Biomedical subjects

P Cavallo-Perin

Publications and source records attributed to P Cavallo-Perin.

At least 19 recordsLinked to original sources

PubMed2006

Effect of age on the association of non-high-density-lipoprotein cholesterol and apolipoprotein B with cardiovascular mortality in a Mediterranean population with type 2 diabetes: the Casale Monferrato study.

AIMS/HYPOTHESIS: Measurement of plasma apolipoprotein (Apo) B may improve prediction of cardiovascular risk, as it provides a measure of the total number of atherogenic particles. The aim of this population-based study was to compare the association of non-HDL-cholesterol, ApoB and the ApoB:ApoA-I ratio with cardiovascular mortality in people with type 2 diabetes. SUBJECTS AND METHODS: We assessed the association of lipids, lipoprotein lipids and apolipoproteins with 11-year mortality from cardiovascular disease in the population-based cohort of the Casale Monferrato Study (1,565 people with diabetes; median age 68.9 years), and determined the effect of age (< or =70 and >70 years) on these relationships. RESULTS: On the basis of 341 deaths from cardiovascular disease in 10,809 person-years of observation, there was a decreasing trend in risk adjusted for multiple factors across quartiles of total cholesterol, and LDL- and non-HDL-cholesterol in people aged >70 years, but no trend in those aged < or =70 years. Age did not affect the protective effect of HDL-cholesterol. ApoB and ApoB:ApoA-I were associated with outcome in people in both age groups independently of non-HDL-cholesterol. After adjustment for multiple factors, including non-HDL-cholesterol, the hazard ratios for ApoB:ApoA-I in the upper vs lower quartile were 2.98 (95% CI 1.15-7.75; p for trend=0.009) for people aged < or =70 years and 1.94 (95% CI 1.20-3.13; p for trend=0.003) for those aged >70 years. CONCLUSIONS/INTERPRETATION: In this cohort of Mediterranean subjects with diabetes, ApoB and the ApoB:ApoA-I ratio were associated with cardiovascular disease mortality independently of non-HDL-cholesterol. Our findings support the recommendation that ApoB and ApoA-I should be measured routinely in all people with diabetes, particularly in the elderly.

Age Distribution↗

PubMed2005

Preserved insulin sensitivity and {beta}-cell activity, but decreased glucose effectiveness in normal-weight women with the polycystic ovary syndrome.

Insulin resistance and hyperinsulinemia are often considered intrinsic features of the polycystic ovary syndrome (PCOS). Nevertheless, conflicting results of insulin sensitivity and secretion have been obtained in the subgroup of normal-weight women with PCOS. Differences in body composition, ethnicity, and diet composition and a family history of metabolic diseases may act as confounding variables in women with PCOS. In the present study, insulin sensitivity and secretion were estimated by an iv glucose tolerance test (IVGTT), analyzed by minimal models, in 20 normal-weight healthy women with PCOS and no family history of type 2 diabetes mellitus and in 20 normally ovulating women, matched for age and body mass index. Insulin sensitivity [mean (95% confidence intervals); PCOS 4.0 (2.8-5.1) vs. controls 4.5 (3.5-5.4) 10(-4) min(-1)/microU.ml], and insulin secretion, expressed as the acute insulin response to glucose [PCOS 3.7 (3.3-4.2) vs. controls 3.7 (3.4-4.0) microU/ml] were similar in the two groups. The women with PCOS showed an increased proportion of total body fat (PCOS 29% vs. controls 27.2%; P < 0.01). They also showed decreased glucose effectiveness, i.e. the proportion of glucose uptake independent from insulin activity [PCOS 2.6 (2.1-3.0) vs. controls 3.8 (3.0-4.6) mg x 100 min(-1); P = 0.01]. The levels of insulin sensitivity and of glucose effectiveness did not correlate in either group. Whether the isolated finding of decreased glucose effectiveness could reflect an early stage in the development of the metabolic aberrations often associated with the syndrome remains to be clarified.

Adult↗

PubMed2005

Fibrinogen and AER are major independent predictors of 11-year cardiovascular mortality in type 2 diabetes: the Casale Monferrato Study.

