A Tura

National Research Council, Roma, Latium, Italy

Are you A Tura?

Claim your profile

Publications (27)91.94 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: In humans, sodium is essential for the regulation of blood volume and pressure. During hemodialysis, sodium measurement is important to preserve the patient from hypo- or hyper-natremia Usually, sodium measurement is performed through laboratory equipment which is typically expensive, and requires manual intervention. We propose a new method, based on conductivity measurement after treatment of dialysate solution through ion-exchange resin. To test this method, we performed in vitro experiments. We prepared 40 ml sodium chloride (NaCl) samples at 280, 140, 70, 35, 17.5, 8.75, 4.375 mEq/l, and some "mixed samples", i.e., with added potassium chloride (KCl) at different concentrations (4.375-17.5 mEq/l), to simulate the confounding factors in a conductivity-based sodium measurement. We measured the conductivity of all samples. Afterwards, each sample was treated for 1 min with 1 g of Dowex G-26 resin, and conductivity measured again. On average, the difference ɛ in the conductivity between mixed samples and corresponding pure NaCl samples (at the same NaCl concentration) was 20.9%. With treatment with the resin, it was 9.9%, only. We conclude that ion-exchange resin treatment coupled with conductivity measures may be a possible simple approach for continuous and automatic sodium measurement during hemodialysis.
    Journal of Physics Conference Series 09/2013; 459(1):2062-.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Women with former gestational diabetes are at increased risk of Type 2 diabetes, which likely relates to hyperlipidaemia and ectopic lipid storage, mainly in the liver. Here, we examined the response of non-esterified fatty acid dynamics to oral glucose loading (oral glucose tolerance test). We studied women with former gestational diabetes with normal glucose tolerance (n = 60) or impaired glucose metabolism (n = 12) and compared them with healthy women after normal pregnancy (control subjects, n = 15). During a 3-h oral glucose tolerance test, glucose, insulin and non-esterified fatty acid were frequently measured to compute the area under the non-esterified fatty acid curve and parameters of β-cell function and insulin sensitivity. Through mathematical modelling, we assessed insulin sensitivity of lipolysis inhibition and the fractional non-esterified fatty acid turnover rate. We also measured some serum liver enzymes. Women with former gestational diabetes were slightly older and had greater body mass than control subjects. Subjects with impaired glucose metabolism had lower oral glucose insulin sensitivity, but higher fasting insulin and area under the non-esterified fatty acid curve, which inversely related to oral glucose insulin sensitivity and independently determined mean glycaemia. Model-derived non-esterified fatty acid parameters were lower in subjects with impaired glucose metabolism than in control subjects, particularly sensitivity of non-esterified fatty acid inhibition to insulin (2.50 ± 0.52 vs. 1.06 ± 0.20 · 10(-2) ml/μU). Also, subjects with impaired glucose metabolism had higher liver transaminases. However, all non-esterified fatty acid parameters showed only modest inverse correlation with liver transaminases. Despite greater insulinaemia, circulating non-esterified fatty acids are higher in women with former gestational diabetes than in control subjects, which likely results from reduced sensitivity of lipolysis inhibition to insulin. This parameter may serve as indicator of an early metabolic derangement in this population at risk for diabetes.
    Diabetic Medicine 03/2012; 29(3):351-8. · 3.24 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background and Aims. Women with former gestational diabetes (fGDM) are characterized by impaired beta-cell function (BC). Incretin hormones contribute to insulin secretion after oral administration of glucose. We aimed to assess the possible role of incretins on altered insulin release in fGDM. Materials and Methods. We studied 104 fGDM women within 6 months after delivery and 35 healthy women after normal pregnancy (CNT) with a 75 g oral (OGTT) and a 0.33 g/kg intravenous (IVGTT) glucose test, both lasting 3 h. The ratio of suprabasal areas under the concentration curves for glucose (dAUC(GL)) and C-peptide (dAUC(CP)) evaluated BC during OGTT (BC(OG)) and IVGTT (BC(IV)). Incretin effect was computed in all fGDM and in fGDM with normal tolerance (fGDM(NGT)) and with impaired glucose regulation (fGDM(IGR)). Results. dAUC(GL) of fGDM was higher (P < 0.0001) than CNT for both tests; while dAUC(CP) were not different. BC(OG) and BC(IV) were lower in fGDM versus CNT (1.42 ± 0.17nmol(CP)/mmol(GLUC) versus 2.53 ± 0.61, P = 0.015 and 0.41 ± 0.03 versus 0.68 ± 0.10, P = 0.0006, respectively). IE in CNT (66 ± 4 %) was not different from that of all fGDM (59 ± 3) and fGDM(NGT) (60 ± 3), but higher than that of fGDM(IGR) (52 ± 6; P = 0.03). IE normalized to BMI was 2.77 ± 0.19 % m(2)/kg in CNT, higher than that of fGDM(IGR) (1.75 ± 0.21; P = 0.02) and also of fGDM(NGT  )(2.33 ± 0.11; P = 0.038). Conclusion. Compromised IE characterizes fGDM(IGR). In both fGDM categories, regardless their glucose tolerance, IE normalized to BMI was reduced, signifying an intrinsic characteristic of fGDM. Therefore, the diminished IE of fGDM seems to reflect an early abnormality of the general beta-cell dysfunction in the progression toward type 2 diabetes.
