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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a muscle bath technique the vascular response to KCl, noradrenaline, angiotensin II, acetylcholine, and sodium nitroprusside were evaluated in 13 patients with diabetes mellitus (DM group) and 15 nondiabetic (non-DM group) chronic renal failure patients treated with haemodialysis. There were no differences in age, duration of haemodialysis, blood pressure and the levels of plasma renin activity, noradrenaline, and parathyroid hormone between groups. After informed consent was obtained, a small piece of forearm vein was resected during the blood access surgery. The ring preparation of the blood vessel was sustained in the muscle bath filled with Krebs-Henseleit solution and the isometric tension development was recorded. All drugs produced concentration dependent responses in the ring preparations of both groups. Although there were no significant differences in Emax values for KCl- and angiotensin-II-induced contractions between groups, the value for noradrenaline in the DM group was significantly less than that in the non-DM group. Sodium nitroprusside completely relaxed the ring preparation precontracted by 10(-5) M noradrenaline. However, the response to acetylcholine in the DM group was significantly weaker than that in the non-DM group. These results suggest a reduced vascular response to noradrenaline and acetylcholine in dialysed diabetic renal failure patients, which may relate to the autonomic nervous system dysfunction.
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PMID:Vascular response to vasoactive agents in dialysed patients with chronic renal failure with and without diabetes mellitus. 817 67

To investigate bone mineral metabolism in insulin-dependent diabetes mellitus, serum osteocalcin, a marker of bone formation, was measured in 31 diabetic children at onset of disease and 15 days after metabolic improvement by insulin therapy. As a control group for osteocalcin levels we studied 31 healthy sex- and age-matched children. Mean values of serum osteocalcin at onset of diabetes were significantly lower than in control group (p < 0.001), but we did not find any difference after 15 days of insulin therapy. Osteocalcin and parathyroid hormone concentrations were significantly greater after 15 days of insulin treatment than at onset of disease (p < 0.001 and p < 0.01, respectively). The osteocalcin levels were negatively correlated both with fructosamine and with glycosylated hemoglobin (p < 0.01 and p < 0.001, respectively), and positively correlated with the degree of metabolic acidosis at onset (p < 0.05). Therefore we postulate that during glycometabolic imbalance there is a decrease in bone turnover that could be one of the etiological factors of diabetic osteopenia.
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PMID:Effect of insulin treatment on osteocalcin levels in diabetic children and adolescents. 822 79

We evaluated 259 dialysis patients using serum parathyroid hormone (PTH, IRMA; normal range 1 to 5.5 pM or 10 to 55 pg/ml), the deferoxamine infusion test and iliac crest bone biopsy to determine the various forms of renal osteodystrophy and their risk factors. Although half of the biopsied patients had low turnover osteodystrophy, evidence of aluminum toxicity was present in only 1/3 of them. Additional risk factors for this bone lesion included treatment with peritoneal dialysis, ingestion of calcium carbonate, diabetes mellitus and advanced age. The PTH levels in patients with the aplastic lesion were significantly lower than in patients with normal or high bone turnover lesions [7.7 +/- 6.1 vs. 36.9 +/- 3.2 pM (77 +/- 61 vs. 369 +/- 32 pg/ml), P < 0.0001]. Aside from hypercalcemia, these patients were relatively asymptomatic. In a second study, 10 patients on peritoneal dialysis with the aplastic lesion had their dialysate calcium lowered from 1.62 to 1.0 mM. This resulted in a significant increase in PTH levels, from [3.7 +/- 0.8 to 10.6 +/- 1.9 pM (37 +/- 8 to 106 +/- 19 pg/ml), P < 0.001] which persisted over the nine-month observation period. In conclusion, the aplastic lesion is the most common form of renal osteodystrophy, with aluminum intoxication implicated in only 1/3 of the cases. In the remainder, factors identified include therapy with peritoneal dialysis using supraphysiological dialysate calcium, oral CaCO3 intake and diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aplastic osteodystrophy without aluminum: the role of "suppressed" parathyroid function. 825 62