AIMS/HYPOTHESIS: Fibrinogen and elevated AER increase cardiovascular mortality, but few data are available in the type 2 diabetic population. We have conducted an 11-year follow-up study of the Casale Monferrato cohort to assess: (1) the long-term predictive role of AER independently of conventional risk factors; (2) the shape of its relationship with cardiovascular mortality; and (3) whether fibrinogen has a predictive effect independent of the increased cardiovascular risk associated with nephropathy. METHODS: During the follow-up period (1991-2001) a population-based cohort of 1,565 patients was regularly examined, and measurements of HbA1c were centralised. Multivariate Cox proportional hazards modelling was employed to assess the role of fibrinogen and AER as predictors of all-cause and cardiovascular mortality, independently of baseline variables and individual cumulative average values of HbA1c during follow-up. RESULTS: In 10,890.2 person-years of observations, 685 deaths were identified, giving an all-cause mortality rate of 63.4 per 1,000 person-years (95% CI 58.8-68.3). In Cox regression analyses, the strongest predictor of cardiovascular mortality was macroalbuminuria (relative risk 2.18, 95% CI 1.62-2.94), which was mainly associated with a high risk of short-term mortality. No increased risk was evident until the upper microalbuminuric range of AER values. Plasma fibrinogen was also a major independent predictor, and its role was not modified by AER, or by the exclusion of subjects developing chronic renal failure or diabetic nephropathy during follow-up. CONCLUSIONS/INTERPRETATION: The results indicate that: (1) AER is the main independent predictor of 11-year cardiovascular mortality; (2) this effect is mainly evident in the upper range of microalbuminuria and in macroalbuminuria; and (3) fibrinogen has an independent effect on cardiovascular mortality, but no synergistic effect with AER, suggesting that both endothelial dysfunction and chronic inflammation are involved in the excess cardiovascular mortality of type 2 diabetic patients.

Aged↗

PubMed2004

QT interval, cardiovascular risk factors and risk of death in diabetes.

A prolonged QT interval is considered an indicator of increased risk of malignant ventricular arrhythmias and/or sudden death. It has been proposed that autonomic neuropathy in diabetes is related to QT interval prolongation and increased mortality rates. Several studies in Type 1 and Type 2 diabetic patients have confirmed the independent relation between prolonged QT interval duration or increased QT interval dispersion and chronic ischemic heart disease. It has been consistently shown that autonomic neuropathy is related to QT interval duration while more controversies exist on the association with QT interval dispersion. In recent years, studies have confirmed the value of QT interval as a predictor of total mortality in both diabetic and non-diabetic subjects. Moreover, several studies have shown a significant relation between QT interval prolongation and cardiovascular disease risk factors. QT interval could be used to stratify the cardiovascular risk in diabetic patients. We still do not know why QT interval is prolonged and how this abnormality leads to death. Nevertheless, QT interval is a simple, low-cost measure, easily obtainable without the need of the patient's compliance and which could help to select patients who need second level diagnostic procedures and strict observation.

Clinical Trials as Topic↗

PubMed2003

Glutamic acid decarboxylase and ICA512/IA-2 autoantibodies as disease markers and relationship to residual beta-cell function and glycemic control in young type 1 diabetic patients.

Circulating autoantibodies (Ab) to islet autoantigens, glutamic acid decarboxylase (GAD(65)), and tyrosine phosphatase ICA512/IA-2 have been proposed as predictive markers of type 1 diabetes mellitus. To ascertain residual beta-cell function and the clinical relevance for monitoring autoimmunity after clinical manifestation of disease, we studied 63 children at diagnosis of type 1 diabetes (mean SD age 7.5 +/- 4 years) and 91 adolescent patients with type 1 diabetes (age 14.7 +/- 1.6 years) with a mean duration of disease of 7 +/- 3.5) years. Forty-two normal adolescent subjects (age 14.6 +/- 1.8 years) without a family history of diabetes were the control group. Anti-GAD(65) and ICA512/IA-2 Ab were assessed by a quantitative radioimmunoprecipitation assay. The relationship between humoral autoimmunity and clinical parameters was explored. GAD(65) and ICA512/IA-2 Ab were detected in 56% and 63% of newly diagnosed children and the prevalence was not different in relationship to clinical characteristics. Levels of GAD(65) Ab positively correlated with diagnosis age (P <.05). Both Ab were associated with islet cell antibodies (ICA) (P <.05), but one fifth of patients had at least 1 of the 2 Ab and absent ICA. At onset, only age showed a significant relationship to residual C-peptide secretion. Among the cohort of patients with diabetes of short-mid duration, GAD(65) and ICA512/IA-2 Ab were present in 44% and 45% of cases (P >.05 and P <.05 v newly diagnosed children, respectively) and more patients were identified by these Ab (68%) than by ICA alone (34%) (P <.05). In this cohort, levels of ICA512/IA-2 Ab negatively correlated with levels of glycosylated hemoglobin (HbA(1c)) (P <.005) and with daily insulin requirement (P <.05). Moreover, the presence of some residual C-peptide secretion was significantly associated with the presence of ICA512/IA-2 Ab (P <.05). Our findings confirm that positivity for either GAD(65) or ICA512/IA-2 Ab is a highly sensitive marker of type 1 diabetes in the pediatric age group, identifying a group of patients with absent ICA immunofluorescence. The persistence of Ab to islet tyrosine phosphatase possibly represents a marker of better glycemic control and less insulin requirement, indicating residual beta-cell function, thus conferring clinical and prognostic relevance to these Ab, as well as potential usefulness in intervention strategies.

