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G Riccardi

Publications and source records attributed to G Riccardi.

At least 55 records · Page 3Linked to original sources
PubMed2000

Invasive and non-invasive determinants of pulmonary hypertension in patients with chronic heart failure.

BACKGROUND: In patients with chronic heart failure, pulmonary hypertension is an important predictive marker of adverse outcome. Its invasive and non-invasive determinants have not been evaluated. OBJECTIVE: This study was performed to evaluate hemodynamic determinants of pulmonary hypertension in chronic heart failure and to compare the predictive value of Doppler indices with that of invasively measured hemodynamic indices. METHODS: Right heart catheterization and transthoracic echo-Doppler were simultaneously performed in 259 consecutive patients with chronic heart failure (ejection fraction 24% +/- 7%) who were in sinus rhythm and receiving optimized medical therapy. Systolic pulmonary artery pressure (sPAP), cardiac index, transpulmonary gradient pressure, and pulmonary wedge pressure (PWP) were measured invasively. Left atrial and ventricular systolic and diastolic volumes, the ratio of maximal early to late diastolic filling velocities (E/A ratio), deceleration time (DT) and atrial filling fraction (AFF) of transmitral flow, systolic fraction of forward pulmonary venous flow (SFpvf), and mitral regurgitation were quantified by echo-Doppler. RESULTS: Patients with pulmonary hypertension had greater left atrial systolic and diastolic dysfunction, more left ventricular diastolic abnormalities, and greater hemodynamic impairment. The correlations between systolic left ventricular indices, mitral regurgitation, and sPAP were generally poor. Among invasive and non-invasive measurements, PWP (r = 0.89, p < 0.0001) and SFpvf (r = -0.68, p < 0.0001) showed the strongest correlation with sPAP. When we compared all patients with those without mitral regurgitation, the correlations between E/A ratio (r = 0.56 vs r = 0. 74, p < 0.002), SFpvf (r = -0.68 vs r = -0.84, p < 0.03), and systolic pulmonary artery pressure were significantly stronger. Multivariate analysis revealed that PWP was the strongest invasive independent predictor of systolic pulmonary artery pressure in patients with (R(2) = 0.87, p < 0.0001) and without (R(2) = 0.90, p < 0.0001) mitral regurgitation. A PWP > or= 18 mm Hg (odds ratio [95% CL], 142 (41-570) was strongly associated with systolic pulmonary hypertension. Among non-invasive variables DT, SFpvf, and AFF were identified as independent predictors of sPAP in patients with (R(2) = 0.56, p < 0.0001) and without (R(2) = 0.78, p < 0.0001) mitral regurgitation. A DT < 130 (odds ratio [95% CL], 3.5 (1.3-8.5), SFfvp < 40% (odds ratio [95% CL], 333 (41-1,007), and AFF < 30% (odds ratio [95% CL], 2 (1.3-7) most strongly predicted systolic pulmonary hypertension. CONCLUSIONS: The results of this study indicate that in patients with chronic heart failure, venous pulmonary congestion is an important determinant of systolic pulmonary artery hypertension. Hemodynamic and Doppler determinants showed similar predictive power in identifying systolic pulmonary artery hypertension.

Blood Flow Velocity↗
PubMed2000

Dietary treatment of the metabolic syndrome--the optimal diet.

