Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary excretion of calcium, inorganic phosphorus, magnesium, glucose, and creatinine was measured in first-void spot urine samples collected 4 days apart in 220 insulin-dependent diabetic (IDDM) children (mean age 11.9 yr) attending a summer camp. A single control urine sample was obtained from 33 healthy nondiabetic siblings (mean age 11.2 yr). Mean +/- SD urinary calcium-creatinine ratios (UCa/Cr) did not significantly differ between IDDM and control subjects (0.14 +/- 0.09 vs. 0.12 +/- 0.09, respectively, P = 0.156). Mean urinary magnesium-creatinine ratios (UMg/Cr) were elevated in IDDM compared with control subjects (0.15 +/- 0.06 vs. 0.08 +/- 0.03, respectively, P = 0.0001). Similarly, mean urinary phosphorus-creatinine ratios (UP/Cr) were significantly increased over those in control subjects (1.12 +/- 0.33 vs. 0.40 +/- 0.22, respectively, P = 0.0001). UCa/Cr, UMg/Cr, and UP/Cr were correlated with increasing mean urine glucose content (P = 0.0001). No correlations were found when UCa/Cr, UMg/Cr, or UP/Cr were compared with patient age, duration of diabetes, glycosylated hemoglobin, or insulin dosage. Urine losses of phosphorus and magnesium were present even when glycemic control was considered good by several methods (glycosylated hemoglobin, short-term glycemic index, or urinary glucose content). Glomerular hyperfiltration was unable to account for increased urinary mineral content. In conclusion, the data indicate that urinary excretion of phosphorus and magnesium is elevated in children with IDDM, regardless of glycemic control. In the presence of glucosuria, this loss is further enhanced. Urinary calcium excretion is significantly higher only during periods of glucosuria. The data suggest that children with IDDM could be at risk for mineral deficiencies in the absence of intensive insulin management.
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PMID:Hyperphosphaturia and hypermagnesuria in children with IDDM. 218 Jun 62

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11

Many authors have described abnormalities of calcium homeostasis in type I diabetes mellitus, but data in the literature are conflicting. Consequently we studied calcium, phosphorus and magnesium (in serum and urine), parathyroid hormone, calcitonin and 25-hydroxyvitamin D (25-OHD) levels in 21 prepubertal diabetic patients and in 21 sex- and age-matched controls. We did not find any significant difference of all the aforementioned parameters between diabetics and controls. Also the value of 25-OHD was similar in diabetic and healthy subjects (24.33 +/- 6.04 vs 22.09 +/- 5.01 ng/ml). The results suggest that the principal parameters of calcium metabolism are normal in prepubertal diabetic children.
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PMID:Calcium homeostasis in prepubertal diabetic children. 322 92

A case of an 18-year-old female with polyglandular autoimmune syndrome (PGA) type 1 complicated by slowly progressive IDDM was described. She had epilepsy at the age of 5, and mucocutaneous candidiasis and hypoparathyroidism at 7 years. At the age of 18, the patient noticed thirst and body weight loss. On admission, she had uneven teeth and chronic mucocutaneous candidiasis. Plasma blood glucose was 312 mg/dl without ketosis, hemoglobin Alc 9.1%, serum calcium 3.5 mEq/l, serum phosphorus 6.0 mg/dl. A CT scan of her brain revealed calcification in the bilateral basal ganglia. Serum intact PTH was less than 10 pg/ml. Ellsworth-Howard's test showed hyperresponsiveness in the secretion of urinary phosphorus and cyclic-AMP. Other endocrinological studies showed no abnormality except for mild hyporesponsiveness in the secretion of urinary C-peptide (39.6 mu g/day). After admission, she was initially treated with diet alone with positive islet cell antibody (ICA). Three months later she was treated with low dose insulin, and ICA became negative. Then 5 months later it became positive again. Sixteen months later she had IDDM with positive ICA and without the secretion of urinary C-peptide. On the basis of these results, we diagnosed this case as PGA type 1 with the manifestations of hypoparathyroidism, chronic mucocutaneous candidiasis and slowly progressive IDDM. This is the second case report in Japan about PGA type 1. Furthermore, this case demonstrates for the first time in Japan that slowly progressive IDDM is complicated by PGA type 1. The patient had this HLA typing: A 24(9), BW52(5), BW60(40), CW3, DR2, DRW12, DQW7. More investigation is necessary to clarify the mechanism of PGA type 1.
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PMID:[A case of polyglandular autoimmune syndrome (PGA) type 1 complicated with slowly progressive IDDM]. 789 66