Adolescent↗

PubMed2002

Anti-CD38 autoantibodies: characterisation in new-onset type I diabetes and latent autoimmune diabetes of the adult (LADA) and comparison with other islet autoantibodies.

AIMS/HYPOTHESIS: Serum anti-CD38 autoantibodies (aAbs) have been reported in 17 to 19% of patients with long-standing Type I (insulin-dependent) diabetes mellitus and Type II (non-insulin-dependent) diabetes mellitus. Whether these aAbs are also found in new-onset Type I diabetes and in Latent Autoimmune Diabetes in Adults (LADA) is not known, as is their relationship with conventional islet aAbs. METHODS: These issues were addressed by studying new-onset Type I and LADA diabetic cohorts with a recently developed anti-CD38 enzymatic immuno-assay. RESULTS: Anti-CD38 aAb prevalence among new-onset Type I patients (3.8%) was lower than previously found in long-standing Type I diabetes (11.7%, as defined with the 97.5 percentile cutoff; p=0.01), suggesting a late appearance of these aAbs. Among LADA patients, 14.9% were anti-CD38(+). Anti-CD38 were only associated with anti-GAD aAbs in new-onset Type I diabetes. Although the CD38 target molecule was expressed in human pancreatic islets, anti-CD38 aAbs did not contribute to the islet cell antibody (ICA) immunofluorescence reactivity. All the positive sera analysed for Ca(2+) release were found to mobilise it. In agreement with these agonistic features, anti-CD38(+) new-onset Type I patients showed higher fasting C-peptide values as compared to negative counterparts; the association was stronger when the analysis was limited to the agonistic anti-CD38(+) sera. A similar trend was found among LADA patients. CONCLUSION/INTERPRETATION: Anti-CD38 aAbs are distinct markers of islet autoimmunity which are more prevalent in long-standing disease, as opposed to the other known islet aAbs. Their in vitro agonistic properties could be operating in vivo as well, as they identify sub-groups of patients with higher residual beta-cell function.

ADP-ribosyl Cyclase↗

PubMed2002

Plasma homocysteine, methylenetetrahydrofolate reductase gene polymorphism and carotid intima-media thickness in Italian type 2 diabetic patients.

BACKGROUND: Moderately elevated levels of homocysteine have been associated with an increased cardiovascular risk in type 2 diabetic patients. The role of methylenetetrahydrofolate reductase gene polymorphism is less clear. MATERIALS AND METHODS: We investigated the contribution of plasma homocysteine levels and the methylenetetrahydrofolate reductase gene polymorphism to the variability of carotid intima-media thickness in 124 consecutive Italian patients with type 2 diabetes mellitus. Fasting plasma homocysteine was measured by high-pressure liquid chromatography with an electrochemical detector; methylenetetrahydrofolate reductase genotypes were determined by polymerase chain reaction and restriction enzyme digestion. The carotid intima-media thickness was evaluated with high-resolution B-mode ultrasonography. RESULTS: Age, creatinine and plasma homocysteine levels showed a positive correlation with mean carotid intima-media thickness values, but only age and creatinine levels were still associated with mean carotid intima-media thickness values in the multivariate analysis. Plasma homocysteine levels were significantly higher in the patients bearing the 677T/677T genotype of the methylenetetrahydrofolate reductase polymorphism; mean carotid intima-media thickness values were not different in the three different methylenetetrahydrofolate reductase genotypes. CONCLUSION: In 124 Italian patients with type 2 diabetes mellitus, basal levels of plasma homocysteine, as well as methylenetetrahydrofolate reductase gene polymorphism, did not explain the variability of mean carotid intima-media thickness.