    International Journal of Endocrinology 01/2012; 2012:247392. · 2.52 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We estimated the heritability of individual differences in beta cell function after a mixed meal test designed to assess a wide range of classical and model-derived beta cell function parameters. A total of 183 healthy participants (77 men), recruited from the Netherlands Twin Register, took part in a 4 h protocol, which included a mixed meal test. Participants were Dutch twin pairs and their siblings, aged 20 to 49 years. All members within a family were of the same sex. Insulin sensitivity, insulinogenic index, insulin response and postprandial glycaemia were assessed, as well as model-derived parameters of beta cell function, in particular beta cell glucose sensitivity and insulin secretion rates. Genetic modelling provided the heritability of all traits. Multivariate genetic analyses were performed to test for overlap in the genetic factors influencing beta cell function, waist circumference and insulin sensitivity. Significant heritabilities were found for insulinogenic index (63%), beta cell glucose sensitivity (50%), insulin secretion during the first 2 h postprandial (42-47%) and postprandial glycaemia (43-52%). Genetic factors influencing beta cell glucose sensitivity and insulin secretion during the first 30 postprandial min showed only negligible overlap with the genetic factors that influence waist circumference and insulin sensitivity. The highest heritability for postprandial beta cell function was found for the insulinogenic index, but the most specific indices of heritability of beta cell function appeared to be beta cell glucose sensitivity and the insulin secretion rate during the first 30 min after a mixed meal.
    Diabetologia 02/2011; 54(5):1043-51. · 6.49 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: CONTEXT: What defects in glucose metabolism are present in offspring of type 2 diabetic patients (FHD(+) with a positive family history of diabetes) and to what extent they depend on line of inheritance are uncertain. OBJECTIVE: The objective of this study was to assess clinical phenotype, insulin sensitivity, and β-cell function in FHD(+) by line of inheritance. SUBJECTS: The subjects included 1221 nondiabetic men and women aged 30-60 yr, of whom 343 were FHD(+), who participated to the Relationship between Insulin Sensitivity and Cardiovascular Disease Investigators study, a multicenter European collaboration. MAIN OUTCOME MEASURES: The main outcome measures included the following: insulin sensitivity by the euglycemic clamp; total insulin secretion, β-cell glucose sensitivity, rate sensitivity, and potentiation by C-peptide deconvolution and oral glucose tolerance test modeling; and acute insulin response to i.v. glucose. RESULTS: Older age, increased adiposity, and dyslipidemia were the dominant features of FHD(+) clinical phenotype. FHD(+) subjects had a 13% reduction in insulin sensitivity [95% confidence interval (CI) of 6,19], which in males was more pronounced (17%, CI: 5,24 vs. 10%, CI: 2,20) and influenced by maternal inheritance (21%, CI: 5,38 vs. 14%, CI: 0,28 paternal). After adjusting for confounders, β-cell glucose sensitivity and rate sensitivity were reduced by 13% (CI: 3,20) and 18% (CI: 5,35), respectively (P < 0.01 for both); the former defect was more severe with maternal (16%, CI: 4,26) than paternal (9%, CI: -2,22) transmission. Independently of line of inheritance, both fasting and total oral glucose tolerance test insulin secretion were increased in proportion to the insulin resistance, whereas acute insulin response and rate sensitivity were not. CONCLUSIONS: Diabetic inheritance is expressed as a characteristic clinical phenotype associated with defects in insulin sensitivity and β-cell glucose sensitivity, which are accentuated along maternal inheritance. β-Cell rate sensitivity is reduced and β-cell dynamic responses to insulin resistance are lost independently of the line of inheritance.