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

We aimed to determine the natural history of borderline increases in albuminuria in adolescents with insulin-dependent (Type 1) diabetes mellitus (IDDM) and factors which are associated with progression to persistent microalbuminura. Fifty-five normotensive adolescents with IDDM and intermittent microalbuminura (overnight albumin excretion ratte of 20-200 micrograms min-1 on one of three consecutive timed collections, n = 29) or borderline albuminura (mean overnight albumin excretion rate of 7.2-20 micrograms min-1 on one of three consecutive timed collections, n = 30) were followed prospectively at 3 monthly intervals. The endpoint was persistent microalbuminuria defined as a minimum of three of four consecutive overnight albumin excretion rates of greater than 20 micrograms min-1. One hundred and forty-two adolescents with IDDM and normoalbuminura were also followed prospectively. Fifteen of the 59 patients (25.4%) with intermittent (9/29) or borderline (6/30) albuminura progressed to persistent microalbuminura (progressors) over 28 (15-50) months [median (range)] in comparison with two of the 142 patients with normoalbuminuria at entry (relative risk = 12.6; p = 0.001). Progressors to persistent microalbuminura were pubertal and had higher systolic (p = 0.02) and diastolic (p = 0.02) blood pressure, and HbA1c (p = 0.004) than non-progressors. All patients remained normotensive. Glomerular filtration rate, apolipoproteins, dietary phosphorus, protein and sodium intakes, and prevalence of smoking did not differ between progressors and non-progressors. Total renin was higher in the diabetic patients without a difference between progressors and non-progressors. In conclusion there is a relatively high rate of progression to persistent microalbuminuria in pubertal adolescents with borderline increases in albuminura and duration greater than 3 years. These patients require attention to minimize associated factors of poor metabolic control and higher blood pressure in the development of incipient nephropathy.
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PMID:Progression of borderline increases in albuminuria in adolescents with insulin-dependent diabetes mellitus. 930 Feb 27

The aim of the study was to evaluate whether in diabetics with good metabolic control and without any diabetic complications, disturbances of calcium, phosphorus and magnesium metabolism or hormonal regulation (parathormone/calcitonin) were present, and if they depended on type of diabetes, duration time of diabetes, kind of hypoglycaemic treatment, sex or age of patients. 83 subjects were examined, including: 14 with type 1 diabetes mellitus, 49 with type 2 diabetes mellitus and 20 healthy persons. All tests were performed in standarized low-calcium diet conditions. In basal conditions both serum concentrations and daily urine excretion of calcium, phosphorus, magnesium were estimated. Oral and intravenous calcium load tests with simultaneous parathormone, calcitonin, calcium, magnesium and phosphorus concentrations estimation were done. The final conclusions were as follow: Both in type 1 diabetes mellitus and type 2 diabetes mellitus subjects with good metabolic compensation and without advanced diabetic complications a tendency to early disturbances of calcium-phosphorus metabolism is observed. Physiological hormonal control (parathormone/calcitonin) is preserved. Correlations between mineral metabolism and type of diabetes, duration time of diabetes, daily insulin dose, body mass index and sex are observed. Kind of hypoglycaemic treatment has only slight influence on the mineral metabolism.
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PMID:[Bone complication in diabetic subjects with good metabolic control and without any late complications: selected problems. Part I: calcium, phosphorus and magnesium metabolism]. 1160 76

The aims of this study were to evaluate bone mineral density (BMD) and bone turnover markers in patients with type 1 diabetes and screening-identified evidence of celiac disease, i.e., celiac autoimmunity. We screened 50 consecutive type 1 diabetic patients for IgA antitissue transglutaminase to identify those with celiac autoimmunity. Eight seropositive patients were identified on this screening, and 12 patients matched for gender and age range were selected as a control group from among the type 1 diabetic patients without celiac autoimmunity. Patients and controls underwent dual-energy X-ray absorptiometry (DEXA) for measurement of bone mineral status and had their blood levels of osteocalcin, carboxy-terminal telopeptide of type I collagen (CTX), calcium, and phosphorus determined. BMD was further adjusted for height, weight, and pubertal stage. Radiographic and blood markers of bone mineralization were compared between patients and controls. BMD (Z-score) at the lumbar spine was -1.44 +/- 0.5 SD for patients and 0.04 +/- 0.2 SD for controls (P = 0.02). Bone mineral content was 37.9 +/- 4.5 g for patients and 49.4 +/- 2.6 g for controls (P = 0.049). Adjusted BMD was -0.62 +/- 0.5 SD for patients and 0.81 +/- 0.09 SD for controls (P = 0.04). After adjustment, four patients and none of the controls presented BMD < -1 SD (P = 0.01). Osteocalcin, CTX, calcium, and phosphorus blood levels were not significantly different between patients and controls. Celiac autoimmunity is associated with reduced bone mineralization in type 1 diabetic patients. The pathophysiological mechanisms and clinical relevance of this finding remain to be further investigated.
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PMID:Bone mineralization in young patients with type 1 diabetes mellitus and screening-identified evidence of celiac disease. 1793 41