Aged↗

PubMed2002

Prevalence of increased QT interval duration and dispersion in type 2 diabetic patients and its relationship with coronary heart disease: a population-based cohort.

OBJECTIVE: To evaluate the prevalence of prolonged QT interval and dispersion in a population-based cohort of type 2 diabetic patients and their relationship with clinical and metabolic variables. DESIGN: Cross-sectional population-based cohort. SETTING: Diabetes clinics and general practitioners in Casale Monferrato (Northern Italy). SUBJECTS: A total of 1357 patients with known type 2 diabetes (70% of the cohort). MAIN OUTCOMES MEASURES: Albumin excretion rate and coronary heart disease (CHD); a standard supine 12-lead electrocardiogram (ECG) was recorded and coded according to the Minnesota code criteria. QT interval corrected for heart rate (QTc) > 0.44 s and QTc dispersion > 0.080 s were considered abnormally prolonged. RESULTS: Prevalence of increased QTc duration and QTc dispersion were 25.8% (95% CI 23.5-28.3) and 33.1% (95% CI 30.6-35.7), with no sex differences. No metabolic differences were found, apart from fibrinogen and creatinine levels, which were higher in patients with increased QTc dispersion. Patients with CHD had higher mean adjusted values of QTc and QTc dispersion, whereas no association was found with albumin excretion rate (AER) and diabetes treatment. QTc duration and QTc dispersion were significantly correlated (0.17, P < 0.001). In multiple regression analysis, only CHD was independently associated with QTc, after adjustment for age and sex (beta=0.010, P < 0.001, R2=2.5%); as regards QTc dispersion, a similar association with CHD was found (beta=0.20, P < 0.001, R2=4.8%). CONCLUSIONS: This population-based study shows a considerably high prevalence of increased QTc and QTc dispersion in type 2 diabetic patients and their association with CHD. These findings have both epidemiological and clinical relevance, as they might be implicated in the excess mortality risk of type 2 diabetic patients.

Aged↗

PubMed2001

Postprandial triglyceride-rich lipoprotein metabolism and insulin sensitivity in nonalcoholic steatohepatitis patients.

Nonalcoholic steatohepatitis (NASH) is a syndrome frequently associated with obesity, diabetes mellitus, and dyslipidemia. Increased fasting insulinemia and blood glucose levels may trigger a reduced catabolism of lipoproteins rich in triglycerides by lipoprotein lipase (LPL) and an increase in their fasting and postprandial levels. An association between postprandial lipemia and coronary heart disease has been observed, and many studies now support this concept. The most important result of our study is the increase in triglyceride-rich lipoproteins response after a fat load in NASH patients, the increase of incremental area under the postprandial curve, and the duration of the hypertriglyceridemic peaks. The persisting postprandial plasma triglyceride elevation in NASH patients was mostly due to the elevated plasma level of large triglyceride-rich particles. These data are coupled with lower plasma HDL2-cholesterol levels. As for lipoprotein analyses, the number of apolipoprotein B100 (ApoB100) particles is not significantly different between the two groups, and the higher content of triglycerides in NASH very low density lipoproteins (VLDL) increases the triglyceride-to-ApoB ratio and the particle size. A decreased enzymatic activity of LPL or a defective assembly and secretion of VLDL from hepatocytes due to a moderate reduction in microsomal triglyceride transfer protein could be involved in the overloading of VLDL. Moreover, the undetectable levels of ApoB48 in triglyceride-rich lipoproteins fraction A could be related to the synthesis of smaller and denser chylomicrons. NASH patients not only are insulin resistant but also tend to present alterations in fatty meal delivery, suggesting that an increase in fasting plasma insulin and glucose, with insulin resistance, joins with depressed metabolism of triglyceride-rich lipoproteins. An increase in postprandial triglyceride levels with production of large VLDL suggests an atherogenic behavior of lipid metabolism, in accordance with the high prevalence of the metabolic syndrome in NASH patients. This paper suggests that a fat load may be useful in early detection of atherogenic risk in the presence of otherwise normal fasting plasma lipids.

Adult↗

PubMed2001

Hypouricemia and hyperuricemia in type 2 diabetes: two different phenotypes.