    The Journal of clinical endocrinology 10/2010; 95(10):4703-11.
  • Source
    Diabetologia 04/2010; · 6.49 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: It is commonly thought that hyperglycaemia results from insufficient compensation of insulin secretion for insulin resistance. To verify this hypothesis, we assessed beta cell function and insulin sensitivity (IS) in a large cohort of volunteers with normal glucose tolerance (NGT) or impaired glucose regulation (IGR), i.e. impaired glucose tolerance or impaired fasting glucose. In men and women with NGT (n=1,123) or IGR(n=156) (age 44 +/- 8 years, BMI 25+/-4 kg/m2, mean +/- SD)we measured: (1) IS by clamp; (2) insulin secretion rates(ISR) and beta cell glucose sensitivity (=slope of the insulin secretion/plasma glucose dose-response) by C-peptide deconvolution and OGTT modelling; and (3) acute insulin response to intravenous glucose. After controlling for centre, sex, age and BMI, fasting and total ISR were inversely related to IS in both groups,whereas beta cell glucose sensitivity was not. Acute insulin response was reciprocally related to IS in both groups, but the relationships were incompatible with inadequate compensation and significance was lost after controlling for fasting ISR. InIGR vs NGT, IS was impaired (92 [75] vs 133 [86] micromol min(-1)[kg fat-free mass](-1) [nmol/l](-1), median [interquartile range],p<0.0001) as was beta cell glucose sensitivity (69 [46] vs 119[83] pmol min(-1) m(-2) [nmol/l](-1), p<0.0001), whereas fasting and total ISR were increased (35% and 25%, respectively, p<0.0001). In fully adjusted models, beta cell glucose sensitivity was the strongest determinant of OGTT glucose levels. Insulin resistance normally upregulates the secretory tone, with no evidence of defective compensation in IGR. In contrast, beta cell glucose sensitivity is independent of insulin resistance, but a key determinant of glucose tolerance. This suggests that hyperglycaemia results from an intrinsic beta cell defect rather than from inadequate compensation for insulin resistance.
    Diabetologia 04/2010; 53(4):749-56. · 6.49 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The Zone diet (ZD) is centreed primarily on protein intake. Previous findings have assessed the role of ZD on glucose metabolism, but the outcomes have been conflicting. So far, there is no clear evidence of the effects of ZD on insulin response. Furthermore, the effect of ZD on insulin sensitivity has never been clearly determined yet. Our aim was to evaluate in healthy subjects how ZD acts on body composition, lipid profile and overall on insulin sensitivity and secretion in dynamic conditions. We also compared ZD effects with those of the Mediterranean diet (MD). Twelve volunteers were studied. Subjects were randomized either to MD or to ZD for 8weeks. A wash-out period followed. Afterwards, subjects were crossed over to the other diet for other 8weeks. At any end-point subjects underwent standard 75g oral glucose tolerance test for measurements of glucose, insulin, C-peptide, proinsulin and glucagon. Lipids and free fatty acids were determined at fasting. Insulin sensitivity was assessed by the oral glucose insulin sensitivity index. Insulin secretion was determined by mathematical modelling of insulin and C-peptide data. No significant differences were observed following both diets in body weight, fat mass and plasma glucose, insulin, C-peptide, proinsulin and glucagon levels. Similarly, insulin sensitivity and secretion were not different in both absolute values and changes from baseline. Decrease in triglyceride and increase in HDL–cholesterol levels were observed after ZD compared with MD. Thus, it was determined that intake of high-protein diet for 2 months does not modify insulin action and secretion, but improves lipid profile. KeywordsDietary carbohydrates-Dietary proteins-Insulin-Cholesterol-Humans
    Mediterranean Journal of Nutrition and Metabolism 01/2010; 3(3):233-237.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Minimal model analysis for insulin sensitivity has been validated against the glucose clamp and is an accepted method for estimating insulin sensitivity from IVGTT. However minimal model analysis requires a 3 h test and relevant expertise to run the mathematical model. The aim of this study was to suggest a simple predictor of minimal model analysis index using only 1 h IVGTT. We studied participants with different clinical characteristics who underwent 3 h regular (n = 336) or insulin-modified (n = 160) IVGTT, or 1 h IVGTT and euglycaemic-hyperinsulinaemic clamp (n = 247). Measures of insulin sensitivity were insulin sensitivity index estimated by minimal model analysis (S(I)) and the mean glucose infusion rate (clamp) (M). A calculated S(I) (CS(I)) predictor, CS(I) = Alpha