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)

Diabetes mellitus is the most common pathological state in which secondary magnesium deficiency occurs. Magnesium metabolism abnormalities vary according to the multiple clinical forms of diabetes: plasma magnesium is more often decreased than red blood cell magnesium. Plasma Mg levels are correlated mainly with the severity of the diabetic state, glucose disposal and endogenous insulin secretion. Various mechanisms are involved in the induction of Mg depletion in diabetes mellitus, i.e. insulin and epinephrine secretion, modifications of the vitamin D metabolism, decrease of blood P, vitamin B6 and taurine levels, increase of vitamin B5, C and glutathione turnover, treatment with high levels of insulin and biguanides. K depletion in diabetes mellitus is well known. Some of its mechanisms are concomitant to those of Mg depletion. But their hierarchic importance is not the same: i.e., insulin hyposecretion is more important versus K+ than versus Mg2+. Insulin increases the cellular inflow of K+ more than that of Mg2+ because there is more free K+ (87%) than Mg2+ (30%) in the cell. The consequences of the double Mg-K depletion are either antagonistic: i.e. versus insulin secretion (increased by K+, decreased by Mg2+) or agonistic i.e. on the membrane: (i.e. Na+K+ATPase), tolerance of glucose oral load, renal disturbances. The real importance of these disorders in the diabetic condition is still poorly understood. Retinopathy and microangiopathy are correlated with the drop of plasma and red blood cell Mg. K deficiency increases the noxious cardiorenal effects of Mg deficiency. The treatment should primarily insure diabetic control.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Magnesium and potassium in diabetes and carbohydrate metabolism. Review of the present status and recent results. 639 45

A significant loss of bone has been observed in diabetes mellitus. The pathogenesis is unknown, but an impairment of vitamin D metabolism might be involved. Consequently, we have studied vitamin D metabolism in five groups of insulin-dependent diabetic patients. Significantly reduced levels of serum 25(OH)D were seen only in patients with diabetic nephropathy. The serum levels of 1,25 (OH)2D were reduced only in diabetic ketoacidosis but normalized during recovery. It is concluded that vitamin D metabolism is largely normal in adult insulin-dependent diabetes, and it seems unlikely that a disturbance of the vitamin D metabolism can explain the bone loss in the ordinarily controlled diabetics.
 ...
PMID:Vitamin D metabolism in insulin-dependent diabetes mellitus. 642 48

Red blood cell (RBC) and polymorphonuclear white blood cell (WBC) calmodulin levels were measured in 25 uremic patients on regular hemodialysis. Uremic patients had significantly higher RBC [11.45 +/- 0.66 (+/-SE) fg/cell] and WBC (590.5 +/- 110 fg/cell) calmodulin levels than normal subjects (8.62 +/- 0.37 and 130 +/- 30 fg/cell; P less than 0.05). An extremely high RBC calmodulin level (20.58 fg/cell) was found in a patient with sickle cell anemia. Uremic patients on dialysis for 2 yr or more had lower RBC (10.99 +/- 0.58 fg/cell) and WBC (390 +/- 50 fg/cell) calmodulin levels than those who were on dialysis for less than 2 yr (RBC, 12.30 +/- 1.56 fg/cell; WBC, 943 +/- 256 fg/cell; P less than 0.05). There were no statistically significant differences in calmodulin levels when different subgroups of uremic patients were compared, e.g. patients with diabetes mellitus or those receiving supplemental vitamin D, anabolic steroids, or antihypertensive medications. We conclude that calmodulin levels are elevated in uremic patients on regular hemodialysis.
 ...
PMID:The effects of chronic renal failure and hemodialysis on human red and white cell calmodulin levels. 672 5

In order to elucidate if changes in vitamin D metabolism play a role for diabetic bone loss, the serum concentrations of the major vitamin D metabolites were studied in 26 adult male ambulatory insulin-treated diabetics, selected to have normal renal function and a duration of diabetes below 11 years. The patients were studied during usual metabolic control and exhibited wide ranges of hyperglycaemia and glycosuria. The serum concentrations of the major metabolites of vitamin D, 25-hydroxyvitamin D(2 + 3) (25OHD), 24,25-dihydroxyvitamin D(2 + 3) (24,25(OH)2D), and 1,25-dihydroxyvitamin D(2 + 3) (1,25(OH)2D), were measured in diabetics, and in age and sex matched controls. The diabetics had slightly decreased serum levels of 25OHD (42.0 nmol/l versus 55.5 nmol/l in normals, P less than 0.05), markedly decreased serum levels of 24,25(OH)2D (2.98 nmol/l versus 5.91 nmol/l, P less than 0.01), but serum levels of 1,25(OH)2D were virtually normal (64.2 pmol/l versus 68.3 pmol/l, ns). The close correlation between serum concentrations of 25OHD and 24,25(OH)2D observed in the normal subjects, was absent in the diabetics. There were no correlations between the serum levels of any of the vitamin D metabolites and the measured indices of glucose and calcium metabolism. It is concluded that insulin-dependent diabetic patients demonstrate definite alterations in serum levels of vitamin D metabolites, the significance of which remains unknown at present.
 ...
PMID:Vitamin D metabolites in diabetic patients: decreased serum concentration of 24,25-dihydroxyvitamin D. 676 Mar 73

