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)

The role of hypercalciuria and hyperphosphaturia in the growth retardation of children with diabetes mellitus was investigated in 157 children with diabetes whose mean height was less than that of 37 nondiabetic siblings of similar age (P less than .025). Hyperglycemia, hypercalciuria, and hyperphosphaturia were assessed coincident with the height measurement of each child in a cross-sectional survey. The distribution of height percentiles of the children with diabetes was skewed to the left with 61% at or below the 50th percentile. Eleven percent of the insulin-dependent children with diabetes mellitus were shorter than would be anticipated by a normal distribution of the 157 children. The duration of diabetes (hyperglycemia) had the greatest influence upon the children's height. Children with diabetes were shorter than the nondiabetic subjects by the fourth year of hyperglycemia, and this difference in height became statistically significant after 7 years or more of diabetes. The degree of hypercalciuria and hyperphosphaturia was more closely associated with reduced height in children with diabetes than was the degree of hyperglycemia, although the renal wastage of calcium and phosphorus seemed to be the result of glucosuria. Because hypercalciuria and hyperphosphaturia impair growth in nondiabetic children, they may also play an important role in the poor growth of children with diabetes mellitus.
 ...
PMID:Hypercalciuria, hyperphosphaturia, and growth retardation in children with diabetes mellitus. 348 37

To determine the effects of very-low-calorie diets on the metabolic abnormalities of diabetes and obesity, we have studied 10 obese, non-insulin-dependent diabetic (NIDDM) and 5 obese, nondiabetic subjects for 36 days on a metabolic ward during consumption of a liquid diet of 300 kcal/day with 30 g of protein. Rapid improvement occurred in the glycemic indices of the diabetic subjects, with mean (+/- SEM) fasting plasma glucose falling from 291 +/- 21 to 95 +/- 6 mg/dl (P less than 0.001) and total glycosylated hemoglobin from 13.1 +/- 0.7% to 8.8 +/- 0.3% (P less than 0.001) (normal reference range 5.5-8.5%). Lipid elevations were normalized with plasma triglycerides reduced to less than 100 mg/dl and total plasma cholesterol to less than 150 mg/dl in both groups. Hormonal and substrate responses were also comparable between groups with reductions in insulin and triiodothyronine and moderate elevations in blood and urinary ketoacid levels without a corresponding rise in free fatty acids. Electrolyte balance for sodium, potassium, calcium, and phosphorus was initially negative but approached equilibrium by completion of the study. Magnesium, in contrast, remained in positive balance in both groups throughout. Total nitrogen loss varied widely among all subjects, ranging from 70 to 367 g, and showed a strong positive correlation with initial lean body mass (N = 0.83, P less than 0.001) and total weight loss (N = 0.87, P less than 0.001). The nondiabetic group, which had a significantly greater initial body weight and lean body mass than the diabetic group, also had a significantly greater weight loss of 450 +/- 31 g/day compared with 308 +/- 19 g/day (P less than 0.01) in the diabetic subjects. The composition of the weight lost at completion was similar in both groups and ranged from 21.6% to 31.3% water, 3.9% to 7.8% protein, and 60.9% to 74.5% fat. The contribution of both water and protein progressively decreased and fat increased, resulting in unchanged caloric requirements during the diet. This study demonstrates that short-term treatment with a very-low-calorie diet in both obese diabetic and nondiabetic subjects results in: safe and effective weight loss associated with the normalization of elevated glucose and lipid levels, a large individual variability in total nitrogen loss determined principally by the initial lean body mass, and progressive increments in the contribution of fat to weight loss with stable caloric requirements and no evidence of a hypometabolic response.
Diabetes 1986 Feb
PMID:Metabolic consequences of very-low-calorie diet therapy in obese non-insulin-dependent diabetic and nondiabetic subjects. 351 Sep 22

Relative low serum levels of parathormone (PTH) and low incidence of secondary hyperparathyroidism have been reported in diabetic uremic patients. The pathogenesis of this reported resistance to uremic secondary hyperparathyroidism in diabetes remains controversial. We have measured the serum C-terminal parathormone (C-PTH) renal phosphorus threshold (TmPO4) and nephrogenous cyclic AMP (N-cCAMP), in 2-hour urine collection in 22 patients with diabetic nephropathy with moderate chronic renal failure and in 27 controls with similar creatinine clearance values (18.16 +/- 9.14 and and 19.1 +/- 8.47 ml/min). In spite of the lower levels of serum C-PTH (1.07 +/- 0.43 ng/ml) diabetic patients exhibited an increased phosphaturia (TmPO4: 1.97 +/- 0.9 mg/100 ml GFR) when compared with the control group (C-PTH: 2.01 +/- 1.17 mg/ml, and TmPO4: 2.5 +/- 0.7 ml GFR). When the C-PTH values were plotted against the logarithm of creatinine clearance values, both groups showed a significant linear relationship reflecting the progressive increase in PTH when GFR fell. This progressive parathyroid stimulus was also present in diabetic patients but in a lower intensity. We believe that increased phosphaturia in diabetics with moderate chronic renal failure may be a major factor in precluding the appearance of secondary hyperparathyroidism in these patients once they reach the dialysis and transplantation programs.
 ...
PMID:Relative hyperphosphaturia in diabetic chronic renal failure: a protective factor of hyperparathyroidism. 367 Feb 26

