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

Thirty-four children were followed up prospectively for 5 years from the onset of diabetes regarding serum magnesium, zinc and some proteins. Serum magnesium decreased to significantly lower values (0.76 +/- 0.05 mmol l-1) than those in matched controls after 2 and 5 years, with the lowest mean values in diabetic girls. Serum zinc concentration was higher in the diabetic group than in the control children, and again the diabetic girls differed most from the controls. Serum prealbumin was significantly lower in the diabetic patients after 2 and 5 years than in the controls. Serum albumin was also slightly reduced in the diabetic patients, while orosomucoid was normal. These data indicate chronic magnesium deficiency and insufficient liver synthesis of certain serum proteins in diabetic children.
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PMID:Serum magnesium and protein concentrations during the first five years of insulin-dependent diabetes in children. 905 31

We investigated the effects of diabetes mellitus on the hypothalamo-hypophysial-thyroid axis in male (R x U) F1 and R-Amsterdam rats, which were found to respond to streptozotocin (STZ)-induced diabetes mellitus with no or marked increases, respectively, in plasma corticosterone. Males received STZ (65 mg/kg i.v.) or vehicle, and were killed 1, 2 or 3 weeks later. At all times studied, STZ-induced diabetes mellitus resulted in reduced plasma TSH, thyroxine (T4) and 3,5,3'-tri-iodothyronine (T3). Since the dialyzable T4 fraction increased after STZ, probably as a result of decreased T4-binding prealbumin, plasma free T4 was not altered during diabetes. In contrast, both free T3 and its dialyzable fraction decreased during diabetes, which was associated with an increase in T4-binding globulin. Hepatic activity of type I deiodinase decreased and T4 UDP-glucuronyltransferase increased after STZ treatment. Thus, the lowered plasma T3 during diabetes may be due to decreased hepatic T4 to T3 conversion. Median eminence content of TRH increased after STZ, suggesting that hypothalamic TRH release is reduced during diabetes and that this is not caused by impaired synthesis or axonal transport of TRH to the median eminence. Hypothalamic proTRH mRNA did not change in diabetic (R x U) F1 rats during the period of observation, but was lower in R-Amsterdam rats 3 weeks after STZ. Similarly, pituitary TSH and TSH beta mRNA had decreased in R-Amsterdam rats by 1 week after STZ treatment, but did not change in (R x U) F1 rats. The difference between the responses in diabetic R-Amsterdam and (R x U) F1 rats may be explained on the basis of plasma corticosterone levels which increased in R-Amsterdam rats only. Hypothalamic TRH content was not affected by diabetes mellitus, but the hypothalami of diabetic rats released less TRH in vitro than those of control rats. Moreover, insulin had a positive effect on TRH release in vitro. In conclusion, the reduced hypothalamic TRH release during diabetes is probably not caused by decreases in TRH synthesis or transport to the median eminence, but seems to be due to impaired TRH release from the median eminence which may be related to the lack of insulin. Inhibition of proTRH and TSH beta gene expression in diabetic R-Amsterdam rats is not a primary event but appears to be secondary to enhanced adrenal activity in these animals during diabetes.
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PMID:Possible role of corticosterone in the down-regulation of the hypothalamo-hypophysial-thyroid axis in streptozotocin-induced diabetes mellitus in rats. 916 15