X K(G)/(DeltaAUC(INS)/T), was suggested, based on the calculation of the rate of glucose disappearance K(G) and the suprabasal AUC of insulin concentration DeltaAUC(INS) over T = 40 min. For all the participants, alpha was assumed equal to the regression line slope between K(G)/(DeltaAUC(INS)/T) and S(I) in control participants. CS(I) and S(I) showed high correlation (R(2) = 0.68-0.96) and regression line slopes of approximately one in the majority of groups. CS(I) tended to overestimate S(I) in type 2 diabetic participants, but results were more reliable when CS(I) was computed with insulin-modified rather than regular IVGTT. CS(I) showed behaviours similar to S(I) as regards relationships with BMI, acute insulin response and sex. CS(I) showed good correlation with M (R(2) = 0.82). A short test can achieve a good approximation of minimal model analysis and clamp insulin sensitivity. The importance of a method such as CS(I) is that it allows analysis of IVGTT datasets with samples limited to 1 h.
    Diabetologia 10/2009; 53(1):144-52. · 6.49 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We investigated whether variation in MTNR1B, which was recently identified as a common genetic determinant of fasting glucose levels in healthy, diabetes-free individuals, is associated with measures of beta cell function and whole-body insulin sensitivity. We studied 1,276 healthy individuals of European ancestry at 19 centres of the Relationship between Insulin Sensitivity and Cardiovascular disease (RISC) study. Whole-body insulin sensitivity was assessed by euglycaemic-hyperinsulinaemic clamp and indices of beta cell function were derived from a 75 g oral glucose tolerance test (including 30 min insulin response and glucose sensitivity). We studied rs10830963 in MTNR1B using additive genetic models, adjusting for age, sex and recruitment centre. The minor (G) allele of rs10830963 in MTNR1B (frequency 0.30 in HapMap Centre d'Etude du Polymorphisme [Utah residents with northern and western European ancestry] [CEU]; 0.29 in RISC participants) was associated with higher levels of fasting plasma glucose (standardised beta [95% CI] 0.17 [0.085, 0.25] per G allele, p = 5.8 x 10(-5)), consistent with recent observations. In addition, the G-allele was significantly associated with lower early insulin response (-0.19 [-0.28, -0.10], p = 1.7 x 10(-5)), as well as with decreased beta cell glucose sensitivity (-0.11 [-0.20, -0.027], p = 0.010). No associations were observed with clamp-assessed insulin sensitivity (p = 0.15) or different measures of body size (p > 0.7 for all). Genetic variation in MTNR1B is associated with defective early insulin response and decreased beta cell glucose sensitivity, which may contribute to the higher glucose levels of non-diabetic individuals carrying the minor G allele of rs10830963 in MTNR1B.
    Diabetologia 06/2009; 52(8):1537-42. · 6.49 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Highly active antiretroviral therapy (HAART) leads to lipodystrophy and is associated with detrimental changes in glucose and lipid metabolism. This study investigated the impact of rosiglitazone on insulin sensitivity, beta cell function, bone mineral density, and body composition in HIV+ nondiabetic subjects under HAART. In this randomized, double blind, placebo controlled parallel group study, 40 HIV+ subjects were treated with rosiglitazone 4 mg/day (R, n=23) or placebo (P, n=17) for 6 months. Glucose, insulin and C peptide concentrations were analyzed for assessing insulin sensitivity and secretion. Adiponectin and leptin were evaluated. Body fluid compartments were measured with bioelectrical impedance spectroscopy, and bone mineral density and body composition with Dual X Ray absorptiometry. Rosiglitazone improved peripheral insulin sensitivity (+36.7+/-15.7 ml/min/m (2), p=0.03, means+/-SEM), while no change was observed in P (+4.5+/-19.5 ml/min/m (2), p=0.55). Liver insulin resistance, beta cell activity, and hepatic insulin clearance did not change. Plasma adiponectin increased (R: +2.47+/-0.86 microg/ml, p=0.01 vs. P: +0.45+/-0.60, p=0.28). Rosiglitazone had no influence on body composition, fat distribution and bone mineral density but expanded extra-cellular fluid volume in HIV infected persons (R: +0.50+/-0.21 l, p=0.02 vs. P: 0.10+/-0.25 l, p=0.32). Lipid metabolism in P remained unchanged, in R total cholesterol and LDL cholesterol levels increased significantly (p<0.05). Rosiglitazone treatment resulted in improved peripheral insulin sensitivity with increased circulating adiponectin in HIV patients under HAART. No effect was seen on body fat distribution, bone mineral density, and weight. These side effects and their potential for cardiac risk must be weighed against the beneficial effects on glucose metabolism.
