Serum selenium levels in diabetic children

The effect of increased selenium uptake on serum selenium in diabetic children was investigated during the first 9 yr of the Finnish nationwide selenium fertilization program, which started in 1984. Serum selenium concentrations were followed in 237 diabetic children (mean age 8.1 yr) and 214 controls from 1984 to 1992. The control group consisted of 107 siblings of the diabetics and of 107 other healthy children of corresponding age groups. Selenium was determined by direct electrothermal atomic absorption spectrophotometry. The effect of the increased uptake was seen in both diabetic and in control persons. Before the autumn of 1985, diabetic patients had significantly higher serum selenium levels than their siblings or the other healthy controls. Toward the end of year 1987, this difference had disappeared. After that, serum selenium levels continued to increase until the year 1990. In 1990 the mean selenium serum level of diabetic patients was 1.36 μmol/L and that of controls 1.33 μmol/L. The duration of diabetes did not have any effect on selenium serum levels. Slightly higher serum selenium in new diabetic patients before the start of therapy was explained by the dehydration state. The patients who were younger than 3 yr had slightly lower selenium serum levels when compared with older age groups. This difference was observed, however, only during the first 3 yr of the study. After that, when the selenium intake increased in general, no age-dependent differences were found anymore. There were no significant differences in serum selenium levels between males and females in either diabetic patients or in controls.     

Selenium and glycogen levels in diabetic patients

Selenium in serum and selenium and glycogen in erythrocytes were determined in diabetic patients divided into noninsulin-dependent (n=50) and insulin-dependent (n=31) groups according to the etiopathogenesis of their diabetes. Selenium was determined by the method of atomic absorption spectrometry. Serum level of selenium was statistically significantly different in patients with either noninsulin-dependent (59.23±12.2 μg/L) or insulin-dependent (58.23±16.7 μg/L) diabetes mellitus as compared with the control group of 62 subjects (64.2±11.5 μg/L; p<0.05). There was no statistically significant difference in the serum levels of selenium between the groups of patients with noninsulin-dependent and insulin-dependent diabetes mellitus. The levels of erythrocyte glycogen were 2.0580±1.326, 2.0380±1.735, and 2.0036±1.3537 μg/g Hb in the control group, noninsulin-dependent group, and insulin-dependent group, respectively, with no statistically significant between-group difference. The decreased levels of selenium in serum and erythrocytes of diabetic patients suggest the possible role of glutathione peroxidase activity.     

Plasma endothelin-1 levels and albumin excretion rate in normotensive,microalbuminuric type 2 diabetic patients

BACKGROUND: Endothelin-1 (ET-1) is able to determine functional and structural renal alterations and plasma levels of this vasoconstrictor peptide are increased in diabetic patients. In a selected group of type 2 normotensive diabetic patients with microalbuminuria, we investigated circulating ET-1 levels compared to a control group and verified whether there is a relationship between ET-1 levels and albumin excretion rate in diabetics. SUBJECTS AND METHODS: Thirty-two microalbuminuric type 2 diabetic patients (12 males and 20 females; mean age 57 +/- 8 years) without hypertension, renal failure, hypercholesterolemia or atherosclerotic damage were selected. The control group was made up of 28 healthy subjects matched for sex and age. Blood pressure, creatinine clearance, serum cholesterol and plasma ET-1 values were determined in diabetic and control group. In diabetic patients, glycosilated hemoglobin and urinary albumin excretion rate were also assayed. Mean ET-1 values in diabetics and controls were compared using Student's t-test. Linear regression test was done to relate two variables. Statistical significance was set at p<0.05. RESULTS: Mean ET-1 values were significantly higher in the diabetic group than in controls (11.77 +/- 1.16 pg/ml vs 8.9 +/- 2.1 pg/ml; p<0.05). No relationship (p>0.05) was found between circulating ET-1 and blood pressure, creatinine clearance, serum cholesterol and metabolic control in diabetics. There was a significant positive correlation (r=0.403; p=0.03) between plasma ET-1 levels and albumin excretion rate in diabetic patients. CONCLUSIONS: Our results showed that circulating ET-1 values were increased in microalbuminuric, normotensive, type 2 diabetic patients and correlated with albumin excretion rate. These findings confirm that endothelial dysfunction, as expressed by ET-1 levels, occurs early in these patients and support the hypothesis of a potential role for this peptide in development of microalbuminuria in diabetic nephropathy.     