The treatment of the metabolic syndrome aims to improve insulin sensitivity and correct/prevent the associated metabolic and cardiovascular abnormalities. Since many individuals with the metabolic syndrome are overweight, dietary treatment should be primarily focused on weight reduction. This approach can improve insulin sensitivity and exert beneficial effects on all the other abnormalities clustering in the syndrome. Insulin sensitivity can also be influenced by diet composition. In this respect, the specific effects of the quality of dietary fat are of great interest, given the considerable evidence in experimental animals that saturated fat in the diet may lead to insulin resistance. In man, there is indirect evidence that a higher saturated fat intake is associated with impaired insulin action. Human studies have also attempted to evaluate the relationship between total fat intake and insulin sensitivity. They are consistent in showing that fat intake is correlated with both plasma insulin values (positively) and insulin sensitivity (negatively). However, these correlations are largely mediated by body weight. Conversely, intervention studies are consistent in showing that when total fat intake is moderately increased (from 20 to 40%), no major effect is observed on insulin sensitivity. We have recently undertaken a large, multicentre intervention study in 162 healthy individuals given either a high-saturated-fat or a high-monounsaturated-fat diet for 3 months. It shows that a high-monounsaturated-fat diet significantly improves insulin sensitivity compared to a high-saturated-fat diet. However, this beneficial effect of monounsaturated fat disappears when total fat intake exceeds 38% of total energy. Independently of its effects on insulin sensitivity, diet composition can influence the factors clustering in the metabolic syndrome. Dietary carbohydrate increases blood glucose levels, particularly in the postprandial period, and consequently also insulin levels and plasma triglycerides. The detrimental effects of a high-carbohydrate diet on plasma glucose/insulin, triglyceride/HDL or fibrinolysis occur only when carbohydrate foods with a high glycaemic index are consumed, while they are abolished if the diet is based largely on fibre-rich, low-glycaemic-index foods. In conclusion, weight reduction is a powerful measure for the treatment of metabolic syndrome. Moreover, the diet for the treatment of the metabolic syndrome should be limited in the intake of saturated fat, while high fibre/low-glycaemic-index foods should be used without specific limitations. Moderate amounts of monounsaturated fat could be permitted as they do not induce detrimental metabolic effects.

Cardiovascular Diseases↗
PubMed2000

Pro12Ala mutation in the peroxisome proliferator-activated receptor gamma2 (PPARgamma2) and severe obesity: a case-control study.

OBJECTIVE: To explore the association of the Pro12Ala mutation in the peroxisome proliferator-activated receptor gamma2 with severe obesity and the features of the metabolic syndrome in a population-based sample of Caucasians. PARTICIPANTS AND METHODS: The study is based on a case-control design: 95 non-diabetic severely obese (body mass index, BMI > 35 kg/m2) cases and 280 normal weight (BMI < 25 kg/m2), age- and sex-matched controls selected from the same population were studied. Height, weight, waist circumference, as well as blood pressure were measured according to a standard protocol. BMI at age 25 y was calculated on the basis of current height and reported weight at age 25 y Biochemical measurements included fasting glucose, triglycerides, high-density lipoprotein cholesterol and insulin. DNA analysis was conducted by PCR and gel electrophoresis. RESULTS: Age and gender distribution were similar in obese and normal weight participants. The percentage of people with the Pro12Ala mutation was not significantly different in obese or normal weight participants (20% and 15%, respectively; P = 0.32). Conversely, in obese participants with obesity starting in early adulthood (ie with BMI at age 25 above 26.9kg/m2 which represents the median of the whole obese group), the Pro12Ala mutation was observed significantly more frequently than in the normal weight controls (29% vs 15%; chi square = 4.5, P < 0.05; odds ratio 2.4; 95% CI 1.03-5.36). No association of the Pro12Ala variant with any of the component of the metabolic syndrome measured in the study was observed in either obese, juvenile obese or normal weight participants. CONCLUSIONS: Results of this study indicate that the Pro12Ala mutation does not play a major role as a determinant of severe obesity and/or features of the metabolic syndrome in the general population. However, this mutation may be of greater importance as a contributor to early onset obesity.

Adult↗
PubMed2000

Is the erythrocyte membrane fatty acid composition a valid index of skeletal muscle membrane fatty acid composition?

