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Articles by E. Ferrannini
Total Records ( 4 ) for E. Ferrannini
  S Bonuccelli , E Muscelli , A Gastaldelli , E Barsotti , B. D Astiarraga , J. J Holst , A Mari and E. Ferrannini

Improved glucose tolerance to sequential glucose loading (Staub-Traugott effect) is an important determinant of day-to-day glycemic exposure. Its mechanisms have not been clearly established. We recruited 17 healthy volunteers to receive two sequential oral glucose tolerance tests (OGTTs), at time 0 min and 180 min (Study I). The protocol was repeated on a separate day (Study II) except that plasma glucose was clamped at 8.3 mmol/l between 60 and 180 min. β-Cell function was analyzed by mathematical modeling of C-peptide concentrations. In a subgroup, glucose kinetics were measured by a triple-tracer technique (infusion of [6,6-2H2]glucose and labeling of the 2 glucose loads with [1-2H]glucose and [U-13C]glucose). In both Studies I and II, the plasma glucose response to the second OGTT equaled 84 ± 2% (P = 0.003) of the response to the first OGTT. Absolute insulin secretion was lower (37.8 ± 4.3 vs. 42.8 ± 5.1 nmol/m2, P = 0.02), but glucose potentiation (i.e., higher secretion at the same glycemia) was stronger (1.08 ± 0.02- vs. 0.92 ± 0.02-fold, P = 0.006), the increment being higher in Study II (+36 ± 5%) than Study I (+19 ± 6%, P < 0.05). In pooled data, a higher glucose area during the first OGTT was associated with a higher potentiation during the second OGTT (rho=0.60, P = 0.002). Neither insulin clearance nor glucose clearance differed between loads, and appearance of glucose over 3 h totalled 60 ± 6 g for the first load and 52 ± 5 g for the second load (P = not significant). Fasting endogenous glucose production [13.3 ± 0.6 µmol·min–1·kg fat-free mass (FFM)–1] averaged 6.0 ± 3.8 µmol·min–1·kg FFM–1 between 0 and 180 min and 1.7 ± 2.6 between 180 and 360 min (P < 0.03). Glucose potentiation and stronger suppression of endogenous glucose release are the main mechanisms underlying the Staub-Traugott effect.

  A. Mari , A. Tura , G. Pacini , A. Kautzky-Willer and E. Ferrannini

Aims 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).

Methods We measured AIR and secretion after a 75-g OGTT in 221 subjects [age 37±11years, body mass index (BMI) 28±5kg/m2; 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.

Results 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 ~0 at ~7mmol/l FPG, whereas B-cell glucose sensitivity declined gradually throughout the FPG range. In addition, for FPG >7mmol/l, AIR was no longer related to FPG, whereas a strong relationship between FPG and B-cell glucose sensitivity was preserved (?=−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.

Conclusions 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.

  A. Antonelli , P. Fallahi , S. M. Ferrari , C. Pupilli , G. D`Annunzio , R. Lorini , M. Vanelli and E. Ferrannini
  Aims   Cell-mediated immunity and pro-inflammatory cytokines are implicated in the pathogenesis of Type 1 diabetes. The aim of this study was to investigate whether circulating chemokines involved in T-helper 1 (CXCL10) and T-helper 2 (CCL2) autoimmunity are increased in children with Type 1 diabetes at onset and follow-up.

Methods   Serum CXCL10 and CCL2 were measured in 96 children with newly diagnosed Type 1 diabetes, 59 age-matched first-degree relatives of diabetic children and 40 age-matched non-diabetic children with no family history of diabetes. In the diabetic children, an additional serum sample was obtained a median of 16 months after diagnosis.

Results   Serum CXCL10 levels were significantly higher in Type 1 children than in relatives or control children (P < 0.001); 44.7% of patients had a serum CXCL10 level ≥ 2 standard deviation above the mean value of the control group vs. 3.4% of relatives (P < 0.0001). In contrast, serum CCL2 levels were similar in patients, relatives and control subjects. In the Type 1 diabetic patients at follow-up, CXCL10 was significantly reduced vs. baseline (P = 0.01), while CCL2 did not change.

Conclusions   In children with newly diagnosed Type 1 diabetes, raised serum CXCL10 and normal CCL2 concentrations signal a predominant T-helper 1-driven autoimmune process, which shifts toward T-helper 2 immunity over the first 12 years from diagnosis.

  A. M. Sironi , R. Petz , D. De Marchi , E. Buzzigoli , D. Ciociaro , V. Positano , M. Lombardi , E. Ferrannini and A. Gastaldelli
  Objective  Previous studies have highlighted the associations between abdominal, cardiac or total fat accumulation and cardiovascular disease. The aim of this study was to investigate the impact of different ectopic fat depots on measurements of metabolic dysfunction and cardiovascular disease risk.

Methods  Using magnetic resonance imaging in 113 subjects, we measured abdominal (visceral and subcutaneous) and cardiac (epicardial and extra-pericardial) fat depots and examined their association with overall (BMI) and abdominal obesity (waist circumference), dyslipidaemia (triglycerides, total and HDL cholesterol), glucose tolerance (by an oral glucose tolerance test) and insulin sensitivity, blood pressure and 10-year coronary heart disease risk by Framingham score.

Results  Fat accumulation was proportional to the degree of obesity, with body fat ranging from 14 to 33 kg, visceral fat from 0.8 to 1.8 kg and cardiac fat from 134 to 236 g. Most cardiac fat (70% on average) was extra-pericardial, with a wide variability for both cardiac depots (epicardial: 172-2008 mm2; extra-pericardial: 100-5056 mm2). Only visceral and extra-pericardial fat, but not epicardial or subcutaneous fat, could discriminate between subjects with three or more factors of the metabolic syndrome or medium-to-high coronary heart disease risk score. Controlling for gender and BMI by multivariable analysis, the best marker of reduced insulin sensitivity was visceral fat (partial = −0.35); extra-pericardial fat was the closest associate of increased blood pressure (partial = 0.26) and both extra-pericardial and visceral fat clustered with hypertriglyceridaemia (partial = 0.29 and 0.24; both P < 0.02).

Conclusion  Increased epicardial fat per se does not necessarily translate into presence or prediction of disease. In contrast, increased deposition of visceral abdominal and extra-pericardial mediastinal fat are both associated with an enhanced cardiovascular disease risk profile.

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