Identification of variables influencing resistin serum levels in patients with type 1 and type 2 diabetes mellitus.

BACKGROUND: Resistin, a peptide hormone, has been discussed controversially as a missing link between obesity and insulin resistance. In contrast to resistin mRNA expression in adipose tissue, data on human serum levels in obesity and diabetes mellitus is scarce. The physiological range of serum resistin levels, reference values or adjusted percentiles have not yet been determined, making the interpretation of serum resistin concentrations quite difficult. METHODS: Resistin serum concentrations were measured systematically by ELISA in 216 healthy controls, 555 patients with type 2 diabetes and 114 patients with type 1 diabetes. Mean values, median, and range were determined, and BMI-, gender-, and disease-adapted percentiles were calculated for all subgroups. RESULTS: Age and gender did not have any influence on resistin levels. BMI and resistin levels were positively correlated in healthy controls (p = 0.02), albeit with a weak correlation coefficient. This correlation was absent in patients with type 1 and type 2 diabetes. In both genders, healthy controls had significantly higher resistin levels than patients with type 1 and type 2 diabetes (7.9 +/- 0.2 ng/ml vs. 5.7 +/- 0.2 ng/ml and 5.5 +/- 0.1 ng/ml, respectively; p < 0.0001). There was no correlation between resistin levels and occurrence of diabetic retinopathy or nephropathy. CONCLUSIONS: Serum resistin levels can be measured by ELISA over a broad range from 0.6 ng/ml up to 27.7 ng/ml, suggesting that percentiles might be helpful in the interpretation of an individuals resistin value. While age and gender do not influence resistin levels, BMI and occurrence of diabetes have to be considered.     

Effect of diabetic duration on serum concentrations of endogenous inhibitor of nitric oxide synthase in patients and rats with diabetes

This study was designed to investigate the effect of diabetic duration on serum concentrations of endogenous inhibitor of nitric oxide synthase N(G), N(G)-asymmetric dimethylarginine (ADMA) in patients and rats with diabetes, and to determine whether elevated endogenous ADMA is implicated in endothelial dysfunction or macroangiopathy in diabetes. Experimental diabetic model was induced by a single intraperitoneal injection of streptozotocin to male Sprague-Dawley rats and fed for 2-, 4- and 8-week, respectively. Type 2 diabetic patients with different diabetic duration were recruited from Xiangya Hospital. Plasma glucose and serum ADMA levels were measured in both patients and rats. Moreover, endothelium-dependent relaxation of thoracic aortas and some parameters of metabolic control were examined in rats. Serum ADMA concentrations were significantly elevated in type 2 diabetic patients compared with healthy subjects (3.44 +/- 0.40 vs 1.08 +/- 0.14 micromol/L, n = 50 in diabetic patients and n = 40 in healthy subjects, P < 0.01). The serum levels of ADMA in patients with macroangiopathy were higher than the patients without macroangiopathy (P < 0.01). But no difference was observed in serum ADMA concentrations between groups of patients with different diabetic duration. Similarly, serum levels of ADMA in diabetic rats were also significantly elevated at 2-week duration compared with duration-matched control (3.71 +/- 0.20 vs 1.04 +/- 0.23 micromol/L, n = 5 approximately 6, P < 0.01). This elevation of ADMA was retained to 4- and 8-week (3.54 +/- 0.76 vs 0.95 +/- 0.06 micromol/L for 4-week, 3.21 +/- 0.50 vs 1.03 +/- 0. 09 micromol/L for 8-week, n = 5 approximately 6, all P < 0.01) and remained unchanged among three diabetic groups. The elevation of ADMA was accompanied by impairment of endothelium-dependent relaxation and poor metabolic control in diabetic rat. These results first reveal that the extent of elevation in serum ADMA in both rats and patients with diabetes is not proportion with the length of their diabetic duration but rather with the metabolic control of this disease. Elevated endogenous ADMA may be implicated in diabetes-induced endothelial dysfunction and macroangiopathy. This study is helpful to prevention and treatment of diabetic-induced endothelial dysfunction or macroangiopathy.     