Recent studies suggest that insulin sensitivity is related to the fatty acid composition of phospholipids in skeletal muscle (SM) membranes. Since it is difficult to obtain muscle biopsies, it may be useful to have information on the fatty acid composition using more accessible cells such as erythrocytes. This would be possible only if the composition of erythrocyte and muscle membranes are very similar. Since no comparative data are available, we evaluated the phospholipid fatty acid composition of erythrocyte and SM membranes in 16 individuals, 10 nondiabetics (male to female ratio, 4:6; age, 50 +/- 11 years; body mass index, 27 +/- 5 kg/m2; mean +/- SD) and 6 type 2 diabetic patients (male to female ratio, 2:4; age, 64 +/- 5 years; body mass index, 27 +/- 4 kg/m2). All patients underwent abdominal surgery, during which a biopsy of the abdominal rectus muscle (50 to 100 mg) was obtained. Erythrocyte and SM phospholipid fatty acids were extracted and then methylated; the methyl fatty acids were separated and quantified by gas chromatography. Compared with erythrocyte membranes, muscle membranes showed a significantly higher proportion of omega-6 polyunsaturated fatty acid ([PUFA] 43.0% +/- 3.1% v29.7% +/- 1.6%, P < .001) and lower saturated fatty acid ([SFA] 41.1% +/- 1.5% v 43.4% +/- 1.2%, P < .001), monounsaturated fatty acid ([MUFA] 11.5% +/- 1.7% v 20.0% +/- 1.9%, P < .001), and omega-3 PUFA (3.8% +/- 0.6% v 7.4% +/- 1.0%, P < .001). The greatest increase involved linoleic acid (26.9% +/- 2.8% v 10.3% +/- 1.6%, P < .001), whereas lignoceric acid (0.8% +/- 0.2% v 5.0% +/- 0.6%, P < .001) and oleic acid (10.4% +/- 1.6% v 13.5% +/- 1.3%, P < .001) were significantly lower. These results show that erythrocyte and muscle membrane phospholipid fatty acids are significantly different. Therefore, data on SM membranes cannot be extrapolated on the basis of measures of erythrocyte phospholipid fatty acid composition.

Adult↗
PubMed2000

Effect of insulin and sulfonylurea therapy, at the same level of blood glucose control, on low density lipoprotein subfractions in type 2 diabetic patients.

The aim of this study was to evaluate the effect of sc insulin (INS) compared with sulfonylurea (SUL) therapy, at the same level of blood glucose control, on the low density lipoprotein (LDL) subfraction profile in normolipidemic type 2 diabetic patients. Nine normolipidemic type 2 diabetic men (age, 56+/-3 yr; body mass index, 26.5+/-0.9 kg/m2; mean +/- SEM), after a 3-week wash-out period, were assigned to INS or SUL for 2 months in a randomized cross-over design. Doses were adjusted only during the first month and then were kept constant. At the end of the treatments, hemoglobin A1c, plasma lipids, LDL, and very low density lipoprotein (VLDL) subfraction profiles and plasma postheparin lipoprotein lipase and hepatic lipase (HL) activities were evaluated. Despite glucose control was similar at the end of both periods (hemoglobin A1c, 7.4+/-0.3% vs. 7.0+/-0.2%, INS vs. SUL), INS compared with SUL significantly reduced plasma triglyceride (0.9+/-0.1 vs. 1.1+/-0.1 mmol/L; P < 0.05). Although INS did not affect the LDL concentration, it induced a decrease in both the amount (59.0 = 9.8 vs. 76.1+/-16.8 mg/dL; P = NS) and the proportion (31.2+/-3.0% vs. 38.3+/-3.8%; P < 0.03) of small LDL. Moreover, the decrease in small LDL was positively related to the reduction of large VLDL (r = 0.67; P < 0.04) and HL (r = 0.69, P < 0.05) induced by insulin therapy. In conclusion, sc insulin therapy, independently of glucose control and even in the presence of quite low plasma triglyceride levels, is able to reduce small LDL particles in type 2 diabetic patients. This change is related to decreases in both HL activity and large VLDL particles.

Blood Glucose↗
PubMed2000

The IR1152 mutant insulin receptor selectively impairs insulin action in skeletal muscle but not in liver.