BACKGROUND AND DESIGN: Conflicting data exist about uric acid levels in type 2 diabetes mellitus, as low levels were found in diabetic patients, while elevated serum uric acid is a feature of hyperinsulinemia and impaired glucose tolerance. The present study was addressed to evaluate the relation between uric acid and metabolic parameters, creatinine clearance and albumin excretion rate in a cohort of type 2 diabetic patients. RESULTS: Hyperuricemic patients were older and had higher values of body mass index (BMI), systolic and diastolic blood pressure, triglycerides, albumin excretion rate, C-peptide and prevalence of hypertension, metabolic syndrome and macroalbuminuria and lower values of high-density lipoprotein (HDL)-cholesterol, creatinine clearance and glycated haemoglobin (HbA1c). The correlations between uric acid levels and triglycerides, BMI, systolic blood pressure, albumin excretion rate, C-peptide, creatinine clearance, HDL-cholesterol and HbA1c remained significant in a multiple regression analysis after adjustment for age, sex and duration of diabetes. After performing multiple logistic regression analyses, uric acid levels were independently associated with hypertension [odds ratio (OR) = 1.8; 95% confidence interval (CI) 1.6--2], after adjustment for age, sex, duration of diabetes and macroalbuminuria (OR = 1.5; 95% CI 1.1--2.0), after adjustment for age, sex, HbA1c levels, creatinine clearance, duration of diabetes and blood pressure levels and the metabolic syndrome (OR = 1.6; 95% CI 1.5--1.8), after adjustment for age, sex and creatinine clearance. CONCLUSIONS: In type 2 diabetes, hyperuricemia seems to be associated with the insulin-resistant syndrome and with early onset or increased progression to overt nephropathy, while hypouricemia is associated with worse metabolic control, hyperfiltration and a late onset or decreased progression to overt nephropathy.

Aged↗

PubMed2001

Plasma lipids and urinary albumin excretion rate in Type 1 diabetes mellitus: the EURODIAB IDDM Complications Study.

AIMS: To examine the relationship between increased urinary albumin excretion rate and fasting plasma lipids among male and female respondents to the EURODIAB IDDM Complications Study, and attempt to explain inconsistencies in previous reports. METHODS: A cross-sectional study of 3250 randomly selected Type 1 diabetic patients from 31 diabetes clinics in 16 European countries was carried out between 1989 and 1990. Plasma lipids and urinary albumin were measured centrally. The present analysis was confined to the subgroup of 2205 patients attending after a 10-12 h overnight fast. Mean age was 33 years (SD 10) and mean duration of Type 1 diabetes mellitus was 15 years (SD 9). RESULTS: The prevalence of microalbuminuria (24-h urinary albumin excretion rate 20-200 microg/min) was 21.7% (95% confidence interval 19.9-23.5) and macroalbuminuria (24-h urinary albumin excretion rate > 200 microg/min) 7.8% (6.6-9.0). In comparison to patients with normal urinary albumin excretion rate (< 20 microg/min), and after controlling for age, sex, glycaemic control, duration of diabetes and current smoking, macroalbuminuria was associated with significantly (P<0.01) increased fasting plasma triglycerides, cholesterol, LDL-cholesterol, cholesterol:HDL-cholesterol ratio and, in women, reduced HDL-cholesterol. In men and women with microalbuminuria, the only significant association was with increased plasma triglycerides. CONCLUSIONS: These data confirm that there is an association between fasting plasma lipids and increasing urinary albumin excretion rate in European Type 1 diabetic patients. In microalbuminuric patients, however, the association was weaker than previously reported and partly explained by confounding factors.

Adult↗

PubMed2001

Myocardial infarction before the age of 40 years is associated with insulin resistance.

Insulin resistance is associated with atherosclerosis, and hyperinsulinemia is predictive of coronary heart disease. However, a quantitative estimation of in vivo insulin sensitivity in juvenile myocardial infarction is still lacking and the mechanism of hyperinsulinemia is unknown. We estimated insulin sensitivity, beta-cell secretion, and hepatic insulin extraction using the minimal model analysis of a frequently sampled intravenous glucose tolerance test (FSIGT) in 25 normal-weight subjects without glucose intolerance and hypertension who had an acute myocardial infarction before the age of 40 years, and 10 control subjects comparable for age, sex, body mass index, and blood pressure. All patients underwent a coronary angiography. Insulin sensitivity was significantly lower in patients than in control subjects (mean +/- SEM, 4.6 +/- 0.6 v8.5 +/- 1.2 10(-4). min(-1)(microU/mL), P = .002). The basal C-peptide secretion rate (P = .02), total C-peptide secretion (P = .005), area under the curve (AUC) of insulin (P = .04) and C-peptide (P = .01), and hepatic insulin extraction (P = .04) were higher in patients versus control subjects. In conclusion, insulin resistance is evident in subjects with early myocardial infarction accurately selected to avoid the influence of other factors known to reduce insulin sensitivity, and hyperinsulinemia is due to an increase in beta-cell secretion rather than a decrease in hepatic insulin extraction.

