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

The principle of iron conservation is the basis of iron metabolism; the normal basal loss of iron from the body is about 1 mg daily in a 70 kg man and 0.8 mg in a 55 kg woman. Iron is lost mainly by the menstrual and gastrointestinal routes. The total iron requirement during pregnancy is 800 mg; in the last month the requirement may amount to 7 to 8 mg/day. Supplementary iron is recommended for many menstruating women, and during the latter part of pregnancy. Correct fetal iron metabolism is ensured by proper maternal iron status, although there are contradictory opinions and findings about the relationship between maternal and fetal iron metabolism. Preterm infants fed on breast milk have a negative iron balance, and require an iron intake of about 0.6 mg/kg/day, and 3.4 mg/1 g haemoglobin, to compensate for intestinal and venesection iron losses, respectively. The absorption of supplementary iron by the preterm infant is a linear function of intake. Preterm infants do not require iron supplements when given repeated blood transfusions. During lactation the total iron losses of the mother are 1 mg/day, and thus no supplementary iron is needed if the iron metabolism has been in balance during the pregnancy. Serum ferritin concentration decreases continuously when iron stores in the body are reduced, and totally empty iron stores are the only known reasons for low serum ferritin concentration. Despite depleted iron stores, serum ferritin concentration can be normal or higher than normal in protein-energy malnutrition, up to 3 months after major surgery, in acute liver damage, in some patients with prolonged hyperglycaemia due to diabetes mellitus, in acute lobar pneumonia, active pulmonary tuberculosis and rheumatoid arthritis on gold therapy, in sepsis secondary to marrow hypoplasia induced by chemotherapy, in heavy drinkers and for a few days after myocardial infarction. In haemochromatosis, iron is deposited in liver (producing fibrosis), pancreas, endocrine glands and heart. The rise in the level of iron in the body is due to increased absorption and/or increased intake. This pathology may occur in transfusions, in alcoholism (especially when alcoholic beverages are contaminated with iron and the diet is low-protein), in several liver diseases, in congenital transferrin deficiency and in idiopathic disease. Patients susceptible to haemochromatosis should receive a low-iron diet. Serum ferritin determination may be helpful in early identification of susceptible members of a family with idiopathic familial haemochromatosis, but transferrin saturation is not a good indicator of either iron depletion or iron overload.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of iron preparations. 267 7

We measured concentrations of transferrin (TRF, in micrograms), and creatinine (Cr, in millimoles) in samples of untimed urine from 53 healthy subjects and 157 non-insulin-dependent diabetic (NIDD) subjects. The urinary TRF/Cr ratio was significantly higher in the NIDD group (P less than 0.001). If NIDD subjects are grouped according to their Alb/Cr ratio into normal albuminuria (Group A, Alb/Cr less than 2.5 mg/mmol), microalbuminuria (Group B, Alb/Cr 2.5-26.8 mg/mmol), and macroalbuminuria (Group C, Alb/Cr greater than 26.8 mg/mmol), the TRF/Cr ratios in all three groups exceeded those for healthy controls. Moreover, this ratio was higher in Group B than in Group A and higher in Group C than in Group B. The value for TRF/Cr was clearly abnormal (i.e., exceeded the 95th percentile value found in healthy subjects) in 61%, 95%, and 100% of Group A, B, and C subjects, respectively. The TRF/Cr ratio was significantly higher in those NIDD subjects with clinical retinopathy, and it correlated with arterial pressure. Evidently, TRF/Cr may be increased early in NIDD subjects, and it may be a sensitive marker for detecting development of complications of diabetes.
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PMID:Urinary excretion of transferrin by non-insulin-dependent diabetics: a marker for early complications? 275 34

Partly desialylated transferrin was measured in the serum of subjects with chronic alcoholism, of patients with non-alcoholic-related steatohepatitis, diabetes, and other non-alcoholic liver diseases, and of healthy controls. In non-alcoholic patients and controls the maximum desialylated transferrin expressed in relation to total transferrin was 1.5%. This value was exceeded in 18 (90%) of the 20 alcoholics. By contrast, gamma-glutamyl transferase was within the reference range in 9 of the alcoholics.
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PMID:Desialylated transferrin as a serological marker of chronic excessive alcohol ingestion. 288 14

Lower limb venous compliance and transcapillary escape rate of transferrin were measured in eight normotensive, insulin-dependent male diabetic patients and eight control subjects using a dual isotope technique. Technetium-99m labelled autologous erythrocytes were used to measure venous compliance and to correct for local changes in blood volume, whilst Indium-113m labelled transferrin was used to measure transcapillary escape of protein. The diabetic patients were found to have reduced venous compliance 1.5 (0.7 to 3.4) x 10(-2) mmHg-1 compared with controls 3.2 (2.4 to 4.1) x 10(-2) mmHg-1 (p less than 0.01). The diabetic patients were also found to have greater transcapillary escape of transferrin -2.7 (-1.5 to -5.3) x 10(-3), compared with control subjects -5.2 (-4.1 to -8.1) x 10(-3) (p less than 0.02) in response to increasing hydrostatic pressure. These results show reduced venous compliance in patients with a mean duration of diabetes of 15 years and with only at most, early complications of diabetes, and confirm previous observations showing increased transcapillary escape of protein.
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PMID:Reduced venous compliance and increased transcapillary escape of protein in insulin-dependent diabetic patients. 297 Sep 19

