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Free access

Salvatore Calanna, Francesca Urbano, Salvatore Piro, Rose Maria Zagami, Antonino Di Pino, Luisa Spadaro, Francesco Purrello and Agata Maria Rabuazzo

Background and aims

Metabolic syndrome (MS) is a high-risk condition for type 2 diabetes, a disease characterized by insulin resistance and insulin secretion abnormalities. Insulin resistance has been widely characterized in MS subjects while insulin secretion has been poorly investigated. The present study was hence undertaken to further investigate the α and β cell function and entero-insular axis in this pre-diabetic condition.

Materials and methods

Using 120′ oral glucose tolerance test (OGTT, 75 g) and 60′ intravenous glucose tolerance test (IVGTT, 0.3 g/kg), we studied α and β cell function, insulin resistance, and incretin levels in 96 subjects with normal fasting glucose and normal glucose tolerance to OGTT, with (MS+, n=29) and without MS (MS−, n=67).


MS+ individuals showed in comparison with MS−: higher insulinogenic index (IG30) and higher area under the curve (AUC) (0–120) for glucose and insulin during the OGTT, P<0.05; higher AUC (0–10) for glucose (P<0.05) but similar first phase insulin secretion (P=NS) as measured by ΔAIRG and AUC (0–10) for insulin during the IVGTT; increased AUC (0–60) for insulin during the IVGTT (P=0.04); higher GIP levels at 30′ (P=0.03), 60′ (P=0.01), 90′ (P=0.003), and 120′ (P=0.004); higher AUC (0–120) for GIP (P=0.007); similar AUC (0–120) for GLP-1 during the OGTT; and delayed glucagon suppression after the OGTT.


NGT subjects with MS showed increased GIP secretion that could be responsible for the delayed glucagon suppression during the OGTT, thereby suggesting a role for incretins in regulating glucose homeostasis in this condition.

Open access

Francesca Urbano, Antonino Di Pino, Roberto Scicali, Agnese Filippello, Stefania Di Mauro, Alessandra Scamporrino, Simona Marchisello, Agata Maria Rabuazzo, Francesco Purrello and Salvatore Piro


Statin therapy has been linked to an increased risk of type 2 diabetes in high-risk populations; however, the pathophysiology of this association remains to be clarified. We investigated glucagon suppression and its relationship with insulin resistance in prediabetic subjects undergoing atorvastatin therapy; in addition, we studied molecular insulin signaling in pancreatic α-cells exposed to atorvastatin in vitro.

Design and methods

Fifty subjects with prediabetes were divided into two groups based on atorvastatin therapy. All subjects underwent an oral glucose tolerance test. Early (0–30 min), late (30–120 min) and overall (0–120 min) glucagon suppression were evaluated. Insulin sensitivity was estimated by the insulin sensitivity index (ISI0–120). Insulin signaling pathway and insulin-mediated glucagon suppression were investigated in pancreatic αTC1-6 cells chronically exposed (24 or 48 h) to atorvastatin (100 ng/mL).


Individuals on statin therapy (n = 26) showed a significantly reduced early (0–30 min) (P = 0.003) and overall (0–120 min) (P = 0.01) glucagon suppression compared with controls (n = 24). In multivariate regression analysis, early glucagon suppression (0–30 min) exhibited a significant correlation with statin therapy. Regression analysis showed a significant association between ISI 0-120 and early0-30 (r = 0.33, P < 0.05) and overall0-120 (r = 0.38, P < 0.05) glucagon suppression. Moreover, in αTC1-6 cells atorvastatin treatment affected insulin-mediated glucagon suppression, insulin receptor phosphorylation and IRS-1-AKT pathway signaling.


Prediabetic patients undergoing statin therapy exhibit impaired glucagon suppression associated with lower insulin sensitivity. Our data revealed a new molecular aspect behind the deregulation of insulin sensitivity secondary to statin exposure.