Effects of ketoacidosis and puberty on basal and TRH-stimulated thyroid hormones and TSH in children with diabetes mellitus

Basal and TRH-stimulated thyroid hormones and TSH were evaluated in two groups of prepubertal and pubertal diabetics: group B - 45 children without ketoacidosis; group C - 16 children with ketoacidosis. The diabetic patients showed no signs of diabetic microangiopathy. Fifty-three healthy subjects served as controls (group A). T4, T3, FT4 and FT3 serum levels were reduced in diabetics, particularly in ketotic ones; T4 and T3 values were lower in pubertal than in prepubertal non-ketotic diabetics and in pubertal than in prepubertal controls, while no significant difference was observed between pubertal and prepubertal ketotic patients. Moreover, no difference in rT3 serum concentrations was found between group A, B and C, but non-ketotic and ketotic pubertals showed a significant rT3 reduction if compared with non-ketotic and ketotic prepubertals and with healthy pubertals. TBG was lower in group B and group C diabetics than in controls. After TRH stimulus, T3 levels showed a significant increase both in controls and in non-ketotic diabetics, while no variation was observed in ketotic children; furthermore, at 120 minutes T3 values were lower in diabetic than in healthy children, particularly in ketotic ones. Basal TSH serum concentrations were reduced in ketotic diabetics, while no difference was found between nonketotic and control subjects. After TRH stimulus, TSH peak was higher in pubertal non-ketotic diabetics than in pubertal controls, while no difference was found between prepubertal and pubertal diabetics, both in non-ketotic and in ketotic status.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibin B levels in adolescents and young adults with type 1 diabetes

OBJECTIVE/METHODS: To assess exocrine and endocrine testicular function in subjects with diabetes, we evaluated serum inhibin B, gonadotrophins and testosterone levels in 33 male adolescent and young adult patients affected by type-1 diabetes (age 21.0 +/- 5 years; range 14.2-33.3), with a mean disease duration of 12.7 +/- 5.8 years (range 1.5-25.3) and various metabolic control (HbA1c 7.8 +/- 1.5%; range 5.5-13.2) and compared them with those of an age-matched group of 36 healthy control subjects (age 19.5 +/- 4.1 years; range 13.6-28.1). Both patients and controls had a testicular volume >or=15 ml. Inhibin B was measured by ELISA method. RESULTS/CONCLUSION: Diabetics and controls had comparable inhibin B (203 +/- 74 vs. 221 +/- 69 pg/ml, respectively) and follicle-stimulating hormone (FSH) levels, while luteinizing hormone (LH) and testosterone levels were significantly higher in the diabetic group. Inhibin B was negatively correlated both in patients and controls with FSH, while a negative correlation with LH was found only in the diabetic group. We conclude that our young diabetic males, after a mean disease duration of 12 years and various metabolic control, had inhibin B and FSH levels comparable to those of normal subjects. Therefore, they seem to have a regular testicular function and in particular a normal seminiferous tubule/Sertoli cell activity despite sustained hyperglycemia.     

Effect of Various Clinical Variables on Total Intracellular Magnesium in Hospitalized Normomagnesemic Diabetic Patients before Discharge

Deficiency of intracellular magnesium (icMg) may coexist with normal serum Mg levels. Little is known about clinical and pharmacological factors affecting icMg in normomagnesemic patients with diabetes mellitus (DM). Moreover, no information exists regarding the icMg state in diabetic patients after acute illness and before hospital discharge. We have evaluated the effect of antihyperglycemic medications and other relevant clinical variables on icMg in 119 such patients. Total icMg was measured in peripheral blood mononuclear cells. Twenty healthy volunteers served as controls. IcMg content (μg/mg cell protein) was lower in DM compared to controls (1.74 ± 0.44 vs 2.4 ± 0.39, p < 0.001). It was also significantly lower in patients treated with insulin (1.57 ± 0.31 vs 1.8 ± 0.46, p = 0.01), while metformin treatment was associated with higher icMg (1.86 ± 0.49 vs 1.63 ± 0.35, p = 0.003). After adjustment for age, gender, and concomitant use of other hypoglycemic drugs, only treatment with metformin was independently associated with increased icMg (p = 0.03). No statistically significant association or correlation was found between icMg content and age, causes of hospitalization, comorbid conditions, treatment with other drugs, concentrations of HbA_1c, serum glucose, Mg, or creatinine. In conclusion, icMg is depleted in normomagnesemic DM patients. Insulin treatment is associated with worsening of icMg status, while metformin treatment may confer protective effect.     