In patients harboring the IR1152 mutant insulin receptor, hepatic glucose production was normally suppressed by insulin. Hepatocytes without the insulin receptor gene and expressing IR1152 (Hep(MUT)) also showed normal insulin suppression of glucose production and full insulin response of glycogen synthase. In contrast, expression of the IR1152 mutant in skeletal muscle maximally increased glucose uptake and storage, preventing further insulin stimulation. IRS-1 phosphorylation was normally stimulated by insulin in both intact Hep(MUT) and L6 skeletal muscle cells expressing the IR1152 mutant (L6(MUT)). At variance, IRS-2 phosphorylation exhibited high basal levels with no further insulin-dependent increase in L6(MUT) but almost normal phosphorylation, both basal and insulin-stimulated, in the Hep(MUT) cells. In vitro, IR1152 mutant preparations from both the L6(MUT) and the Hep(MUT) cells exhibited increased basal and no insulin-stimulated phosphorylation of IRS-2 immobilized from either muscle or liver cells. IR1152 internalization in liver and muscle cells closely paralleled the ability of this mutant to phosphorylate IRS-2 in vivo in these cells. Block of receptor internalization (wild-type and mutant) in the liver and muscle cells also inhibited IRS-2, but not IRS-1, phosphorylation. Thus, the mechanisms controlling insulin receptor internalization differ in liver and skeletal muscle cells and may enable IR1152 to control glucose metabolism selectively in liver. In both cell types, receptor internalization seems necessary for IRS-2 but not IRS-1 phosphorylation.

Animals↗
PubMed2000

Long-term dietary treatment with increased amounts of fiber-rich low-glycemic index natural foods improves blood glucose control and reduces the number of hypoglycemic events in type 1 diabetic patients.

OBJECTIVE: To evaluate in type 1 diabetic patients 1) the long-term feasibility of a high-fiber (HF) diet composed exclusively of natural foodstuffs and 2) the efficacy of this diet in relation to blood glucose control and incidence of hypoglycemic episodes. RESEARCH DESIGN AND METHODS: The study was randomized with parallel groups. Participants were part of a larger multicenter study on the effects of acarbose on glucose control in diabetes. A total of 63 type 1 diabetic patients, age 28 +/- 9 years, BMI 24 +/- 0.6 kg/m2, after a 4-week run-in period on their habitual diet, were randomized to either an HF (n = 32) or a low-fiber (LF) diet (n = 31) for 24 weeks. The two diets, composed exclusively of natural foodstuffs, were weight-maintaining and, aside from their fiber content, were similar for all nutrients. At the end of the run-in period and the dietary treatment, fasting blood samples for the measurement of plasma cholesterol, HDL cholesterol, triglyceride, and HbA(1c) were collected. A daily glycemic profile was performed on a day in which the participants had consumed a standard menu representative of their treatment diet (HF or LF). RESULTS: Of the 63 study subjects, 29 in the HF group (91%) and 25 in the LF group (81%) completed the study Compared with the LF diet, the HF diet after 24 weeks decreased both mean daily blood glucose concentrations (P < 0.05) and number of hypoglycemic events (P < 0.01). When compliance to diet was taken into account, 83% of the subjects on the HF diet and 88% on the LF diet were compliant. In this subgroup, compared with the LF diet, the HF diet significantly reduced mean daily blood glucose concentrations (P < 0.001), HbA(1c) (P < 0.05), and number of hypoglycemic events (P < 0.01). CONCLUSIONS: In type 1 diabetic patients, an HF diet is feasible in the long term and, compared with an LF diet, improves glycemic control and reduces the number of hypoglycemic events.

Adult↗
PubMed2000

Cardiac abnormalities in type 1 diabetes.

BACKGROUND: Left ventricular (LV) structural and hemodynamic consequences of type 1 diabetes mellitus are not fully understood. METHODS: To evaluate LV geometry, systolic and diastolic function in type 1 diabetes, Doppler echocardiograms were performed in 40 normotensive, type 1 diabetic patients without coronary heart disease or valvular lesions (22 men, 18 women, mean age 43 +/- 6 years, body mass index 24.7 +/- 2.8 kg/m2) and in 40 age and sex-matched non-diabetic normotensive controls (22 men, 18 women, mean age 43 +/- 5 years, body mass index 23.2 +/- 2.8 kg/m2), in a case-control design. RESULTS: Patients had higher systolic blood pressure than controls (p < 0.03) and comparable diastolic blood pressure and heart rate. LV dimension and mass were higher in patients than in controls (both p < 0.0001) whereas relative wall thickness did not differ. For comparable levels of end-systolic stress, patients exhibited a higher ejection fraction than controls (p < 0.01) and normal midwall shortening. Cardiac output was also higher (p < 0.001), whereas total peripheral resistance was lower in patients than in controls (p < 0.0001). Isovolumic relaxation time and E deceleration were prolonged in patients and peak A velocity was greater than in controls (all p < 0.01), whereas the difference in duration between A and pulmonary vein peak reverse flow at atrial contraction was comparable. In subgroup analyses, all reported features were independent of a) presence of target organ damage; b) duration of disease; c) levels of glycosylated hemoglobin. CONCLUSIONS: In normotensive patients with type 1 diabetes: 1) there was a moderate increase in LV mass; 2) LV chamber function was supernormal and wall mechanics was normal; 3) LV active relaxation was impaired but chamber stiffness was normal.