Needs for virtually all nutrients increase during pregnancy and lactation but those for iron are the most difficult to meet from a normal diet. During pregnancy, nutritional objectives include helping the woman to increase the quality of her diet in protective nutrients as well as energy to meet the elevated needs of gestation, ensuring satisfactory weight gain patterns, prescribing iron and possible folic acid supplements, ensuring that intakes of alcohol, drugs, and other potentially harmful substances are moderate, preparing her for feeding the infant, and coping with any special diet-related problems that may arise. These issues and the management of edema, high blood pressure, and diabetes mellitus are discussed. Prenatal preparations for lactation and diet during lactation are also discussed. Specific objectives of nutritional education on lactation include helping the mother to make the decision to breast or bottle feed, taking steps to prepare her nipples if this is necessary and planning her diet. Dietary adjustments are discussed and a food guide presented. Iron supplements for ther lactating mother and iron, vitamin D, and fluoride supplements for the infant are recommended.
 ...
PMID:Nutritional support during pregnancy and lactation. 692 84

Recent autoradiographic studies demonstrated that B-cells concentrate 1,25 (OH)2 D3 in their nuclei, suggesting a genomic action on B-cell function. This study was undertaken to investigate the effects of 1,25 (OH)2 D3 on insulin secretion in vitamin D-deficient rats. Mature vitamin D-deficient rats were injected with 1,25 (OH)2 D3 or the ethanol-isotonic saline vehicle. Administration of 1,25 (OH)2 D3 to 10 rats resulted in a 17 microunits/ml (113%) increase in insulin levels and 0.9 mg/dl (16%) increase in plasma calcium. No changes were found in insulin or calcium levels in 5 control rats given vehicle alone. A group of vitamin D-deficient rats with plasma calcium levels of 5.4 +/- 0.1 mg/dl had insulin levels that were the same as those observed in a group of vitamin D-deficient rats with plasma calcium levels of 6.3 +/- 0.1 mg/dl. The difference in calcium levels between these two groups is similar to the increase in plasma calcium found after 1,25 (OH)2 D3 administration. The results of these studies indicate that 1,25 (OH)2 D3 action on pancreatic B-cells affects insulin secretion. Since insulin increases synthesis of 1,25 (OH)2 D3, the existence of a feedback loop between B-cells and kidney proximal tubule cells is suggested.
Diabetes 1981 May
PMID:Effect of 1,25 dihydroxyvitamin D3 on insulin secretion. 701 6

Several vitamins have been demonstrated to interfere with the pathogenesis of some metabolic diseases, mainly by three different mechanisms: 1) vitamin malabsorption, 2) errors in vitamin metabolism, 3) vitamin dependent syndromes. The latter is due to a deficiency of the apoenzyme whose coenzyme is the vitamin itself. In this case pharmacological, instead of nutritional doses of the vitamin may be needed. The vitamins which interfere with inborn metabolic errors are reviewed; for each vitamin the corresponding diseases which may be treated are indicated. The vitamins are: 1) thiamine (leucinosis); b) nicotinic acid (hyperlipoproteinemia); c) biotin (beta-methyl-crotonyl-glycinuria, propionic aciduria); d) pyridoxine (infantile convulsions, familial pyridoxine responsive anemia, homocystinuria, cystathioninuria, xanthurenicaciduria); e) cobalamins (congenital intrinsic factor deficiency, cobalamin malabsorption, transcobalamin deficiency, methylmalonic aciduria) f) folic acid (congenital folic acid malabsorption, formimino-transferase deficiency, methylenetetrahydrofolic reductase deficiency, Lesch-Nyhan syndrome); g) vitamin D (phosphatic diabetes, Prader's type rickets, Albright's syndrome; essential hereditary hypophosphatemia, etc). It is noteworthy that the vitamin therapy of these diseases, not only corrects the metabolic errors, but can also promote the healing or the amelioration of the psycho-physical growth, of central nervous system alterations and of other lesions.
 ...
PMID:[Vitamins in metabolic diseases]. 702 68