Dietary supplementation with high-carbohydrate, guar gum fiber (HCF) is effective in acutely blunting postprandial blood glucose levels. We report the effect of such supplementation on the diet and nutritional status of a group of 16 subjects with non-insulin-dependent diabetes mellitus (NIDDM) who incorporated either HCF bars (35.7 g carbohydrate and 6.6 g guar gum/bar) or placebo bars (identical except for the absence of guar gum) into the diet for 6 mo as part of a double-blind, randomized clinical trial. The HCF subjects achieved mean daily intake of 4.8 +/- 0.4 bars, constituting 51.2 +/- 3.1% of total calories and providing 29.7 +/- 2.6 g guar gum daily. Energy intakes and body weight did not change significantly in either group. Food consumption patterns and nutrient intakes did change, although not enough to impair the nutritional integrity of the diet because the bars themselves served as a source of nutrients. The bars were rich in thiamin, B6, folacin, phosphorus, iron, zinc, and copper, adequately replacing any decrease in nutrient intake as a result of foods being dropped from the diet. In fact, daily intakes of B6, folacin, and copper actually increased due to contributions from the bars. Nutrients in which the bars were poor (vitamins A, C and B12) resulted in suboptimal intakes (less than 66% RDA). Although no significant change in nutritional status of the HCF group occurred as determined by arm muscle area, arm fat area, hemoglobin, hematocrit, or serum albumin, transferrin, iron, ferritin, calcium, phosphate, B12, and magnesium levels, these indicators of nutritional status are rather insensitive.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Care
PMID:Nutritional risk of high-carbohydrate, guar gum dietary supplementation in non-insulin-dependent diabetes mellitus. 302 7

In 67 patients (mean age 51 years, range 26-79), at diagnosis of primary haemochromatosis (PH), grade III or IV liver iron overload was present in all cases, cirrhosis in 85%, transferrin saturation greater than 80% in 75%, serum ferritin greater than 1000 micrograms/l in 84%, and overt diabetes in 48%. Alcohol intake was greater than 150 g/day in 11 patients; six were chronic hepatitis B surface antigen (HBsAg) carriers. HLA-A3 and B7 antigens were present in 64% and 23% versus respectively 22% (p less than 0.01) and 9% (p less than 0.025) in controls. Iron overload was found in the stomach, duodenum, skin and bone marrow in 57, 43, 45 and 59% of the patients studied. Sixty-three patients were followed for 1-260 months (median 24); 43 received regular iron-depleting treatment and 20 did not because of liver failure, cancer or refusal. Cumulative survival was 79%, 67% and 61% at 1, 4 and 10 years, respectively. Ten patients died from hepatocellular carcinoma and two from extrahepatic cancer. The early high mortality rate was due to some cases of advanced disease or cancer. Cumulative survival in the regularly treated group was 95% at 1 year and 91% at 4 and 10 years, which was higher than in the untreated group.
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PMID:Clinical, biochemical and histological features of primary haemochromatosis: a report of 67 cases. 302 81

Previous studies of patients with end-stage renal disease (ESRD) indicate that the prevalence of goiter varies from 0 to 58% while that of hypothyroidism ranges from 0 to 9.5%. In addition, altered serum thyroid hormone levels are present in euthyroid patients with ESRD and may be related to nonthyroidal disorders including malnutrition. To examine these issues further, 306 patients with ESRD were compared to 139 hospitalized patients without renal disease (control population). Goiter was present in 43% with ESRD compared to 6.7% of controls (P less than 0.001). Goiter frequency was greater (49.6%, P = 0.047) and serum parathyroid hormone levels higher (mean: 238.6 microlitersEq/ml, P less than 0.001; normal: less than 15 microlitersEq/ml) in 115 patients dialyzed for longer than 1 year than in 191 dialyzed for less than 1 year or not at all (38.7%, and 61.5 microlitersEq/ml, respectively). In addition, goiter was more common in females (50.0%) than in males (35.1%, P = 0.008) with ESRD. No significant relationships were observed between goiter frequency and age, race, diabetes mellitus, or elevated antimicrosomal antibody titers. The prevalence of primary hypothyroidism was higher in ESRD (2.6%) than in 2122 in- and out-patients (1.1%) (P = 0.024). Compared to the total group of ESRD patients, the hypothyroid patients were predominantly female (88% vs. 50%) and had a higher frequency of positive antimicrosomal antibody titers (50% vs. 6.7%, P = 0.029). The frequency of hyperthyroidism was not significantly different, being 1.0% in ESRD compared to 0.3% in the general population (P = 0.057). There was a higher frequency of reduced free T4 index values in the 287 euthyroid patients with ESRD (12.9%) than in controls (3.6%) (P = 0.002). Similarly, free T3 index values were reduced below 100 in 65.5% with ESRD compared to 33.8% of controls (P less than 0.001). In addition, serum albumin levels were lower in euthyroid patients with ESRD (3.5 g/dl, P less than 0.001) than in controls (3.8 g/dl). Serum T3 levels correlated directly with both serum albumin (r = 0.57, P less than 0.001) and transferrin (r = 0.54, P less than 0.001) levels in ESRD as well as in controls (r = 0.74, P less than 0.001, and r = 0.69, P less than 0.001, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The thyroid in end-stage renal disease. 325 81