Adult↗
PubMed2000

Plasma homocysteine and microvascular complications in type 1 diabetes.

BACKGROUND: Homocysteine is involved in a complex and dynamic system of vascular injury and repair and may thus contribute to the development of diabetic microangiopathy. This still debated issue has important scientific and clinical implications, since hyperhomocysteinemia can be corrected nutritionally. AIMS: 1) To evaluate the association between fasting plasma homocysteine, type 1 diabetes and its microvascular complications; 2) to elucidate the basis of this association by investigating the major determinants of plasma homocysteine in relation to diabetic microangiopathy. METHODS: We studied sixty-six consecutive patients with type 1 diabetes mellitus of > 10 years duration and normal serum creatinine (< 115 mumol/L, 1.3 mg/dL), and free from clinically detectable cardiovascular diseases. Forty-four non-diabetic controls were also studied. Plasma concentrations of homocysteine, folate and vitamin B12 were investigated together with the C677T mutation in the gene coding for methylenetetrahydrofolate reductase (MTHFR), a key enzyme in homocysteine metabolism. Renal and retinal diabetic complications were evaluated as albumin/creatinine ratio on early-morning, urine spot collection and fundus photographs. FINDINGS: Fasting plasma homocysteine levels were very similar in patients and controls. Patients with microalbuminuria or proliferative retinopathy had significantly higher values than those without: 9.4 +/- 3.1 vs 7.4 +/- 2.8 mumol/L, p < 0.02 and 9.5 +/- 2.6 vs 7.3 +/- 3.0 mumol/L, p < 0.05. This difference was not attributable to confounders, such as age, sex and smoking, nor to dissimilar plasma folate and vitamin B12 concentrations. In contrast, homozygosity for the C677T mutation in the MTHFR gene--the commonest genetic defect linked to moderately increased plasma homocysteine--was significantly more frequent in patients with microalbuminuria and/or proliferative retinopathy (50% vs 13%, p < 0.004), odds ratio 6.7 (95% CI 1.7-27.6). CONCLUSIONS: Type 1 diabetes as such is not associated with increased plasma homocysteine levels, though patients with microalbuminuria and/or proliferative retinopathy display significantly higher values than those without. This difference is not attributable to obvious confounders, nor to differences in vitamin status, and may be partly mediated by genetic factors. Plasma homocysteine, together with other diabetes-related noxae, may thus be in a position to contribute to the development of nephropathy and the progression of retinopathy.

Adult↗
PubMed1999

Long-term effects of fish oil on lipoprotein subfractions and low density lipoprotein size in non-insulin-dependent diabetic patients with hypertriglyceridemia.