    Hormone and Metabolic Research 04/2009; 41(7):573-9. · 2.15 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotrophic peptide (GIP) are released from intestinal endocrine cells in response to luminal glucose. Glucokinase is present in these cells and has been proposed as a glucose sensor. The physiological role of glucokinase can be tested using individuals with heterozygous glucokinase gene (GCK) mutations. If glucokinase is the gut glucose sensor, GLP-1 and GIP secretion during a 75 g OGTT would be lower in GCK mutation carriers compared with controls. We compared GLP-1 and GIP concentrations measured at five time-points during a 75 g OGTT in 49 participants having GCK mutations with those of 28 familial controls. Mathematical modelling of glucose, insulin and C-peptide was used to estimate basal insulin secretion rate (BSR), total insulin secretion (TIS), beta cell glucose sensitivity, potentiation factor and insulin secretion rate (ISR). GIP and GLP-1 profiles during the OGTT were similar in GCK mutation carriers and controls (p = 0.52 and p = 0.44, respectively). Modelled variables of beta cell function showed a reduction in beta cell glucose sensitivity (87 pmol min(-1) m(-2) [mmol/l](-1) [95% CI 66-108] vs 183 pmol min(-1) m(-2) [mmol/l](-1) [95% CI 155-211], p < 0.001) and potentiation factor (1.5 min [95% CI 1.2-1.8] vs 2.2 min [95% CI 1.8-2.7], p = 0.007) but no change in BSR or TIS. The glucose/ISR curve was right-shifted in GCK mutation carriers. Glucokinase, the major pancreatic glucose sensor, is not the main gut glucose sensor. By modelling OGTT data in GCK mutation carriers we were able to distinguish a specific beta cell glucose-sensing defect. Our data suggest a reduction in potentiation of insulin secretion by glucose that is independent of differences in incretin hormone release.
    Diabetologia 10/2008; 52(1):154-9. · 6.49 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We evaluated insulin sensitivity and beta cell function in patients with chronic heart failure (CHF), and investigated a possible correlation of these metabolic parameters with specific biomarkers of heart failure. Additionally, we investigated the effects of two angiotensin receptor blockers (ARBs), namely telmisartan and candesartan, that were administered over a 5 month treatment period, as additional therapy to standard care. The study group consisted of 94 CHF patients. Insulin sensitivity (OGIS index) and insulin secretion parameters were investigated by frequently sampled oral glucose tolerance tests and consecutive mathematical modelling. In total, 94.6 % of patients had clinically overt diabetes, impaired glucose tolerance or insulin resistance at the time of enrolment HbA1c was found to correlate to NT-proBNP, MR-proADM, CT-proET-1, and MR-proANP, but not to Copeptin. NT-proBNP correlated inversely to OGIS. None of the metabolic parameters were altered significantly after candesartan or telmisartan treatment in either the patient or standard care group. Insulin sensitivity and insulin secretion are impaired in CHF and biomarkers of heart failure and atherosclerotic disease correlate to glucose metabolism.