Adult↗

PubMed2001

The metabolic syndrome in twins: a consequence of low birth weight or of being a twin?

BACKGROUND: To evaluate if being a twin is a condition at risk of developing metabolic abnormalities in the adult life 'per se' or as a consequence of the lower birth weight. METHODS: 48 monozygotic twins and 50 non-twin controls, both with parental diabetes, were compared; the two groups were comparable for age, sex and body mass index. RESULTS: Twins showed higher values of blood pressure, triglycerides, insulin resistance, fasting insulin, insulin AUCs and higher prevalence of the metabolic syndrome, and, inversely, lower birth weight. After adjustment for birth weight, no significant association was evident with the twin status. Birth weight was inversely associated with the presence of the metabolic syndrome or of at least one or more of its components, while the positive association with the twin status was not significant. CONCLUSIONS: Our data suggest that low birth weight is more relevant than the twin status as a risk factor for the metabolic syndrome and its components.

Adolescent↗

PubMed2001

Autoantibody response to CD38 in Caucasian patients with type 1 and type 2 diabetes: immunological and genetic characterization.

Insulin secretion is one of the functions mediated by CD38, a nonlineage pleiotropic cell surface receptor. The molecule is the target of an autoimmune response, because serum autoantibodies (aAbs) to CD38 have been detected in diabetic patients. In the healthy Caucasian population, the CD38 gene is bi-allelic (86% CD38*B and 14% CD38*A), whereas an Arg140Trp mutation has been identified in Japanese diabetic patients. We investigated the relationship between CD38 and diabetes in Caucasian patients by characterizing anti-CD38 aAbs in terms of prevalence and function (agonistic/nonagonistic activity) and by exploring the potential influence of the CD38 genetic background. A novel enzymatic immunoassay, using recombinant soluble CD38 as the target antigen, was developed for the analysis of anti-CD38 aAb titers. Sera from 19.15% of type 1 and 16.67% of type 2 diabetic patients were positive. The majority of anti-CD38 aAbs (57.14%) displayed agonistic properties, i.e., they demonstrated the capability to trigger Ca2+ release in lymphocytic cell lines. In agreement with these functional features, the presence of anti-CD38 aAbs in type 2 diabetic patients was associated with significantly higher levels of fasting plasma C-peptide and insulin, as compared with anti-CD38-counterparts. No diabetic subject carrying the Arg140Trp mutation and no preferential association between diabetes or aAb status and the CD38*A allele was found in the study population. These results show the significance of anti-CD38 aAbs as a new diagnostic marker of beta-cell autoimmunity in diabetes. Moreover, the prevalent agonistic activity of these aAbs suggests that they could mediate relevant effects on target cells by means of Ca2+ mobilization.

ADP-ribosyl Cyclase↗

PubMed2001

Low HDL-cholesterol: a component of the metabolic syndrome only in the presence of fasting hypertriglyceridemia in type 2 diabetic patients.

The relation between isolated low HDL-cholesterol and the components of the metabolic syndrome is poorly known in type 2 diabetes. We evaluated cardiovascular risk parameters in type 2 diabetic patients with low HDL-cholesterol, compared to those with low HDL-cholesterol and hypertriglyceridemia, isolated hypertriglyceridemia and normal lipid parameters. Patients with low HDL-cholesterol/high triglycerides had higher BMI (29.6 +/- 5.7 vs 27.9 +/- 4.4 or vs 28.1 +/- 5.2 kg/m(2) ), prevalence of obesity (69% vs 55% or vs 54%), higher levels of uric acid (339.0 +/- 83.3 vs 303.3 +/- 95.2 or vs 303.3 +/- 89.2 micromol/l) and C-peptide (0.76 +/- 0.40 vs 0.63 +/- 0.33 or vs 0.63 +/- 0.36 nmol/l) and number of components of the metabolic syndrome (27% patients with all the components) compared to patients with isolated low HDL-cholesterol or normal subjects, respectively. A similar pattern of values was evident in patients with isolated hypertriglyceridemia. With logistic regression analysis, BMI and uric acid levels were significantly associated with the presence of hypertriglyceridemia (both isolated or associated with low HDL-cholesterol), while patients with isolated low HDL-cholesterol and those without dyslipidemia displayed a similar more favourable metabolic pattern. These results indicate that low HDL-cholesterol is a component of the metabolic syndrome only in the presence of fasting hypertriglyceridemia in type 2 diabetic patients.