Glucose intolerance and diabetes mellitus are both prevalent in patients with chronic liver diseases. We examined the efficacy and systemic safety of therapy with an alpha-glucosidase inhibitor, acarbose, in diabetes mellitus associated with chronic liver diseases. Twenty patients with chronic hepatitis or liver cirrhosis and overt diabetes mellitus received acarbose (taken orally) for 8 weeks. The initial dosage of acarbose was 50 mg three times daily, taken before meals; this was increased to 100 mg three times daily after 2 weeks. The mean fasting plasma glucose level was 173.7 +/- 18.6 mg/dl (mean +/- SE) at entry, and was significantly decreased to 132.9 +/- 7.5 mg/dl (P < 0.05) after 8 weeks of acarbose treatment. The improved glycemic control was reflected by a significant decrease in glycosylated hemoglobin (HbA1c) from 7.2 +/- 0.3% at entry to 6.3 +/- 0.2% (P < 0.05) after 8 weeks. Serum levels of both aspartate and alanine aminotransferases fluctuated during acarbose treatment, probably due to the natural course of chronic liver diseases, but the mean values had decreased after 8 weeks of treatment. Plasma ammonia levels increased, from 61.3 +/- 10.7 micrograms/dl to 71.1 +/- 9.6 micrograms/dl after 8 weeks of acarbose treatment but the increase was not significant. Clinically significant elevation of plasma ammonia concentration was seen in 2 cirrhotic patients (121 and 124 micrograms/dl); this was asymptomatic and gradually returned to the normal range despite continuous acarbose treatment in one patient, and was reversed after the withdrawal of acarbose with the concomitant administration of lactulose in the other patient. No other blood tests results, including albumin, cholinesterase, and prothrombin time, or lipid profile and nutritional status, in terms of rapid turnover proteins, prealbumin, retinol binding protein, and transferin, were altered throughout the study period. These results indicate that diabetes mellitus associated with chronic liver diseases may be safely and effectively treated with acarbose. However, clinicians must be aware of the possibility of hyperammonemia when they prescribe acarbose for patients with diabetes mellitus and advanced liver cirrhosis.
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PMID:Safe and effective treatment of diabetes mellitus associated with chronic liver diseases with an alpha-glucosidase inhibitor, acarbose. 943 16

This study assessed glucose tolerance, insulin sensitivity and lipid parameters in HIV-infected patients presenting with lipodystrophy during HAART including protease inhibitors. Fourteen consecutive patients from Rothschild Hospital treated with HAART and presenting with marked facial lipoatrophy were evaluated. A 75 g oral glucose tolerance test (OGTT) with measurement of plasma glucose, insulin, proinsulin and free fatty acids at T0, 30, 60, 90 and 120 min was performed. Lipid parameters (triglycerides, cholesterol, apolipoproteins A1 and B) were studied as well as nutritional and inflammatory markers (albumin, prealbumin, transferrin, haptoglobin, orosomucoid, C-reactive protein), endocrine and cytokine parameters (thyrotropin, cortisol, leptin, interleukin-6), HIV viral load and CD4-lymphocyte count. These patients were compared with 20 non-lipodystrophic protease inhibitor-treated patients. The measurements performed during OGTT showed that among the 14 lipodystrophic patients, 11 (79%) presented with diabetes (5 patients) or normal glucose tolerance but with insulin resistance (6 patients). This frequency was strikingly different in the group of nonlipodystrophic patients, which included only 4 (20%) presenting with diabetes (1 patient), or impaired glucose tolerance (2 patients), or normal glucose tolerance but with insulin resistance (1 patient). Hypertriglyceridaemia was present in 11 lipodystrophic (79%) versus 7 nonlipodystrophic patients (35%). Nutritional and endocrine measurements were normal. An abnormal processing of proinsulin to insulin was excluded. Thus, lipodystrophy during HAART was associated with diabetes, insulin resistance and hypertriglyceridaemia. Diabetes, diagnosed by basal and/or 120 min-OGTT glycaemia, seems more frequent than previously described. The therapeutic consequences of these results deserve evaluation in clinical trials.
Diabetes Metab 1999 Sep
PMID:Diabetes, insulin resistance and dyslipidaemia in lipodystrophic HIV-infected patients on highly active antiretroviral therapy (HAART). 1049 91