This study has investigated the relationship of glycaemic control, blood pressure and proteinuria to early renal dysfunction in a cohort of 50 type I and 65 type II diabetics, with renal function ranging from normal to mildly impaired (serum creatinine less than 0.2 mM). Repeated measurements were made over a mean interval of 7 years and mean data from each subject were analysed by stepwise multiple linear regression. This enabled associations to be determined independently of the confounding influence of age and duration of disease. In type I diabetics, mean creatinine clearance was inversely related to systolic blood pressure (P less than 0.001), glycosylated haemoglobin (P less than 0.05), fasting plasma glucose (P less than 0.05) and to the renal clearance of albumin (P less than 0.001), transferrin (P less than 0.01) and IgG (P less than 0.05). By contrast, in type II diabetics, none of these associations were significant. No significant relationships were found with the rate of decline of creatinine clearance in either type of diabetic. Further studies will be needed to determine whether the changes in blood pressure and glycaemic control precede or follow the development of renal disease. However, these findings raise the possibility of a difference in the pathogenesis of renal disease in type I and type II diabetes.
Diabetes Res Clin Pract 1988 Jan 07
PMID:Comparison of early renal dysfunction in type I and type II diabetes: differing associations with blood pressure and glycaemic control. 334 32

Free radical medicated oxidative damage has previously been implicated in the pathogenesis of diabetic microangiopathy. Caeruloplasmin and transferrin act as antioxidants in serum by oxidizing and chelating ferrous iron which could otherwise act as a catalyst in free radical reactions. We have measured the serum anti-oxidant activity in 67 diabetics, 25 of whom had retinopathy and in 37 controls. Serum iron concentrations were normal in diabetics in comparison with controls (21.5 +/- 10 v 19.5 +/- 6.7 mumol/L) although transferrin and iron binding capacity were increased in the diabetics (3.7 +/- 0.8 v 2.9 +/- 0.9 g/L, p less than 0.001 and 69.9 +/- 10.8 v 59.0 +/- 14 mumol/L, p less than 0.002 respectively). Caeruloplasmin, measured by its ferroxidase activity, was increased in both male (46 +/- 11 v 36 +/- 9 mu/mL, p less than 0.002) and female diabetics (57 +/- 13 v 47 +/- 11 mu/mL, p less than 0.002). Ferritin was also increased in both male (124 +/- 113 v 44 +/- 38 ng/mL, p less than 0.001) and female diabetics (132 +/- 118 v 25 +/- 12 ng/mL, p less than 0.001). The presence of retinopathy, the degree of glycaemic control and duration of diabetes had no effect on these findings. We conclude that increased concentrations of iron-oxidizing and iron-binding proteins occur in diabetic serum, and that the increased serum antioxidant activity may be a response to oxidative stress.
Diabetes Res 1988 Feb
PMID:Serum antioxidant activity in diabetes mellitus. 339 68

This study has attempted to document a specific haemovascular action of gliclazide on the reversal of early diabetic microangiopathy. A prospective double-blind controlled study was performed over 2 years, comparing gliclazide versus placebo in insulin-treated and gliclazide versus glibenclamide in non-insulin-treated diabetic subjects, after a 1-year run-in period. Glycaemic control was not significantly different in gliclazide- and non-gliclazide-treated subjects before or after the commencement of active therapy. Following treatment with gliclazide in 17/32 insulin-treated and 8/17 non-insulin-treated subjects with Albustix-negative proteinuria, there was no difference in retinopathy score, total proteinuria or the renal clearance of creatinine, albumin, transferrin and immunoglobulin G. In the insulin-treated group, progression of retinopathy was observed in approximately one-third of subjects, but no parameter of proteinuria progressed over 2 years. Thus, this study did not detect a reversal of the parameters measured and does not support an action of gliclazide on diabetic microangiopathy, independent of its hypoglycaemic action.
Diabetes Res Clin Pract
PMID:Lack of effect of gliclazide on early diabetic nephropathy and retinopathy: a two-year controlled study. 355 37


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