The effects of fish oil on lipoprotein subfractions and low density lipoprotein (LDL) size in non-insulin-dependent diabetes mellitus (NIDDM) patients with hypertriglyceridemia are unknown. To elucidate this, 16 NIDDM hypertriglyceridemic patients (plasma triglyceride 2.25- 5.65 mmol/l, plasma cholesterol < or = 7.75 mmol/l) were randomly assigned to a 6-month period with either moderate amounts of fish oil (n = 8) or placebo (n = 8) after 4 weeks of wash-out and 3 weeks of run-in. Diet and hypoglycemic treatment were unchanged throughout the experiment. LDL size were evaluated at baseline and after 6 months. Three VLDL and LDL subfractions were measured at the end of the two periods. The total lipid concentration of all very low density lipoprotein (VLDL) subfractions was lower at the end of fish oil treatment compared with placebo (large VLDL 124.3 +/- 19.7 mg/dl vs 156.7 +/- 45.5 mg/dl; intermediate VLDL 88.5 +/- 9.5 mg/dl vs 113.9 +/- 23.2 mg/dl; small VLDL 105.9 +/- 9.7 mg/dl vs 128.9 +/- 40.7 mg/dl) (mean +/- SEM), although the difference was not statistically significant. Moreover, at the end of the two treatments, the percentage distribution of VLDL subfractions was very similar (large 37.5 +/- 3.3% vs 37.6 +/- 2.6%, intermediate 27.6 +/- 0.9% vs 31.0 +/- 2.4%; small 34.9 +/- 3.7% vs 31.4 +/- 2.1%). Concerning LDL, no significant change in LDL size was observed after the two treatments (255.4 +/- 2.2 A vs 254.2 +/- 1.7 A, fish oil; 253.7 +/- 2.0 A vs 253.3 +/- 1.7 A, placebo). LDL subfraction distribution was also very similar (large 17 +/- 3% vs 17 +/- 2%; intermediate 62 +/- 3% vs 65 +/- 3%; small 21 +/- 3% vs 18 +/- 2%), at the end of the two periods, confirming the lack of effects on LDL size. In conclusion, our study indicates that in NIDDM patients with hypertriglyceridemia, fish oil does not induce any improvement in LDL distribution and LDL size despite its positive effects on plasma triglycerides.

Adult↗
PubMed1999

Efficacy and safety of acarbose in the treatment of Type 1 diabetes mellitus: a placebo-controlled, double-blind, multicentre study.

AIMS: The aim of the study was to evaluate the efficacy and safety of acarbose in patients with Type 1 diabetes mellitus (DM). METHODS: A multicentre double-blind, randomized, placebo-controlled study was performed. After a 6-week run-in, 121 patients were randomized to acarbose or placebo and to high- or low-fibre diet for 24 weeks. Acarbose dose was 50 mg t.d.s. for the first 2 weeks and 100 mg t.d.s. for the subsequent weeks. RESULTS: At the end of 24 weeks of treatment the intention to treat analysis showed that acarbose compared with placebo decreased 2 h postprandial plasma glucose levels (12.23 +/- 0.83 vs. 14.93 +/- 0.87 mmol/l; F = 6.1, P < 0.02) (least square means +/- SEM). No significant effect of acarbose was recorded on HbA1c or on the number of hypoglycaemic episodes. The effect of acarbose on blood glucose control was not influenced by the amount of carbohydrate and/or fibre intake. The incidence of adverse events were 75% and 39% in acarbose and placebo groups, respectively; they were mild and confined to the gastrointestinal tract. CONCLUSIONS: The use of acarbose in combination with insulin reduces postprandial plasma glucose levels in Type 1 diabetic patients who are not satisfactorily controlled with insulin alone but without significant effect on HbA1c.

Acarbose↗
PubMed1999

Pro12Ala substitution in the peroxisome proliferator-activated receptor-gamma2 is not associated with type 2 diabetes.

Peroxisome proliferator-activated receptor (PPAR)-gamma is a major regulator of adipogenesis and insulin sensitivity. The PPAR-gamma gene generates two isoforms through alternative splicing, PPAR-gamma1 and -gamma2, the latter having an additional stretch of 28 amino acids at its NH2-terminus in the ligand-independent activation domain. This extension renders PPAR-gamma2 more sensitive to insulin action. Since there is a Pro12Ala substitution in this domain, we tested whether it is related to type 2 diabetes or insulin resistance. Therefore, 131 type 2 diabetic patients and 312 normoglycemic control subjects were screened for the presence of the mutation and for major clinical and metabolic features. The frequency of the mutation did not differ significantly between diabetic patients and control subjects. BMI, insulin, and other metabolic and anthropometric variables were also not associated with the mutation. Although the study was carried out on a sufficiently large sample, the conclusions do not support a major role for the Pro12Ala substitution of the PPAR-gamma gene in the etiology of type 2 diabetes.