Nutritional factors and dialysis adequacy are associated with outcome in hemodialyzed patients, but their relative contribution remains controversial, particularly when dialysis adequacy complies with current recommendations (Kt/V >1.2). Survival, clinical, and nutritional data from a cohort of prevalent 1,610 patients treated by hemodialysis in 20 centers in France have been collected over a 2.5-year period, from January 1996 to July 1998. Data including age, sex, cause of end-stage renal disease (ESRD), clinical outcome, time on dialysis, body mass index (BMI), blood levels of midweek predialysis albumin, prealbumin, and bicarbonate were analyzed. Normalized protein catabolic rate (nPCR), dialysis adequacy parameters, and estimation of lean body mass (LBM) from creatinine generation were computed from pre- and postdialysis urea and creatinine levels. The characteristics of the patients were as follows: age 59.6 +/- 16.5 years, 58.8% males, 11% of diabetics, time on dialysis 63.2 +/- 64.5 m. Weekly dialysis time was 12.18 +/- 1.78 hrs, Kt/V 1.34 +/- 0.34, nPCR 1.10 +/- 0.35 g/kg body weight/day. Albumin concentration was 39.4 +/- 5.3 g/L, prealbumin was 0.33 +/- 0.09 g/L, BMI was 23.0 +/- 4.5 kg/m(2). Overall survival was 89.7% +/- 0.8% and 78.4% +/- 1.1% after 1 and 2 years. In the Cox proportional hazard model, survival was significantly influenced by age, the presence of diabetes, and by concentrations of albumin and prealbumin, but not by other variables, including Kt/V and urea reduction ratio. These results indicate that nutritional protein concentrations were predictive of dialysis outcome, whereas variables reflecting actual body composition and dialysis dose were not. Furthermore, in this well-dialyzed population, dialysis adequacy had no influence on survival. In conclusion, when adequacy targets are met in hemodialyzed patients, survival is mainly dependent on age and nutritional status. Efforts should be focused on the most efficient ways to maintain nutritional status in these patients.
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PMID:Influence of nutritional factors and hemodialysis adequacy on the survival of 1,610 French patients. 1115 68

The incidence of malnutrition is widely held to be greater in the elderly, but this specific factor has not been extensively studied in elderly dialysis patients. In a 30-month follow-up prospective study, we evaluated the role of nutrition on the outcome of 290 stable hemodialysis (HD) outpatients aged older than 75 years followed up in 20 French HD centers (167 men, 123 women; age, 79.8 +/- 4.2 years; previous time on dialysis, 41 +/- 38 months). On the same day in January 1996, predialysis and postdialysis blood samples were collected according to recommended procedures for dialysis quantification. Normalized protein catabolic rate, dialysis adequacy parameters, and estimation of lean body mass (LBM; expressed as observed/expected LBM values [obs/exp LBM]) were computed from predialysis and postdialysis urea and creatinine levels. Overall survival rates were 80% and 65% after 1 and 2 years of follow-up, respectively, and were significantly less in patients with the lower quartile of obs/exp LBM. In univariate analysis using the Cox proportional hazards model, survival was significantly influenced by age, albumin level, prealbumin level, body mass index, and diabetes, but not by sex, Kt/V, duration of dialysis, cholesterol level, hemoglobin level, or obs/exp LBM. In multivariate analysis, no variable remained significant. Cardiovascular mortality accounted for 52.1% of the patient deaths. We conclude that in elderly HD patients, malnutrition influences overall survival despite adequate dialysis treatment.
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PMID:Factors influencing survival in hemodialysis patients aged older than 75 years: 2.5-year outcome study. 1132 82