    Experimental and Clinical Endocrinology & Diabetes 10/2008; 117(3):99-106. · 1.56 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Novel type 2 diabetes-susceptibility loci have been identified with evidence that individually they mediate the increased diabetes risk through altered pancreatic beta cell function. The aim of this study was to test the cumulative effects of diabetes-risk alleles on measures of beta cell function in non-diabetic individuals. A total of 1,211 non-diabetic individuals underwent metabolic assessment including an OGTT, from which measures of beta cell function were derived. Individuals were genotyped at each of the risk loci and then classified according to the total number of risk alleles that they carried. Initial analysis focused on CDKAL1, HHEX/IDE and TCF7L2 loci, which were individually associated with a decrease in beta cell function in our cohort. Risk alleles for CDKN2A/B, SLC30A8, IGF2BP2 and KCNJ11 loci were subsequently included into the analysis. The diabetes-risk alleles for CDKAL1, HHEX/IDE and TCF7L2 showed an additive model of association with measures of beta cell function. Beta cell glucose sensitivity was decreased by 39% in those individuals with five or more risk alleles compared with those individuals with no risk alleles (geometric mean [SEM]: 84 [1.07] vs 137 [1.11] pmol min(-1) m(-2) (mmol/l)(-1), p = 1.51 x 10(-6)). The same was seen for the 30 min insulin response (p = 4.17 x 10(-7)). The relationship remained after adding in the other four susceptibility loci (30 min insulin response and beta cell glucose sensitivity, p < 0.001 and p = 0.003, respectively). This study shows how individual type 2 diabetes-risk alleles combine in an additive manner to impact upon pancreatic beta cell function in non-diabetic individuals.
    Diabetologia 09/2008; 51(11):1989-92. · 6.49 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Acute insulin release (AIR) in response to intravenous glucose injection (IVGTT) can be abolished in diabetic subjects when their response to oral glucose is maintained. To elucidate this phenomenon, we examined the relationships between fasting plasma glucose (FPG) and the secretory responses to an IVGTT and an oral glucose test (OGTT). We measured AIR and secretion after a 75-g OGTT in 221 subjects [age 37 +/- 11 years, body mass index (BMI) 28 +/- 5 kg/m(2); mean +/- SD] with normal glucose tolerance (NGT, n = 147), impaired FPG/impaired glucose tolerance (IFG/IGT, n = 28) and Type 2 diabetes (n = 46). Insulin secretion was calculated by C-peptide deconvolution; pancreatic B-cell glucose sensitivity was obtained by OGTT modelling. Both AIR [186 (185), 142 (164) and 10 (16) pmol/l, median (interquartile range)] and B-cell glucose sensitivity [98 (64), 66 (53) and 16 (20) pmol min(-1) m(-2) l mmol(-1)] decreased across glucose tolerance category (P < 0.0001). However, AIR became approximately 0 at approximately 7 mmol/l FPG, whereas B-cell glucose sensitivity declined gradually throughout the FPG range. In addition, for FPG > 7 mmol/l, AIR was no longer related to FPG, whereas a strong relationship between FPG and B-cell glucose sensitivity was preserved (rho = -0.71, P < 0.0001). In a multivariate regression model, adjusting for sex, age and BMI, glucose sensitivity [standardized regression coefficient (std.r.) = -0.67, P < 0.0001], but not AIR (std.r. = 0.03, P = 0.55), was an independent predictor of FPG. AIR vanishes at fasting or 2-h glucose levels, at which levels some B-cell glucose sensitivity is retained; therefore, AIR has a limited ability to quantify B-cell function in hyperglycaemic states.
    Diabetic Medicine 06/2008; 25(6):671-7. · 3.24 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Women with former gestational diabetes mellitus (fGDM) often show defects in both insulin sensitivity and beta-cell function but it is not clear which defect plays the major role or which appears first. This might be because fGDM women are often studied as a unique group and not divided according to their glucose tolerance. Different findings might also be the result of using different tests. Our aim was to study insulin sensitivity and beta-cell function with two independent glucose tolerance tests in fGDM women divided according to their glucose tolerance. A total of 108 fGDM women divided into normal glucose tolerance (IGT; N = 82), impaired glucose metabolism (IGM; N = 20) and overt type 2 diabetes (T2DM; N = 6) groups, and 38 healthy control women (CNT) underwent intravenous (IVGTT) and oral glucose tolerance tests (OGTT). Measurements Insulin sensitivity and beta-cell function were assessed by both the IVGTT and the OGTT. Both tests revealed impaired insulin sensitivity in the normotolerant group compared to controls (IVGTT: 4.2 +/- 0.3 vs. 5.4 +/- 0.4 10(-4) min(-1) (microU/ml)(-1); OGTT: 440 +/- 7 vs. 472 +/- 9 ml min(-1) m(-2)). Conversely, no difference was found in beta-cell function from the IVGTT. However, some parameters of beta-cell function by OGTT modelling analysis were found to be impaired: glucose sensitivity (106 +/- 5 vs. 124 +/- 7 pmol min(-1) m(-2) mm(-1), P = 0.0407) and insulin secretion at 5 mm glucose (168 +/- 9 vs. 206 +/- 10 pmol min(-1) m(-2), P = 0.003). Both insulin sensitivity and beta-cell function are impaired in normotolerant fGDM but the subtle defect in beta-cell function is disclosed only by OGTT modelling analysis.
