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)

To assess the effects of diabetes mellitus on renal osteodystrophy, we examined the database of 256 patients (45% on hemodialysis and 55% on peritoneal dialysis) who were prospectively studied in three Toronto dialysis centers between October of 1987 and 1989. All patients had serial documentation of their clinical, laboratory and risk parameters of bone disease, and completed a series of investigations that included the deferoxamine test, measurement of intact 1-84 PTH levels, and an iliac crest bone biopsy. Twenty-five percent of these patients were diabetic. When compared to non-diabetic patients, they were on dialysis for a shorter duration (2.4 +/- 0.3 vs. 4.7 +/- 0.3 years; P < 0.0002), used calcium carbonate as the only phosphate binder more frequently (40 vs. 25%; P < 0.007), and had lower parathyroid hormone levels (12 +/- 1.4 vs. 24 +/- 2.3 pmol/liter; P < 0.002). High-turnover bone disorders (that is, osteitis fibrosa and mixed disorder) were distinctly uncommon (8 vs. 33%; P < 0.01 by Fisher's exact test), while the mild (19 vs. 9%; P = NS) and the aplastic disorders (with mean stainable bone surface aluminum of 6.5 +/- 0.7%) (46 vs. 31%; P = NS) tended to be more common in diabetic patients. The prevalence of aluminum bone disease was the same in both groups (27%). Diabetic patients ingested a smaller cumulative dose of aluminum gels (3.7 +/- 0.6 vs. 9.3 +/- 1.1 kg; P < 0.005), yet had a higher rate of aluminium accumulation on bone surfaces than non-diabetic patients (1.5 +/- 0.19 vs. 0.96 +/- 0.10% per month on dialysis; P < 0.015).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy in diabetic patients. 835 57

Both the cancellous and the cortical envelopes of the vertebral bone of osteopenic rats were histomorphometrically evaluated to elucidate the effect of an intermittent administration of h-PTH (1-34) on bone remodeling. Seven-eight-month-old female Wistar rats were used, and osteopenia was produced by ovariectomy, by prednisolone administration, or by streptozotocin-induced diabetes mellitus. The rats were divided into 10 groups; as base line control rats, vehicle administered rats, and h-PTH administered rats for each of the three kinds of osteopenia, and sham operated rats. Vehicle or h-PTH was administered subcutaneously six times a week from the 9th to the 12th week of the experiment. The dosage of h-PTH was 6.0 micrograms/kg. Ovariectomy developed a high turn-over osteopenia, and prednisolone administration and diabetes mellitus caused a low turn-over osteopenia. All 3 kinds of osteopenia showed similar changes in histomorphometric parameters after h-PTH treatment. In the cancellous envelope, the bone volume increased significantly in all groups. The trabecular thickness, osteoid surface, mineralizing surface, mineral apposition rate, and the bone formation rate increased in all groups after the treatment with h-PTH. The eroded surface significantly decreased except in the diabetes mellitus rats. In the endocortical envelope, the osteoid surface, mineralizing surface and the mineral apposition rate increased in all groups. The eroded surface significantly decreased in all groups after the treatment with h-PTH. The cortical thickness significantly increased except in the ovariectomized rats. The results of the present study suggested that an intermittent administration of h-PTH stimulated bone formation without increasing bone resorption in all three kinds of osteopenia induced by ovariectomy, corticosteroid, or diabetes mellitus.
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PMID:[Effect of intermittent administration of human PTH on experimental osteopenia in adult rat: a histomorphometric study of both trabecular and cortical bone of the vertebrae]. 855 Oct 88

We have evaluated changes in bone volume, bone marrow tissue, and the density of osteoclasts caused by intermittent administration of human parathyroid hormone (h-PTH) to experimental osteopenia induced in rat by ovariectomy (OVX) or by diabetes mellitus (use of streptozotocin: STZ). A bone and marrow histomorphometric study was performed on HE-stained and tartrate-resistant acid phosphatase-stained (TRAP-stain) tibial bone sections. Retired Wistar rats, 7-8 months old, were used. They were separated into the following nine groups; sham operated, base line control, vehicle administered, low or high dosage h-PTH administered OVX and STZ groups. 6.0 micrograms/kg/day of h-PTH (1-34) as a low dosage, and 60.0 micrograms/kg/day as a high dosage, was injected subcutaneously six times a week for 4 weeks from 9 weeks after ovariectomy or injection of streptozotocin. The bone volume decreased in both the OVX and STZ groups, while the fat tissue volume increased in the bone marrow in the OVX groups to compensate for this decrease, and the foamy marrow tissue volume increased in the STZ groups. The bone volume and the mean trabecular thickness in both the OVX and STZ groups increased by the intermittent administration of h-PTH, while the TRAP positive trabecular surface and the number of osteoclasts decreased. There was no significantly different bone changes between the low and high dosage groups. It is thought that the TRAP positive trabecular surface represented not only the active bone resorption surface but also the related contiguous uneroded surface.
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PMID:[Effect of h-PTH on bone and bone marrow tissue in experimental osteopenia in rat]. 855 Nov