Malnutrition is a major factor contributing to the high mortality rate in hemodialysis (HD) and peritoneal dialysis (PD) patients. We and others have reported previously that single enrollment levels of serum biochemical markers, such as albumin, cholesterol, creatinine, and prealbumin, are correlated directly with mortality in HD and PD patients. We have studied prospectively the relationship of enrollment prealbumin levels, demographic characteristics, and other biochemical markers to all causes of mortality in 130 HD and 128 PD patients who were monitored for 10 years. The Kaplan-Meier method was used to compute observed survival, and the Cox proportional hazards model was used to identify independent predictors of mortality risk. For HD patients, enrollment serum prealbumin remained a strong independent predictor of long-term survival after adjusting for age, race, gender, months on dialysis, diabetic status, and other nutritional markers. In PD and HD patients, observed and adjusted survivals (after adjusting for aforementioned confounding variables) of patients with prealbumin greater than 30 mg/dL were significantly higher than survivals of patients with prealbumin less than 30 mg/dL. For HD and PD patients, age and diabetes were associated inversely with prealbumin concentration, whereas levels of albumin, creatinine, and total cholesterol were associated directly with prealbumin concentration. In this study, prealbumin was the best biochemical predictor of mortality for HD patients and a useful tool to assess nutritional risk in HD and PD patients.
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PMID:Serum prealbumin predicts survival in hemodialysis and peritoneal dialysis: 10 years of prospective observation. 1172 75

Malnutrition is highly prevalent in peritoneal dialysis (PD) patients and is associated with higher mortality. Lower serum levels of markers of nutrition--such as albumin, creatinine, prealbumin, and total cholesterol--are important risk factors in PD patients. Usefulness of bioimpedance analysis (BIA) in hemodialysis (HD) patients has been reported. In the present study, we prospectively examined the relationship of bioimpedance indexes to the nutrition status and survival of 45 PD patients who were followed for more than 1 year. On patient enrollment, a BIA was performed (Bioelectrical Impedance Analyzer, Model BIA-101: RJL Systems, Clinton Township, MI, U.S.A.). Monthly blood was analyzed for biochemical markers. The mean age of the study group was 50 +/- 15 years. Of the 45 patients, 56% were female and 24% were diabetic. Mean body mass index was 25.7 +/- 5.1. Mean resistance, reactance, capacitance, and phase angle were 524 +/- 106 omega 57 +/- 20 omega, 678 +/- 223 pF, and 6.2 +/- 1.7 degrees respectively. Patients with diabetes had lower capacitance (555 pF vs. 713 pF, p = 0.007) and phase angle (5.35 degrees vs. 6.4 degrees, p = 0.05) than patients without diabetes. During the study period, 4 patients died. Patients who survived had higher capacitance (486 +/- 163 pF vs. 697 +/- 218 pF, p = 0.07) and phase angle (4.65 +/- 0.73 degrees, vs. 6.34 +/- 1.67 degrees, p = 0.008) than those who did not survive. The Kaplan-Meier method was used to compute observed survival. The cumulative observed survival of PD patients with an enrollment phase angle > or = 6 degrees was significantly (p = 0.01) higher than that of patients with an enrollment phase angle < 6 degrees. Reactance was directly correlated with albumin (r = 0.52, p < 0.0001) and total protein (r = 0.44, p < 0.05). Capacitance was directly correlated with body mass index (r = 0.35, p < 0.05), albumin (r = 0.32, p < 0.05), and blood urea nitrogen (BUN) (r = 0.44, p < 0.01), and inversely correlated with body weight (r = -0.51, p < 0.0001). Phase angle was directly correlated with all of the biochemical markers of nutrition, such as albumin (r = 0.54, p < 0.01), total protein (r = 0.38, p < 0.05), creatinine (r = 0.28, p < 0.01), and BUN (r = 0.39, p < 0.05). By stepwise multivariate regression analysis, body weight (beta = -0.60, p < 0.0001) and total protein (beta = 0.32, p = 0.012) were significant determinants of resistance. Body weight (beta = -0.31, p = 0.02) and albumin (beta = 0.59, p < 0.0001) were significant predictors of reactance. Serum albumin (beta = 0.53, p < 0.0001) was the only best predictor of phase angle in PD patients. The BIA indices reflect nutrition status in PD patients, and may be useful in monitoring nutrition interventions.
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PMID:Usefulness of bioelectrical impedance analysis in monitoring nutrition status and survival of peritoneal dialysis patients. 1240 18