Comparison of whole-blood glutathione peroxidase activity,levels of serum selenium,and lipid peroxidation in subjects from the fishing and rural communities of "Rabo de Peixe" village,San Miguel Island,the Azores' Archipelago,Portugal

The activity of glutathione peroxidase (GSH-Px), serum selenium (Se), and thiobarbituric acid reactive substances (TBARS) were measured in the whole blood of 148 healthy adults aged 20–60 yr from the fishing and rural communities of “Rabo de Peixe,” The Azores, Portugal. The subjects did not live in the same household and had different socioeconomic profiles and dietary habits. The serum lipid profile and selected life habits were also considered in this study. No significant differences in the activity of GSH-Px were found in the interpopulation or intrapopulation analyses, classified by age or lipid profile. An age-dependent GSH-Px increase was noted in the younger male (M) subgroups (20–39 yr). The Se levels were higher in fishers (f) of both genders (M, F) than in subjects living in the rural (r) environment: 110±25 μg/L (f, M), 89±20 μg/L (f, F), 88±22 μg/L (r, M) and 80±17 μg/L (r, F). In the fishers, but not in the rural population, Se was higher in the males, but it did not show significant variation with age. The levels of TBARS were lower in the f than in the r male group. The Se level was lower and TBARS higher in the hyperlipemic women in the f group, compared to the corresponding controls. Our results suggest that the fishers (mainly men) show a better antioxidant status than that of their rural counterparts, due to differences in dietary habits between the study populations and between genders.     

Antioxidant status and lipid peroxidation in type II diabetes mellitus

Diabetes Mellitus (DM), a state of chronic hyperglycaemia, is a common disease affecting over 124 million individuals worldwide. In this study, erythrocyte glutathione levels, lipid peroxidation, superoxide dismutase, catalase, and glutathione peroxidase and some extracellular antioxidant protein levels of patients with type II diabetes mellitus and healthy controls were investigated. Thirty-eight patients (21 males; with age of mean +/- SD, 53.1+/-9.7 years) and 18 clinically healthy subjects (10 males; with age of mean +/- SD, 49.3+/-15.2 years) were included in the study. Levels of erythrocyte lipid peroxidation, serum ceruloplasmin and glucose levels, HbA1C levels, and erythrocyte catalase activity were significantly increased, whereas serum albumin and transferrin levels, erythrocyte glutathione levels, and glutathione peroxidase activity were significantly decreased compared to those of controls. There was no significant difference in superoxide dismutase activity compared to controls. The results suggest that the antioxidant deficiency and excessive peroxide-mediated damage may appear in non-insulin dependent diabetes mellitus.     

Osteoprotegerin--does it play a protective role in the pathogenesis of bone loss in obese perimenopausal women?

INTRODUCTION: Assessment of serum osteoprotegerin (OPG) concentrations in obese patients in comparison to healthy controls and evaluation of a possible correlation between OPG and other markers of bone turnover or calcitropic hormones. MATERIAL AND METHODS: 50 obese perimenopausal women without concomitant diseases (BMI 36.7 +/- 4.1 kg/m(2), mean age 50.4 +/- 4.9 yrs). The control group consisted of 19 healthy women (BMI 24.2 +/- 2.1 kg/m(2); mean age 53.8 +/- 5.1 yrs). In all patients serum concentration of OPG, C telopeptide of type I collagen containing the crosslinking site (CTX), osteocalcin, parathormone (PTH) and vitamin D (25-OH-D(3)) was assessed. Dual energy x-ray absorptiometry (the DXA method) of the lumbar spine and femoral neck was performed using a Lunar DPXL to measure bone marrow density (BMD). RESULTS: In obese perimenopausal women serum OPG, osteocalcin and 25-OH-D(3) levels were significantly lower, and the serum PTH level was significantly higher in comparison to healthy controls. A significantly positive correlation was found between serum OPG level and age in both obese and control subjects. CONCLUSION: The serum OPG level in obese perimenopausal women is significantly lower in comparison to healthy controls and does not correlate significantly with biochemical markers of bone turnover, calcitropic hormones and BMD. It probably cannot play a protective role in the pathogenesis of bone loss in obese perimenopausal women.     