To assess the effect of different dialysis modalities on calcium turnover, we studied 57 patients on maintenance hemodialysis treatment (HD) and 38 patients on continuous ambulatory peritoneal dialysis (CAPD) with tracer kinetic studies using two calcium isotopes (45Ca by mouth and 47Ca intravenously). The two groups were comparable in age, sex and prevalence of diabetes. The groups did not differ in their serum concentrations of intact parathyroid hormone (iPTH), calcium, inorganic phosphate and 1,25-dihydroxyvitamin D. 25-hydroxy-vitamin D and alkaline phosphatase were found to be significantly higher in HD patients. Despite these similarities, CAPD patients showed a significantly lower calcium kinetic response as measured by calcium retention and plasma calcium efflux than HD patients. Mean calcium retention was 39.5% in HD patients compared to 31.2% in the CAPD group (p < 0.05). Plasma calcium efflux was significantly lower in the CAPD group (2.7 vs 3.2 respectively; p < 0.01). iPTH correlated with calcium retention and plasma calcium efflux in HD patients (r = 0.69 and r = 0.67 respectively). In CAPD patients, the correlation coefficient between iPTH and calcium retention was markedly lower (r = 0.54), whereas no correlation was found between iPTH and plasma calcium efflux (r = 0.08). In addition, the slope of the correlation curve were higher in HD patients (p < 0.01 and p < 0.001, respectively), indicating a better response of this patient group to the action of parathyroid hormone. Our data are in accordance with recently published results showing that the dialysis modality has a major impact on bone turnover and on the progression of uremic bone disease. It has been shown that CAPD is an independent risk factor for the development of the adynamic form of renal bone disease. This finding may be explained by the lower response of calcium turnover to the action of PTH as shown here with tracer kinetic studies.
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PMID:Differences in calcium kinetic pattern between CAPD and HD patients. 857 26

We report 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 NIDDM in this patient may have been related to an insulin secretory defect as a result of hypocalcemia in addition to the hereditary risk.
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PMID:Non-insulin-dependent diabetes mellitus complicated with idiopathic hypoparathyroidism. 858 May 67

To analyze the relative contribution of endocrine and physical factors to bone mineral density (BMD) in late menopause, we studied biochemical markers of bone turnover as well as sex and calciotropic hormones in 53 women (mean age 61 +/- 5.3 years), 5 to 23 years after natural menopause. BMD was measured at the lumbar spine and proximal femur by dual energy radiography. Stepwise regression analysis showed that age and PTH levels were the two major factors that significantly accounted for spinal BMD, with a final r2 = 0.27. Plasma androstenedione was the only other variable that contributed, albeit not significantly, to spine BMD increasing the r2 by 2%. Conversely, body mass was the main contributor to femoral BMD at all sites. While serum calcium and urinary hydroxyproline were significant determinants of neck BMD, urinary hydroxyproline and age provided significant source of variation for trochanteric BMD, and circulating FSH for BMD in the Ward's area. The final models gave r2 values of 0.35, 0.31, and 0.23, for neck, trochanter and Ward's areas, respectively. Thus, determinants of bone density differentially affect the vertebral and proximal femoral sites. While increasing age and PTH, probably reflecting a subclinical vitamin D deficiency, explain a decreased vertebral bone density, body mass appears to affect mostly the proximal femur. Circulating androgens play a secondary role. A persistently increased bone turnover state is conducive to lower bone density in late postmenopausal women.
Exp Clin Endocrinol Diabetes 1996
PMID:Endocrine and physical determinants of bone mass in late postmenopause. 881 45

This paper presents a 59-year-old man who was admitted to our hospital because of abdominal pains in 1973. He had pancreatic calcification and showed high levels of serum amylase, Ca, and PTH. He was diagnosed as primary hyperparathyroidism with chronic pancreatitis. After excision of an ectopic parathyroid adenoma, serum Ca levels were decreased and normalized by dihydrotachysterol p.o. At the same time his symptoms disappeared. The exocrine and endocrine pancreatic functions, however, decreased gradually. Diabetes mellitus appeared in 1975 and he required insulin injection since 1983. In spite of the treatment, his diabetic control was poor. Seventeen years later in 1992, he showed hypertension and edema (nephrotic syndrome). Because of renal failure, he underwent hemodialysis and passed away due to myocardial infarction in 1993. Autopsy findings showed existence of diabetic nephropathy as the cause of renal failure. Clinical course of this patient suggests that severe complications occur even in pancreatic diabetes and that we have to control diabetes strictly in pancreatic diabetes as well as in primary diabetes.
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PMID:[An autopsy case of renal failure as its cause of death in a patient with primary hyperparathyroidism associated with chronic pancreatitis]. 894 Aug 1