    Clinical Endocrinology 02/2008; 69(2):237-43. · 3.40 Impact Factor
  • A. Tura
    Biophysical Chemistry - BIOPHYS CHEM. 01/2008; 132(2):167-168.
  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to evaluate the contribution of insulin processing to the improved meal-related B-cell function previously shown with the DPP-4 inhibitor vildagliptin. Fifty-five patients with type 2 diabetes (56.5+/-1.5 years; BMI=29.6+/-0.5 kg/m(2); FPG=9.9+/-0.2 mmol/l; HbA1c=7.7+/-0.1 %) were studied: 29 patients were treated with vildagliptin and 26 patients with placebo, both added to an ongoing metformin regimen (1.5-3.0 g/day). A standardized breakfast was given at baseline and after 52 weeks of treatment, and proinsulin related to insulin secretion was measured with C-peptide in the fasting and postprandial (over 4 h post-meal) states to evaluate B-cell function. The between-treatment difference (vildagliptin-placebo) in mean change from baseline in fasting proinsulin to C-peptide ratio (fastP/C) was -0.007+/-0.009 (p=0.052). Following the standard breakfast, 52 weeks of treatment with vildagliptin significantly decreased the dynamic proinsulin to C-peptide ratio (dynP/C) relative to placebo by 0.010+/-0.008 (p=0.037). Importantly, when the P/C was expressed in relation to the glucose stimulus (i.e., the fasting glucose and glucose AUC(0-240 min), respectively), the P/C relative to glucose was significantly reduced with vildagliptin vs. placebo, both in the fasting state (p=0.023) and postprandially (p=0.004). In conclusion, a more efficient B-cell insulin processing provides further evidence that vildagliptin treatment ameliorates abnormal B-cell function in patients with type 2 diabetes.
    Hormone and Metabolic Research 12/2007; 39(11):826-9. · 2.15 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Impedance spectroscopy has been proposed as possible approach for non-invasive glycaemia monitoring. However, few quantitative data are reported about impedance variations related to glucose concentration variations, especially below the MHz band. Furthermore, it is not clear whether glucose directly affects the impedance parameters or only indirectly by inducing biochemical phenomena. We investigated the impedance variations in glucose-water, glucose-sodium chloride, and glucose-blood samples, for increasing glucose values (up to 300 mg/dl). In all the frequency range (0.1-10(7) Hz) glucose-water samples showed impedance modulus increases for increasing glucose values (up to 135%). In blood and sodium chloride samples the impedance modulus showed only slight variations (2% and 1.4%), but again in wide frequency ranges. Therefore: i) glucose directly affects the impedance parameters of solutions; ii) effects are more relevant at frequencies below the MHz band; iii) the influence on the impedance is decreased in high conductivity solutions, but still clearly present.
    Biophysical Chemistry 10/2007; 129(2-3):235-41. · 2.28 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Impedance spectroscopy has been proposed as possible approach for non-invasive glycaemia monitoring. However, few quantitative data are reported about impedance variations related to glucose concentration variations, especially below the MHz band. Furthermore, it is not clear whether glucose directly affects the impedance parameters or only indirectly by inducing biochemical phenomena. We investigated the impedance variations in glucose-water and glucose-blood samples, for increasing glucose values (up to 300 mg/dl). In all the frequency range (0.1–107 Hz) glucose-water samples showed huge impedance modulus increases for increasing glucose values (up to 135%). In blood the impedance modulus showed only slight variations (2%), but again in a wide frequency range. Therefore: i) glucose directly affects the impedance parameters of solutions; ii) the influence on the impedance seems to decrease in high conductivity solutions, but it is still clearly present.
    12/2006: pages 194-197;