Adipose Tissue↗
PubMed1999

Risk of diabetes in the new diagnostic category of impaired fasting glucose: a prospective analysis.

OBJECTIVE: To prospectively evaluate progression to diabetes in individuals with impaired glucose regulation as defined according to fasting glucose alone or an oral glucose tolerance test (OGTT) (i.e., both fasting and postload glucose) to compare the ability of these two screening methods to identify people at high risk of developing diabetes. RESEARCH DESIGN AND METHODS: A working population of 1,245 nondiabetic telephone company employees aged 40-59 years was studied by OGTT in 1980. Participants were classified according to baseline fasting glucose only (as encouraged by the American Diabetes Association [ADA]) or OGTT (as recommended by the 1998 World Health Organization [WHO] consultation). Progression to diabetes was evaluated 11.5 years later according to the 1997 ADA criteria of a fasting plasma glucose level > or =7.0 mmol/l. RESULTS: With the use of the OGTT, baseline prevalence of impaired glucose regulation was substantially higher than that with fasting glucose alone (7.2 vs. 3.2%); the two groups only overlap for 40.9% of the cases because a fairly large number of people with postload hyperglycemia (59.1%) have normal fasting glucose. Progression to diabetes in participants with normal fasting glucose and postload hyperglycemia is significantly more frequent than that of people with normoglycemia (32.5 vs. 7.2%; P < 0.001) and not significantly different from that of people with both fasting and postload hyperglycemia (i.e., 44.0%). However, the former are not identified as being at unusually high risk of diabetes unless an OGTT is performed. When the use of fasting glucose alone or OGTT was validated as a marker of progression to diabetes, sensitivity was substantially higher for the OGTT (33.3 vs. 9.0%) without major differences in specificity (92.6 vs. 97.0%). CONCLUSIONS: These data (the only data so far available in Caucasians) support the viewpoint that for the identification of people at high risk of diabetes, the use of the OGTT should be maintained.

Administration, Oral↗
PubMed1998

Effects of dietary cholesterol on plasma lipoproteins and their subclasses in IDDM patients.

To compare the effects of dietary cholesterol supplementation in insulin-dependent diabetic (IDDM) patients and normal subjects, 10 male IDDM patients in good glycaemic control (HbA1c 7.3+/-0.9%) (mean+/-SD) and normal plasma lipid levels, and 11 control male subjects of similar age, body mass index and lipid plasma levels underwent a double blind, cross-over, sequential study. Cholesterol supplementation of 800 mg/day or placebo were given for consecutive periods of 3 weeks. The concentration of plasma total cholesterol increased significantly with the dietary cholesterol supplementation compared to placebo in IDDM patients by 6% (p < 0.05) and in control subjects by 9% (p < 0.05). No changes were observed in the concentration of plasma triglycerides in either group. The LDL cholesterol level increased by 12% (p < 0.01) in patients and by 7% (p < 0.05) in control subjects. In patients plasma HDL cholesterol concentration remained the same, while in control subjects it tended to increase after cholesterol supplementation (from 1.14+/-0.26 to 1.23+/-0.27 mmol/l, p = 0.06). During the cholesterol intake period the mean concentration of LDL1, LDL2 and LDL3 subclasses in patients showed a significant increase by 21.0 (p < 0.05), 20.4 (p < 0.001) and 11.1% (p < 0.05), respectively, resulting in an 18.0% increase in mean total LDL mass (p < 0.001) without major changes in LDL composition. In the control subjects the changes in the concentrations of LDL subclasses during cholesterol intake were less and not significant. In the IDDM patients the cholesterol intake did not affect the concentration or composition of HDL subclasses or total HDL mass. In contrast, in control subjects cholesterol intake increased the mean concentration of HDL2a by 12.2.% (p < 0.05) and this increase was significantly different if compared to changes obtained in the patients. In conclusion, compared to normal subjects, in IDDM patients, dietary cholesterol intake increased the LDL particle mass significantly and had no positive effect on HDL.

Adult↗