Amniotic fluid for fetal lung maturity studies was obtained from 287 healthy and 198 diabetic women. Classes of diabetes were as follows: Class A, 111; Class B, 58; Class C, 13; Class D, 11; Class F, 4; and Class R, 1. The regression lines representing the relationship of amniotic fluid lecithin phosphorus concentration to gestational age at amniocentesis in each of the groups of diabetic patients were not statistically different from those of the control subjects. Each of the diabetic patients was then matched with a control subject of the same race, sex of newborn infant, and gestational age at amniocentesis. The regression lines of the nonhypertensive, hypertensive, and all diabetics were not different from those of their respective matched control subjects. Also there was no difference in the proportion of mature lecithin phosphorus concentrations at different weeks between diabetic and normal women. The absence of a significant influence of diabetes on fetal lung maturation is probably due to improvement in diabetic control resulting in normalization of the fetal metabolic environment.
 ...
PMID:Effect of maternal-fetal disorders on lung maturation. I. Diabetes mellitus. 375 75

Choline metabolism and phosphatidylcholine biosynthesis were studied in renocortical slices of rats rendered diabetic with streptozotocin. The rates of [14C]choline incorporation into both acid-soluble and acid-insoluble fractions were increased in diabetic relative to control kidneys. While choline uptake into the control kidneys reached a plateau after 30 min of incubation, the tissue uptake of choline by the diabetic kidneys showed a time-dependent increase over 120 min, rising to a level exceeding that of control kidneys. In the control kidney, the oxidation of choline to betaine was similar to the level of phosphocholine accumulation during the first 30 min, while the formation of phosphocholine in the diabetic kidney was 1.9-fold higher than that in the control kidney (P less than 0.02) and 1.4-fold higher than the formation of betaine in diabetics (P less than 0.05). These data suggest that most of the choline transported into cells enters the Kennedy pathway by phosphorylation to phosphocholine in diabetic kidneys. The diabetic kidney also demonstrated a marked increase in the formation of three choline-containing phospholipids; phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin. The treatment of diabetes with insulin restored these abnormalities toward normal. The absolute content of phosphatidylcholine significantly increased in diabetic kidneys (P less than 0.05) while contents of other major phospholipids and total lipid phosphorus in diabetic kidneys were not different from those in control kidneys. Our results indicate that renal hypertrophy in experimental diabetes is associated with a stimulation of the biosynthesis of renal phosphatidylcholine, presumably caused by an enhanced tissue uptake of choline and a stimulation of choline kinase. Since an enhancement of the membrane phosphatidylcholine biosynthesis is one of the early responses to growth signals, an alteration in phosphatidylcholine biosynthesis may contribute to the development of renal hypertrophy in experimental diabetes.
 ...
PMID:Stimulation of phosphatidylcholine biosynthesis in diabetic hypertrophic kidneys. 380 92

We studied phosphorus and calcium metabolism in 50 adult insulin dependent and non insulin dependent diabetics arranged in 4 groups according to therapy and control of diabetes. We observed: a low level of blood magnesium in all diabetics a lower level of P T H, more pronounced with poorly controlled diabetes. a decrease of 1-25 (OH) 2 D levels without modification of the 25 (OH) D levels in badly controlled diabetics. This decrease may be related to the low level of PTH with a 1 alpha hydroxylation defect. These results are in favor of the hypothesis of a primary bone problem leading to the pre-senile and subclinical osteoporosis observed in diabetics. Hyperglycaemia rather than insulinopenia may be involved. Rigorous diabetes control significantly decreases all the observed differences, except the low magnesium level.
 ...
PMID:[Calcium and phosphorus metabolism in insulin dependent and non-insulin dependent diabetics, well-controlled and poorly-controlled]. 384 Oct 78