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

Glucagon and the glucagon receptor are a primary source of control over blood glucose concentrations and are especially important to studies of diabetes in which the loss of control over blood glucose concentrations clinically defines the disease. A complementary DNA clone for the glucagon receptor was isolated by an expression cloning strategy, and the receptor protein was expressed in several kidney cell lines. The cloned receptor bound glucagon and caused an increase in the intracellular concentration of adenosine 3', 5'-monophosphate (cAMP). The cloned glucagon receptor also transduced a signal that led to an increased concentration of intracellular calcium. The glucagon receptor is similar to the calcitonin and parathyroid hormone receptors. It can transduce signals leading to the accumulation of two different second messengers, cAMP and calcium.
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PMID:Expression cloning and signaling properties of the rat glucagon receptor. 838 75

We have assessed the bone histology in 259 chronic dialysis patients, all of whom were in the same dialysis program. All patients had bone biopsies with quantitative histomorphometry, intact parathyroid hormone (PTH) measurements, basal and deferoxamine stimulated serum aluminum levels. Results demonstrate the increased incidence of the recently described aplastic bone lesion, particularly in patients treated with peritoneal dialysis (PD). Aluminum-related bone disease is much less common than previously described, perhaps in relation to the declining use of aluminum as a phosphate binder. A different pattern of bone lesions is seen in PD as compared with hemodialysis (HD), with low turnover disorders comprising 66% of the lesions seen in PD and high turnover lesions accounting for 62% of the bone histologic findings in HD. The difference in these patterns may relate to alterations in PTH levels, as mean PTH levels in HD patients were 2-1/2 times the levels found in PD patients (P < 0.0005), while older age, higher prevalence of diabetes and a shorter duration of dialysis may also have contributed to the findings in the PD patients. We suggest that PD, perhaps by maintaining calcium at higher levels, may more effectively suppress the parathyroid gland.
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PMID:The spectrum of bone disease in end-stage renal failure--an evolving disorder. 844 Dec 40

Reduced bone mass occurring with increased frequency in diabetes mellitus has been attributed to poor blood glucose control but the pathogenetic mechanisms remain unknown. To evaluate the role of calcium metabolism, 59 patients with diabetes and normal renal function (22 Type 1, 37 Type 2) were studied. In all patients plasma calcium (Ca), serum phosphate (PO4), serum parathyroid hormone (PTH), and 24-h urinary calcium (uCa) were determined under both poor and improved control (for at least 7 days) as ascertained by four blood glucose determinations daily. Improvement of blood glucose control (p = 0.001) was associated with reduction of uCa both in Type 1 (6.9 +/- 1 vs 4.9 +/- 0.9 mmol day-1, mean +/- SEM, p = 0.02) and in Type 2 patients (4.2 +/- 0.4 vs 3.2 +/- 0.4 mmol day-1, mean +/- SEM, p = 0.002). Considerably more Type 1 patients (10 out of 22) had PTH values below the detection limit (1.5 pmol l-1) during poor than during improved control (2 out of 22). Comparison between the two types of diabetes showed that in Type 1 under poor control, Ca and PTH were lower (p = 0.03), while uCa was higher (p = 0.003), and after improved control, only uCa continued to be higher (p = 0.035). These findings suggest that increased uCa excretion in association with 'functional hypoparathyroidism' (especially in Type 1 diabetes) is observed during poor blood glucose control, and may be one of the factors leading to reduced bone mass in diabetes mellitus.
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PMID:Calcium metabolism in diabetes mellitus: effect of improved blood glucose control. 850 17

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

Activation of osteoclasts by parathyroid hormone (PTH) is mediated by PTH stimulation of osteoblasts, and is dependent on a PTH-induced rise in protein kinase C activity. Physiological levels of insulin reduce the ability of PTH to activate protein kinase C in osteoblasts, suggesting that insulin may be a physiological antagonist of bone resorption. In addition, insulin is known to promote collagen production by osteoblasts. These findings imply that efficient insulin activity may exert an anabolic effect on bone, and rationalize the many clinical studies demonstrating reduced bone density in Type I diabetes. Recently, the insulin-sensitizing nutrient chromium picolinate has been found to reduce urinary excretion of hydroxyproline and calcium in postmenopausal women, presumably indicative of a reduced rate of bone resorption. This nutrient also raised serum levels of dehydroepiandrosterone-sulfate, which may play a physiological role in the preservation of postmenopausal bone density. The impact of chromium picolinate (alone or in conjunction with calcium and other micronutrients) on bone metabolism and bone density, merits further evaluation in controlled studies.
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PMID:Anabolic effects of insulin on bone suggest a role for chromium picolinate in preservation of bone density. 856 46

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


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