An increased level of total plasma homocysteine (tHcy) is a risk factor for poor cardiovascular outcome in the general population. However, a decreased, rather than an increased, tHcy concentration may predict poor outcome in maintenance hemodialysis (MHD) patients, a phenomenon referred to as reverse epidemiology. Associations were examined between tHcy level and markers of malnutrition-inflammation complex syndrome and 12-mo prospective hospitalization and mortality in 367 MHD patients, aged 54.5 +/- 14.7 (mean +/- SD) years, who included 199 men and 55% individuals with diabetes. tHcy was 24.4 +/- 11.8 micro mol/L, and 94% of the patients had hyperhomocysteinemia (tHcy >13.5 micro mol/L). tHcy had weak to moderate but statistically significant bivariate and multivariate correlations with some laboratory markers of nutrition (serum albumin, prealbumin, creatinine, and urea nitrogen) but no significant correlation with serum C-reactive protein or two proinflammatory cytokines (IL-6 and TNF-alpha). During 12 mo of follow-up, 191 MHD patients were hospitalized, 37 died, nine underwent renal transplantation, and 38 transferred out. Hospitalization rates were significantly higher in patients with lower tHcy levels. Mortality rate in the lowest tHcy quartile (17.4%) was significantly higher compared with other three quartiles (6.5 to 9.8%; Kaplan-Meier P = 0.04). Relative risk of death for the lowest tHcy quartile, even after adjustment for case-mix and serum albumin, was 2.27 (95% confidence interval, 1.14 to 4.53; P = 0.02). Hence, tHcy may be a more exclusive nutritional marker in MHD patients with no association with inflammatory measures. Despite a very high prevalence of hyperhomocysteinemia in MHD patients, lower values of tHcy are paradoxically associated with increased hospitalization and mortality. The lowest tHcy quartile confers a twofold increase in risk of death independent of hypoalbuminemia. The nutritional feature of tHcy in MHD patients may explain its reverse association with outcome.
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PMID:A low, rather than a high, total plasma homocysteine is an indicator of poor outcome in hemodialysis patients. 1474 92

Cardiovascular disease is common in patients with chronic kidney disease (CKD). As renal function fails, many patients become progressively malnourished, as evidenced by reduced levels of albumin, prealbumin, and transferrin. Malnourished patients have increased levels of C reactive protein (CRP), interleukin-6 (IL-6), and concomitant cardiovascular disease when they reach end stage. Many diseases that cause CKD, diabetes, and hypertension are also associated with cardiovascular disease. Thus the direct effect of renal failure per se directly contributing to the inflammation-malnutrition-atherosclerosis paradigm is not completely established in early stages of CKD. Some aspects of progressive renal failure, however, cause changes in plasma composition and endothelial structure and function that favor vascular injury. As renal function fails, hepatic apo A-I synthesis decreases and HDL levels fall. HDL is an important antioxidant and defends the endothelium from the effects of cytokines. Inflammation causes further structural and functional abnormalities in HDL. Apolipoprotein C III (apo C III), a competitive inhibitor of lipoprotein lipase is increased in CKD. Serum triglyceride levels increase as a result of accumulation of intermediate-density lipoprotein (IDL) comprising VLDL and chylomicron remnants. These impede vascular relaxation and are associated with cardiovascular disease. Activation of the renin angiotensin axis is a component of many renal diseases and adaptation to loss of renal mass. Angiotensin II (AngII) activates NADPH oxidases, leading to production of the superoxide anion and decreased availability of nitric oxide (NO), further impairing vascular function. H(2)O(2), produced as a consequence of superoxide dismutation, stimulates vascular cell proliferation and hypertrophy. Leukocyte-derived myeloperoxidase functions as an "NO Oxidase" in the inflamed vasculature and contributes to decreased NO bioavailability and compromised vascular reactivity. The changes in lipoprotein composition and structure as well as AngII-mediated alterations in endothelial function amplify the effect of subsequent inflammatory events.
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PMID:The role of oxidative stress-altered lipoprotein structure and function and microinflammation on cardiovascular risk in patients with minor renal dysfunction. 1497 55


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