Epidemiological studies suggest a link between vitamin D deficiency in early life and the later onset of type 1 diabetes. The aim of this matched case-control study was to find the association between vitamin D and T1DM then to study the difference in the level of vitamin D in T1DM and healthy subjects, and to determine the associated environmental risk factors in young Qatari population. The study was carried out among T1DM children and healthy subjects below 16 years at the pediatric endocrinology outpatient clinics of the Hamad General Hospital and the Primary Health care Clinics (PHCs). The survey was conducted over a period from 6 August to 25 December 2007. The subjects were Qatari nationals male and female aged below 16 years. The study is based on matching by age, gender and ethnicity of 170 cases with those of 170 controls. Face-to-face interviews were based on a questionnaire that included variables such as socio-demographic information, assessment of non-dietary covariates, assessment of dietary intake, vitamin D intake, type of feeding, clinical manifestations and laboratory investigations. Their health status was assessed by medical conditions, family history, BMI, past or present clinical manifestations, 25 (OH)D, Calcium, alkaline phosphatase, phosphorus, HbA1C, PTH, Mg and creatinine analysis. The study revealed that vitamin D deficiency was considerably higher in T1DM children (90.6%) compared to non-diabetic children (85.3%). There was a significant difference found in the mean value of vitamin D between T1DM and non-diabetic children (P = 0.009). There were statistically significant differences between type 1 diabetic and healthy subjects with respect to the occupation of parents (P < 0.001) and consanguinity rate (P < 0.047). Family history of vitamin D deficiency was considerably higher among T1DM children (35.3%) with a significant difference between diabetic and non-diabetic children (22.9) (P < 0.012). Vitamin D supplement with breast milk was very poor in diabetic children (37.4%) compared to non-diabetic children (47.7%). Majority of the studied subjects were breast-fed children (95.1% of diabetic children and 97.2% of healthy children). Multivariate logistic regression analysis revealed that fathers and mothers occupation, family history of DM, physical activity, low duration of time under sun light, breast feeding less than 6 months and low vitamin D level were considered as the main factors associated with the T1DM. In conclusion, the present study revealed that vitamin D deficiency was higher in T1DM children compared to non-diabetic. Moreover, vitamin D deficiency was common in Qatari young population. Vitamin D intake was very poor in children and it shows that supplementing infants with vitamin D might be a safe and effective strategy for reducing the risk of T1DM.
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PMID:High prevalence of vitamin D deficiency in type 1 diabetes mellitus and healthy children. 1884 17

1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), the active form of vitamin D, is known to regulate calcium and phosphorus metabolism, thus being a key-player in bone-formation. However 1,25(OH)(2)D(3) also has a physiological role beyond its well-known role in skeletal homeostasis. Here, we describe 1,25(OH)(2)D(3) as an immunomodulator targeting various immune cells, including monocytes, macrophages, dendritic cells (DCs), as well as T-lymphocytes and B-lymphocytes, hence modulating both innate and adaptive immune responses. Besides being targets, immune cells express vitamin D-activating enzymes, allowing local conversion of inactive vitamin D into 1,25(OH)(2)D(3) within the immune system. Taken together, these data indicate that 1,25(OH)(2)D(3) plays a role in maintenance of immune homeostasis. Several epidemiological studies have linked inadequate vitamin D levels to a higher susceptibility of immune-mediated disorders, including chronic infections and autoimmune diseases. This review will discuss the complex immune-regulatory effects of 1,25(OH)(2)D(3) on immune cells as well as its role in infectious and autoimmune diseases, more in particular in tuberculosis and type 1 diabetes (T1D).
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PMID:Vitamin D: modulator of the immune system. 2042 38


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