Comparison of serum sodium and potassium by direct ion-selective electrode analysis between Chinese and American people

The serum levels of sodium and potassium in healthy Chinese were 144 +/- 1.7 mmol/L and 4.3 +/- 0.4 mmol/L respectively; in Americans, the levels were 138 +/- 2.4 and 4.3 +/- 0.3 mmol/L. I found that the serum sodium of Chinese is higher than that of Americans, the serum potassium level is almost the same. It may be due to differences between eating habits of the two races.     

Growth hormone secretion, serum, and cerebral spinal fluid insulin and insulin-like growth factor-I concentrations in pigs with streptozotocin-induced diabetes mellitus.

Diabetes mellitus was induced using streptozotocin in five gilts between 8 and 12 weeks of age. Gilts were maintained with exogenous insulin (INS) except during experimental periods. Four litter-mate gilts served as controls. At 9 months of age, all gilts were ovariectomized, and 30 days after ovariectomy, Experiment (Exp) 1 was conducted. Jugular vein catheters were inserted and blood samples were collected every 10 min for 8 hr. Experiment 2 was conducted when gilts were 11 months of age. Venous blood and cerebrospinal fluid (CSF) samples were collected in the absence (Phase I) or presence (Phase II) of INS therapy. In Experiment 1, plasma glucose concentrations were greater (P < 0.05) in diabetic (465 +/- 17 mg/100 ml) than in control (82 mg +/- 17 mg/100 ml) gilts, whereas serum INS was lower (P < 0.0001) in diabetic gilts (0.3 +/- 0.02 vs 0.9 +/- 0.05 ng/ml) and insulin-like growth factor-I was similar in diabetic and control gilts (32 +/- 3 vs 43 +/- 4 ng/ml, respectively). Mean serum GH concentration was 2-fold greater (P < 0.02) in diabetics (2.8 +/- 0.4 ng/ml) than in control gilts (1.2 +/- 0.2 ng/ml). Diabetic gilts exhibited a greater (P < 0.05) number of GH pulses than control gilts (3.2 +/- 0.4 vs 1.5 +/- 0.3/8 hr, respectively). In addition, GH pulse magnitude was markedly elevated (P < 0.02) in diabetic (5.8 +/- 0.4 ng/ml) compared with control gilts (3.3 +/- 0.6 ng/ml). Mean basal serum GH concentrations were greater (P < 0.07) in diabetic (2.2 +/- 0.5 ng/ml) compared with control gilts (1.0 +/- .1 ng/ml). In Experiment 2, CSF concentrations of insulin-like growth factor-I, INS, GH, and protein were similar for diabetic and control gilts in both phases. Serum GH levels were similar for diabetics and controls in Phase I, but were greater (P < 0.05) in diabetics than in controls in Phase II. CSF glucose levels were greater in diabetic than in control gilts in both the presence (P < 0.003) and absence (P < 0.0002) of INS therapy, whereas plasma glucose was greater (P < 0.003) in diabetic than in control gilts in the absence of INS, but returned to control concentrations in the presence of INS. However, serum GH levels were unchanged after INS therapy in the diabetic gilts. In conclusion, altered GH secretion in the diabetic gilt may, in part, be due to elevated CSF glucose concentrations, which may alter GH-releasing hormone and/or somatostatin secretion from the hypothalamus.     