We report a 17-year-old girl with short stature, external ophthalmoplegia, atypical retinal pigmentary degeneration, sensorineural hearing loss, and cardiac conduction defect (Kearns-Sayre syndrome). A large-scale deletion (6741 base pairs) in mitochondrial DNA was found in her muscle specimen. She also had insulin-dependent diabetes mellitus (IDDM). On admission, her plasma glucose level was elevated at 31.0mmol/l with mild ketoacidosis, and haemoglobinA1c elevated at 16.5%. After improvement of diabetic ketoacidosis, she was placed on insulin 24-30 units/day despite her small body weight of 25 kg. There was reduced excretion of urinary C-peptide at 3.97 nmol/day. In addition, she had idiopathic hypoparathyroidism with a serum calcium level of 2.15 mmol/l, phosphate 1.7 mmol/l, and intact PTH below 10 ng/l. Human leucocyte associated antigen typing showed A24, A26; B54, B61; CW1, CW3; DR8, DR14; DQ1 and DQ3, suggesting that the presence of HLA-A24 and CW3 antigen contributed to the association of IDDM and hypoparathyroidism, similar to Japanese patients with polyglandular autoimmune syndrome, complicated by hypoparathyroidism and IDDM. We suggest that a genetic linkage, as well as mitochondrial dysfunction, may be responsible for the association of the two disease states. This is an extremely rare case of Kearns-Sayre syndrome, presenting in association with IDDM and idiopathic hypoparathyroidism.
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PMID:Hypoparathyroidism and insulin-dependent diabetes mellitus in a patient with Kearns-Sayre syndrome harbouring a mitochondrial DNA deletion. 897 63

An elevation in intracellular calcium ([Ca2+]i) in rats with chronic renal failure and elevated blood levels of PTH is associated with down-regulation of the mRNA of many proteins. Similarly, in phosphate depleted animals that have normal renal function and low blood levels of PTH, [Ca2+]i is elevated and the mRNA of PTH-PTHrP receptor is down-regulated. The effect of elevation in [Ca2+]i on molecular machinery of many proteins may represent a generalized phenomenon. Diabetes mellitus may also be associated with a rise in [Ca2+]i and therefore down-regulation of the mRNA of proteins may also occur. The present study examined the effect of streptozotocin-induced diabetes mellitus in rats on the [Ca2+]i of the renal proximal tubular cells and on their mRNAs of the PTH-PTHrP, V1a and AT1 receptors. The basal levels of [Ca2+]i of these cells increased significantly (P < 0.01) after one day of diabetes and remained elevated thereafter. There was a significant (r = 0.67, P < 0.01) direct correlation between the [Ca2+]i of the cells and blood levels of glucose up to 350 mg/dl, and the value of [Ca2+]i plateaued with higher concentrations of glucose. Three days of amlodipine therapy prevented and reversed the elevated levels of [Ca2+]i despite marked hyperglycemia. The mRNA of all three receptors in the kidney were down-regulated and this defect was prevented by amlodipine which normalized the [Ca2+]i of the cells. The results show that: (1) the hyperglycemia of IDDM in rats causes a significant elevation in the basal levels of [Ca2+]i of the renal proximal tubular cells and down-regulation of their mRNA of PTH-PTHrP, V1a and AT1 receptors; (2) normalization of the [Ca2+]i of these cells by treatment of the diabetic rats with amlodipine prevented the elevation of [Ca2+]i and the down-regulation of the mRNA of these receptors; (3) these effects occurred in the presence of normal renal function and normal blood of PTH and phosphorus.
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PMID:Elevation of [Ca2+]i of renal proximal tubular cells and down-regulation of mRNA of PTH-PTHrP, V1a and AT1 receptors in kidney of diabetic rats. 918 88

Na+/H+ exchange (NHE) was measured as maximal initial velocity of pH-dependent H+ efflux from red cells into an alkaline medium containing Na+ in patients with insulin-dependent or noninsulin-dependent diabetes, with and without hypertension and in normoglycemic, essential hypertensives and normal controls (50 subjects in each subgroup). Maximal velocities of NHE were found in microalbuminuric patients in all subgroups, and NHE correlated with the rate of micro-albuminuria (r = 0.61, p = 0.02). Daily insulin requirements were greater in those with elevated NHE (84 +/- 8 vs 42 +/- 4 U/day). There was no correlation between NHE and levels of plasma glucose, HbA1 and plasma aldosterone and lipid profile and PRA. NHE was correlated with plasma prolactin (r = 0.51, p = 0.02) and PTH r = 0.24, p = 0.05). In uremic patients, NHE was inversely correlated with creatinine clearance (r = -0.48, p = 0.03). Since calphostin C, a selective inhibitor of protein kinase C, lowered increased NHE in vitro, the protein kinase C-dependent pathway of the exchanger regulation was concluded to be responsible for NHE activation in diabetes mellitus and essential hypertension.
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PMID:[Red cell Na+/H+ exchange and role of protein kinase C in its stimulation in diabetes mellitus, essential hypertension and nephropathy]. 922 70


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