To assess the relationship between the decreased bone mass observed in young insulin-requiring diabetic patients and vitamin D metabolism, we measured serum 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D, and 1,25-dihydroxyvitamin D concentration in 45 white, insulin-dependent diabetic subjects, 7-18 yr of age. Metacarpal cortical thickness in 87% of these diabetics was below the mean for their respective ages, while 16% had a cortical thickness value greater than 2 sDs below the mean. Serum calcium and phosphate concentrations were normal, immunoreactive parathyroid hormone was in the low normal range, and total serum alkaline phosphatase was elevated compared to age- and sex-matched controls. Circulating 24,25-dihydroxyvitamin D concentrations were significantly elevated, and 1,25-dihydroxyvitamin D was significantly decreased. The increase in 24,25-dihydroxyvitamin D was greater in the diabetics with the most severe bone loss and was maximally increased during the first 5 yr of clinical diabetes. No apparent correlation was seen between metabolic control, as measured by hemoglobin A1C and urine and plasma glucose, and the circulating levels of the vitamin D metabolites. Despite appropriate insulin replacement, alterations in vitamin D metabolism occur in the young insulin-dependent diabetic and could relate to the decrease in cortical bone mass observed in these patients.
 ...
PMID:Alterations in circulating vitamin D metabolites in the young insulin-dependent diabetic. 702 72

Aplastic bone disease (ABD) is a common form of renal osteodystrophy and is characterized by a defect in bone matrix formation and mineralization without an increase in osteoid thickness. The prevalence and pathogenesis of ABD in predialysis patients is largely unknown. We prospectively studied 92 unselected predialysis patients with a creatinine clearance < 10 ml/min/1.73 m2 and a mean age of 45 +/- 2 years (61 M, 31 F). None of the study patients had received any form of vitamin D therapy, and CaCO3 was the primary phosphate binder. Aplastic bone disease was observed in 30 (32%) patients. Stainable bone aluminium surface was < 3% in all ABD patients. Patients with ABD were older (52 +/- 3 versus 42 +/- 2 years; P < 0.01) and had reduced serum intact PTH compared to non-ABD patients (199 +/- 25 versus 561 +/- 87 pg/ml; P < 0.001). Patients with diabetes mellitus showed lower PTH values (179 +/- 31 versus 432 +/- 62 pg/ml; P < 0.001) and a lower incidence of advanced hyperparathyroidism bone lesions (16% versus 46%; P < 0.05) than non-diabetic patients. However, diabetes was not clearly associated with low bone turnover disease (56% in diabetics versus 41% in non-diabetics; P = 0.1). A second bone biopsy was obtained in eleven ABD patients after a period of 16.6 +/- 2.2 months on maintenance dialysis with a dialysate calcium of 7 mg/dl. Bone histology was unchanged in 10 patients, and one evolved to mild hyperparathyroidism. Trabecular bone volume did not change (22.7 +/- 1.7 versus 20.7 +/- 1.7%), and the stainable bone aluminium surface remained < 3%.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Adynamic bone disease with negative aluminium staining in predialysis patients: prevalence and evolution after maintenance dialysis. 752 7

Several studies of diabetes mellitus patients have demonstrated abnormalities in calcium, phosphate and vitamin D metabolism. In an earlier study, the authors reported impaired renal processing of phosphate in spontaneously diabetic GK rats, an animal model of type II diabetes mellitus. In the present study, which represents an extension of the earlier study, vitamin D metabolism and response are examined in 20-week-old GK rats. Serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] was found to be lower in GK rats than in Wistar rats. After intraperitoneal administration of 0.5 micrograms/kg 1,25-(OH)2D, serum calcium increased in GK rats, but not in Wistar rats, while serum phosphate remained unchanged in GK rats, but increased in Wistar rats. Although serum 1,25-(OH)2D rose abruptly in 3 h and decreased thereafter in both GK and Wistar rats, the decrease in serum 1,25-(OH)2D at 6 h was more marked in GK rats than in Wistar rats. Serum 24,25-dihydroxyvitamin D was consistently higher in GK rats than in Wistar rats. Northern blotting and dot blotting with use of a cDNA probe for the 24-hydroxylase gene showed an increased expression of the gene in the kidney of GK rats. These results demonstrate impaired vitamin D metabolism in GK rats. Increased activity of 24-hydroxylase, in addition to impaired phosphate metabolism, may play a role in impaired vitamin D metabolism in GK rats.
 ...
PMID:Impaired vitamin D metabolism and response in spontaneously diabetic GK rats. 756 51


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