Subnormal follicular-phase serum progesterone levels and elevated follicular-phase serum estradiol levels in young women with insulin-dependent diabetes

In a search for possible hormonal reasons for the loss of protection from myocardial infarction seen in diabetic women, serum levels of estradiol, progesterone, and luteinizing hormone were compared throughout a menstrual cycle (17 points) in eight healthy nonsmoking women and five otherwise healthy nonsmoking insulin-dependent diabetic women. The total length of the menstrual cycle and the lengths of the follicular and luteal phases did not differ between the groups. During the periovulatory and luteal phases, there was no significant intergroup difference with respect to any of the three hormones. During the follicular phase, in both groups, there was a plateau in serum progesterone concentration, with the level approximately 42% lower in the diabetic group (12.0 +/- 6.6 ng/dl versus 20.7 +/- 5.7; P less than 0.0001). Follicular-phase serum estradiol showed a rising curve in both groups; day-by-day comparison (days -10 to -3 before the luteinizing hormone peak) showed consistently higher levels in the diabetic group (mean, 108 pg/ml versus 95 pg/ml; P less than 0.001). The follicular-phase serum estradiol to progesterone ratio was nearly twice as high in the diabetic group as in the normal group (8.9 versus 4.6), a difference that was highly significant. The finding of elevated serum estradiol and subnormal serum progesterone concentrations during the follicular phase is so far unique to women with insulin-dependent diabetes mellitus. The possibility that this pronounced abnormality in diabetic women may be related to coronary disease merits testing in suitable in vivo and in vitro models of atherogenesis.     

Levels of zinc and magnesium in senile and diabetic senile cataractous lenses

Zinc and magnesium in serum, hair, and lens were determined in diabetic and nondiabetic patients who have been operated because of senile cataract. Both trace elements were measured by atomic absorption spectrometry, after acidic digestion of the lens and hair samples. Although there was no difference in serum, lens, and hair levels of magnesium between the two groups, the lens levels of zinc in diabetic patients (0.56+/-0.05 micromol/g dry weight) were significantly higher as compared with nondiabetic group (0.42+/-0.03 micromol/g dry weight). There was no statistically significant difference in serum and hair levels of zinc between the groups. The increased concentration of zinc in the lens of diabetic patients suggests that zinc might play a role in developmental mechanism of the diabetic senile cataract.     

Serum selenium levels in healthy slovak children and adolescents

Blood serum selenium levels were measured in 891 healthy children and adolescents (aged 11–18 yr, 450 girls and 441 boys) residing in both rural and urban areas from eight regions of Slovakia. Subjects were divided into four age groups (11–12 y, 13–14 y, 15–16 y, and 17–18 y). Serum selenium concentration was determined by the electrothermal atomic absorption spectrometric method. The mean (±SD) serum selenium concentrations were 0.750 ±0.255 μmol/L in girls and 0.773 ±0.235 μmol/L in boys. A large proportion of the individuals (25.7% in girls, 18.1% in boys) exhibited serum selenium levels under 0.57 μmol/L (45 μg/L). An increasing trend of the serum selenium values with age has been observed in both boys (p < 0.01) and girls (p < 0.05). Boys had higher serum selenium levels in the all age groups but the differences were not statistically significant.     

Lack of induction of serum gamma-glutamyltransferase in diabetes mellitus

Some authors have suggested that carbohydrates can induce hepatic microsomal enzymes, resulting in increased serum gamma-glutamyltransferase (GGT) in diabetes mellitus. Previously we demonstrated the lack of serum GGT increases in patients with acute diabetic crises. In this work we studied serum GGT activity, blood glucose levels and glycosylated hemoglobin levels (HB A1) in 35 patients with diabetes mellitus and 27 healthy volunteers. We did not see differences in the serum GGT activity among controlled (25.05 +/- 2.72 U/l) and uncontrolled (26.44 +/- 4.05 U/l) diabetics and the control group (22.51 +/- 2.95 U/l). Also, there was no significant correlation between serum GGT and HB A1 levels in diabetic patients (r = 0.279). We think that our observations may be relevant because they support the hypothesis that hyperglycemia does not act as an enzyme-inducing agent in chronically uncontrolled diabetics and, furthermore, they indicate that in the presence of abnormal serum GGT levels in diabetics it is necessary to investigate other associated diseases.     

