specific variables could be identified that would predict which CAPD patients would require infrequent EPO dosing, we reviewed the charts of all our CAPD patients who were receiving EPO as of 1 June 1992. Patients had to have been on CAPD for 3 months and EPO for 3 months to be considered for analysis. We identified 12 patients who required EPO once per week or less frequently (infrequent EPO) and 9 patients who required EPO more than once per week (frequent EPO). Parameters that were analyzed included age, gender, race, time on CAPD, history of gastrointestinal bleeding, exit-site infection or peritonitis in the last 60 days, diabetes, amount of dialysate instilled per day, and the number of exchanges per day. Laboratory data that were analyzed included hemoglobin, hematocrit, serum iron, total iron-binding capacity, ferritin, blood urea nitrogen (BUN), creatinine, BUN/creatinine ratio, albumin, total protein, parathyroid hormone, and aluminum. Categorical data were analyzed via chi-square, and numerical data were analyzed via the t-test. The infrequent EPO group required only 35% as much EPO as the frequent group to maintain hemoglobin and hematocrit, which were significantly greater. The only parameter that was different between the two groups was age (infrequent EPO 42 +/- 13.2 vs frequent EPO 55.8 +/- 11.9 years, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infrequent dosing of subcutaneous erythropoietin for the treatment of anemia in patients on CAPD. 810 57

Recent studies have revealed that altered mineral and vitamin D metabolism is observed in diabetic patients with the complication of osteopenia. In order to elucidate the role of parathyroid hormone-related peptide (PTHrP) on calcium homeostasis in diabetes, we have measured the serum level and urinary excretion of PTHrP as well as other serum calcium-regulating hormones in 106 patients with non-insulin-dependent diabetes mellitus (NIDDM) and 43 control subjects. The serum concentration of intact PTH was 2.34 +/- 0.13 (mean +/- SEM) pmol/l in NIDDM patients, which is significantly lower than the value of 3.11 +/- 0.14 pmol/l in the controls (p < 0.01). Both serum calcium and calcitonin, however, were not statistically different from controls. On the other hand, circulating PTHrP in NIDDM was 40.1 +/- 1.4 pmol/l, which is significantly elevated when compared to 27.3 +/- 1.3 pmol/l in the controls (p < 0.01). Moreover, urinary excretion of PTHrP also was significantly higher in NIDDM (p < 0.01). In the present study, the circulating calcium level was well preserved in NIDDM patients, although the PTH levels were shown to be decreased. The elevated serum PTHrP might, therefore, have a physiologically compensatory role on the calcium regulatory systems in NIDDM. Furthermore, this elevation is most likely due to the excess production of this peptide and not to the decrease in urinary excretion.
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PMID:Possible compensatory role of parathyroid hormone-related peptide on maintenance of calcium homeostasis in patients with non-insulin-dependent diabetes mellitus. 810 85

Hormonal control of skeletal growth, modeling, and remodeling is characterized by a complex interaction between the calciotropic hormones (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, parathyroid hormone, and calcitonin), growth, and thyroid hormones in addition to the estrogenic and androgenic gonadal hormones. Although both growth and thyroid hormones are essential skeletal growth and modeling and also can produce detrimental skeletal effects in adults when circulating in excess concentrations, these hormones assume a minor role in the day-to-day bone remodeling of the mature skeleton. Following the attainment of the peak bone mass, bone mineral content begins to decline in the fourth and fifth decades of life, accelerating in females in the first 5-7 years after the menopause as a result of estrogen deficiency. Associated with this age-dependent loss in skeletal mass are decreases in calcitonin reserve primarily in the 5-7 years following the menopause, decreases in circulating 25-hydroxycholecalciferol, intestinal resistance to 1,25-dihydroxycholecalciferol, and a gradual progressive rise in blood parathyroid hormone. These changes in calciotropic hormone profiles, together with poor nutritional habits, anticonvulsant, glucocorticoid, and thyroid medications, diseases such as type I diabetes, immobilization, or decreased physical activity all serve to weaken the aging skeleton. The result is a gradual and subtle change in skeletal anatomy, which progresses to alterations in vertebral structure, such as kyphosis, scoliosis, and pseudospondylolisthesis, and a variety of sciatic and nerve entrapment syndromes. Vertebral, forearm, and hip fractures and edentulism ultimately comprise the syndrome of age-related bone loss, resulting in lifestyle disabilities, extensive morbidity, analgesic drug abuse, hospitalization, and escalating annual health care expenditures.
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PMID:Hormonal alterations and osteoporotic syndromes. 812 20

The plasma membrane enzyme (Ca2+ + Mg2+)-adenosine triphosphatase [(Ca2+ + Mg2+)-ATPase] is hormonally regulated, and may participate in Ca2+ signaling by removing excess Ca2+ from the cell. Insulin increases ATPase activity in kidney cortical basolateral membranes (BLM) from normal rats, but fails to do so in membranes from insulin-resistant non-insulin-dependent diabetic (NIDDM) rats. To investigate mechanisms of insulin regulation of ATPase and to evaluate whether the loss of this regulation in diabetes is hormone-specific and depends on blood glucose levels, (Ca2+ + Mg2+)-ATPase function and its hormonal regulation were studied in kidney BLM from rats with mild and severe NIDDM. Km values for ATP and Ca2+ affinity of the ATPase were similar in diabetic and control rats, but the maximal velocity (Vmax) of the enzyme was higher in diabetic groups. Insulin, the protein kinase C (PKC) stimulator 12-0-tetradecanoylphorbol 13-acetate (TPA), parathyroid hormone (PTH), and cyclic adenosine monophosphate (cAMP) all increased the ATPase activity in BLM from controls by increasing the enzyme's affinity for Ca2+. A protein kinase A (PKA) inhibitor (H8 in low concentrations) abolished cAMP and PTH effects, but not those of insulin, whereas the PKC inhibitors (sphingosine and high concentrations of H8) did abolish the effects of insulin. Stimulations of ATPase activity by insulin and by PTH and cAMP were additive. Insulin and TPA lost their stimulatory effects on ATPase in BLM from rats with either mild or severe NIDDM, but PTH and cAMP maintained their stimulatory effects in these membranes. The data show [1] (Ca2+ + Mg2+)-ATPase activity is increased in NIDDM, and a hormone-specific loss of insulin stimulation of ATPase occurs; (2) these defects are not dependent on the level of glycemia; and (3) the stimulatory effects of insulin on the ATPase may be mediated in part via PKC. We suggest that the hormone-specific defect in insulin regulation of ATPase seen in the NIDDM rats may contribute to their insulin resistance.
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PMID:Hormone-specific defect in insulin regulation of (Ca2+ + Mg2+)-adenosine triphosphatase activity in kidney membranes from streptozocin non-insulin-dependent diabetic rats. 817 49


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