In order to ascertain whether or not abnormal mineral and vitamin D metabolism in diabetes can be reversed by insulin therapy, plasma calcium, ionized calcium, phosphorus, parathyroid hormone (PTH) and vitamin D metabolites were measured in control, streptozotocin (STZ) diabetic and insulin-treated diabetic rats. Blood glucose levels in diabetic rats treated with insulin decreased to normal. The low plasma calcium and ionized calcium levels in diabetic rats were found to be normal in insulin-treated diabetic rats. An elevated PTH level was observed in the diabetic group, but it was at normal levels in the insulin-treated diabetic group. Plasma 25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)2D) in the diabetic group were decreased compared to those in control rats, but these were also fully restored to control levels by insulin therapy. However, plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) levels in the untreated diabetic group tended to be lower than in controls, and the values in insulin-treated rats were significantly decreased compared to the control group. The ratio of 1,25(OH)2D to 25(OH)D in diabetic rats was higher than in controls, but it was decreased after insulin therapy and was significantly lower than in the control group. It is suggested, therefore, that the negative calcium balance and decreased 25(OH)D and 24,25(OH)2D levels are derived from the metabolic derangement due to the insulin deficiency. Furthermore, insulin seems to suppress the conversion of 25(OH)D to 1,25(OH)2D in experimental diabetes in vivo.
 ...
PMID:Effects of insulin on altered mineral and vitamin D metabolism in streptozotocin-induced diabetes. 388 88

Previous studies have shown that there is an impairment in renal production of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the major biologically active metabolite of vitamin D3, in diabetes. This impairment is not due to a deficiency in the parathyroid hormone (PTH), a major stimulator of renal 1,25(OH)2D3 production. Therefore, we have investigated the capacity of PTH to stimulate 1,25(OH)2D3 production in insulin deficiency and with insulin replacement. Experiments were performed in rats fed a 0.6% calcium, vitamin D sufficient diet for 2 weeks. Thyroparathyroidectomy was performed on all rats. Rats to be rendered diabetic were injected with streptozotocin immediately after surgery. In non-diabetic rats, PTH administration significantly increased renal 1,25(OH)2D3 production (11 +/- 2 vs 46 +/- 5 pg/min/g; P less than 0.05). In diabetic rats, however, PTH caused only a modest increase in 1,25(OH)2D3 production (11 +/- 1 vs 19 +/- 4 pg/min/g; P less than 0.05). With insulin replacement, PTH stimulation of 1,25(OH)2D3 production was markedly increased over that seen in diabetic rats (48 +/- 12 vs 19 +/- 4 pg/min/g; P less than 0.05). PTH was equally effective in raising serum calcium, depressing serum phosphorus and tubular reabsorption of phosphate in non-diabetic as well as in diabetic rats. These results demonstrate that insulin is necessary for the maximal stimulation of renal 1,25(OH)2D3 production by PTH. However, insulin is not necessary for PTH action in terms of renal handling of phosphate and inducing hypercalcaemia. These results suggest multiple pathways for the action of PTH, only some of which are insulin requiring.
 ...
PMID:Insulin modulates the stimulation of renal 1,25-dihydroxyvitamin D3 production by parathyroid hormone. 389 9

The dynamic changes in serum phosphorus levels in 69 episodes of ketoacidosis in 48 diabetic patients were retrospectively evaluated. The mean age was 41 +/- 2 years (mean +/- SEM), and the duration of diabetes mellitus was 7 +/- 1 years. The serum phosphorus levels determined within the first six hours of admission were analyzed. Before initiation of therapy, the incidence of hyperphosphatemia was 94.7 percent. At the end of 12 hours, the mean serum phosphorus level fell from 9.2 +/- 0.6 to 2.8 +/- 0.3 mg/dl. Before therapy, the serum phosphorus level correlated positively with the serum glucose level, the effective plasma osmolality, and anion gaps, and correlated negatively with the serum chloride level. It is concluded that hyperphosphatemia is common in diabetic ketoacidosis before therapy. The increase in serum phosphorus is likely to be due to a transcellular shift. Potential factors responsible for the shift are serum glucose, through its osmotic effect, and the organic anions.
 ...
PMID:Dynamic changes in serum phosphorus levels in diabetic ketoacidosis. 393 41

Dietary intakes of essential nutrients were measured as part of a population-based investigation of diabetes and cardiovascular risk factors in Mexican-Americans and Anglo-Americans in San Antonio, Texas. Twenty-four hour dietary recalls were conducted on 2134 individuals residing in three socioeconomically distinct neighborhoods: low-income, middle-income, and upper-income. Mean intakes of calcium, vitamin A and vitamin C were significantly lower among Mexican-Americans than among Anglos. Intake of vitamin C was most affected by socioeconomic status. Females of both ethnic groups consumed less than their RDA for calcium and iron. Intakes of B vitamins, phosphorus, and potassium were adequate, with few ethnic or socioeconomic differences.
 ...
PMID:Dietary intakes of essential nutrients among Mexican-Americans and Anglo-Americans: the San Antonio Heart Study. 402


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