Transforming growth factor beta1 and soluble Fas serum levels in hepatocellular carcinoma

In this study we assessed the usefulness of serum Transforming Growth Factor-beta1 (TGF-beta1) and soluble Fas (sFas) in distinguishing liver cirrhosis (LC) with and without hepatocellular carcinoma (HCC) as compared with alpha-fetoprotein (AFP). Serum TGF-beta1 and sFas levels were measured by ELISA in 51 LC patients, 54 patients with HCC and 30 healthy donors. Considering as a cut-off limit (mean+1SD of controls) 74 pg/ml and 637 pg/ml for TGF-beta1 and sFas, respectively, we computed serum concentrations of TGF-beta1 and sFas as a score (mean+/-SD). The positive frequency of serum TGF-beta1 levels in HCC patients (54%) was greater than in LC patients (26%) and healthy donors (3%). TGF-beta1 levels were higher in HCC (1.6+/-0.5) than in LC (1.1+/-0.2) (P<0.0001) and healthy donors (0.6+/-0.2). Using a cut-off limit of 82 pg/ml (mean+2SD), the positive frequency of TGF-beta1 was 20% in HCC patients. None of the controls and LC patients had TGF-beta1 levels higher than 82 pg/ml. The positive frequency of serum sFas levels was 100% in HCC patients, 98% in LC patients and 3% in healthy controls. Serum sFas levels were higher in HCC (2.5+/-0.7) than in LC (1.9+/-0.5) (P<0. 001) and healthy donors (0.6+/-0.3). No significant change of positive frequency was obtained by setting sFas cut-off at higher levels. sFas values did not correlate with TGF-beta1 levels. No relationship was found between TGF-beta1 amounts and AFP levels. However, in the 23% of HCC patients, with normal AFP values TGF-beta1 levels were higher than the cut off. These findings suggest the potential usefulness for TGF-beta1 assay in AFP-negative HCC.     

Oxidative protein damage in plasma of type 2 diabetic patients.

In this study, we evaluated protein oxidation in 84 patients with Type 2 diabetes with no complications and in 61 healthy volunteers who formed the control group, whose ages matched those of the patients. We determined plasma carbonyl and plasma thiol levels as markers of oxidative protein damage and erythrocyte glutathione, plasma ceruloplasmin and transferrin as markers of free radical scavengers. The concentrations (mean +/- SD) of both of plasma carbonyl (1.24 +/- 0.46 vs. 0.72 +/- 0.17 nmole/mg protein; p < 0.0001) and lipid hydroperoxides (1.8 +/- 0.63 vs. 1.3 +/- 0.21 micromole/l; p < 0.0001) were increased, and the concentration of plasma transferrin (3.85 +/- 0.65 vs. 4.59 +/- 0.79 g/l; p < 0.05) was decreased, respectively, in Type 2 diabetic patients compared with those of the controls. There were no significant differences in the concentrations of plasma thiol (0.0064 +/- 0.001 vs. 0.0068 +/- 0.001 micromole/mg protein), erythrocyte glutathione (2.54 +/- 0.57 vs. 2.65 +/- 0.56 mg/g Hb), plasma ceruloplasmin (548 +/- 107.30 vs. 609 +/- 93.34 mg/l) between the patients and the controls. These changes observed in diabetic patients contribute to the imbalance in the redox status of the plasma. We attribute this imbalance to oxidative protein damage in Type 2 diabetic patients clinically free of complications.     

Type II collagen peptides for measuring cartilage degradation

This paper describes two new immunoassays for a peptide of the triple helix of type II collagen (Coll 2-1) and its nitrated form (Coll 2-1 NO(2)). In healthy subjects aged between 20 and 65 years old, Coll 2-1 and Coll 2-1 NO(2) levels in serum were in means 125.13+/-3.71 and 0.16+/-0.08 nmol/l, respectively. These levels did not significantly vary with age. However, up to 45 years of age, Coll 2-1 NO(2) levels in women were significantly higher than in men. In patients with knee osteoarthritis (OA), Coll 2-1 in serum was found to be elevated compared to healthy controls (267.45+/-26.42 nmol/l vs 126.78+/-6.61 nmol/l). Further, we have demonstrated that an increase of the urinary levels of Coll 2-1 or Coll 2-1 NO(2) over 1 year was predictive of joint space narrowing progression in OA patients. In conclusion, these preliminary results indicate that Coll 2-1 could be a predictive marker of knee OA progression.