Aged↗

PubMed2000

Relationship of residual beta-cell function, metabolic control and chronic complications in type 2 diabetes mellitus.

As the relationships between C-peptide levels and metabolic control and chronic complications are poorly known in type 2 diabetes, due to the slow decline of beta-cell function, we evaluated these associations in a cohort of type 2 diabetic patients. After excluding insulin-treated subjects, 1,533 patients were divided according to their C-peptide fasting levels in quartiles. Patients within the lowest C-peptide quartile showed significantly higher duration of diabetes, prevalence of retinopathy and values of HDL-cholesterol, albumin excretion rate and HbA1c, while BMI, diastolic blood pressure, percentages of hypertension and metabolic syndrome, and values of triglycerides and uric acid were significantly higher in the highest C-peptide quartile. The associations between C-peptide and duration of diabetes, AER, HbA1c, retinopathy and the components of the metabolic syndrome remained significant, after multiple adjustments. In conclusion, these data support the hypothesis that a reduced insulin secretion is associated with a longer duration of diabetes and a greater prevalence of microvascular complications, while higher insulin levels are associated with the components of the metabolic syndrome.

Aged↗

PubMed2000

Lack of association of fibrinogen, lipoprotein(a), and albumin excretion rate with low birthweight.

An excess of cardiovascular morbidity has been related to low birthweight. The aim of this study was to evaluate the relationship between low birthweight and levels of fibrinogen, lipoprotein(a), and albumin excretion rate, which are known risk factors for coronary artery disease. Seventy-two twins, with the same within-pair gender and normal glucose tolerance, were analyzed in order to avoid confounding factors, such as gestational age, birth order, or sex. Twins with the highest birthweights within the couple showed no significant difference of fibrinogen, lipoprotein(a), and albumin excretion rates compared with the twins with the lowest birthweights among the two co-twins. Moreover, no relevant correlation was found between birthweight and intra-pair birthweight differences and fibrinogen, lipoprotein(a), and albumin excretion rates. The lack of correlation between fibrinogen, lipoprotein(a), albumin excretion rate and birthweight, suggests that these factors do not contribute to the link between intrauterine malnutrition and increased cardiovascular risk.

Albuminuria↗

PubMed2000

Low birthweight and metabolic abnormalities in twins with increased susceptibility to Type 2 diabetes mellitus.

AIMS: To evaluate the role of environmental intra-uterine factors in determining the birthweights of twins with increased susceptibility to diabetes and discordant for abnormal responses to the oral glucose tolerance test (OGTT) and verify the possible association of within-pair birthweight differences and metabolic abnormalities in adult life. METHODS: Forty-six monozygotic (MZ) and 32 dizygotic (DZ) twins were enrolled; 13 MZ twins were discordant for impaired glucose tolerance (IGT) and/or hyperinsulinaemia compared to their co-twins. RESULTS: The 13 MZ discordant twins showed significantly lower birthweights than their normal co-twins (P < 0.001). When dividing all twins in those with the highest birthweights within the couple and those with the lowest, all subjects with abnormal OGTT were found in the latter group (P < 0.0001). Within-pair birthweight difference was significantly higher in MZ twins with abnormal OGTT and the metabolic syndrome compared to normal MZ twins. The relative risk of developing the metabolic syndrome was 8.7 (1.6-46.9) when comparing the higher tertile of within-pair birthweight differences (> or = 0.450 kg) to the two lower tertiles (< 0.450 kg). Logistic regression analysis confirmed within-pair birthweight difference as a significant predictor of abnormal responses to the OGTT and the metabolic syndrome. CONCLUSIONS: These data suggest a causative role for environmental intrauterine factors on the determination of birthweight and support the hypothesis that within-pair birthweight difference, rather than an absolute low birthweight, is responsible for the metabolic abnormalities in the adult life.

Adult↗