Acute fall and long-term rise in oxygen saturation in response to meditation.

The effects of meditation on arterial and tissue oxygenation are unknown and difficult to assess because respiration is often altered, directly or indirectly, during meditation practice. Thus, changes in respiration may affect cardiovascular responses independently from meditation. In this study, we aim to isolate the specific effect of meditation on arterial and tissue oxygenation and other cardiorespiratory indexes while systematically controlling for the role of respiration. Furthermore, we aim to clarify to what extent prior expertise in meditation practice is needed to observe reliable changes. Eighty participants, half with and half without prior meditation experience, were tested while pacing breathing at predetermined rates, in the presence or absence of mantra meditation instructions, and in a body scan meditation that did not involve controlled breathing. Continuous recordings were acquired for arterial and brain oxygenation, respiratory excursion, electrocardiogram, skin vasomotion, and blood pressure. In both groups, meditation acutely decreased arterial and cerebral oxygen saturation, reduced chemoreflex sensitivity, and prolonged the RR interval, independently of respiration. Conversely, slow breathing improved heart rate variability, independently of concurrent meditation. In addition to the immediate effects of meditation, the individuals with long-term practice of meditation had overall higher arterial and cerebral oxygen saturation, overall lower blood pressure, and slower baseline respiration. Meditation acutely lowers arterial and tissue oxygenation. A repeated exposure to this condition may lead to long-term adaptation and, through increased ventilatory efficiency and improved gas exchanges, to an increase in baseline oxygenation. Meditation induces favorable changes in cardiovascular and respiratory end points of clinical interest.

Retraction notice to "Acarbose on insulin resistance after an oral fat load: a double-blind, placebo controlled study".

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). The article is a substantial duplication of an earlier published paper by the same group of authors (below), to which no reference was made during the manuscript submission or review process: Acarbose actions on insulin resistance and inflammatory parameters during an oral fat load. Giuseppe Derosa, Pamela Maffioli, Ilaria Ferrari, Elena Fogari, Angela D'Angelo, Ilaria Palumbo, Sabrina Randazzo, Lucio Bianchi, Arrigo FG Cicero. European Journal of Pharmacology 651 (2011) 240-250. http://doi:10.1016/j.ejphar.2010.11.015. The authors had declared during the editorial process that the article had not been published or was under consideration elsewhere. The article is being retracted per journal policy and academic standards.

Laparoscopy in children and its impact on brain oxygenation during routine inguinal hernia repair.

BACKGROUND: The systemic impact of intra-abdominal pressure (IAP) and/or changes in carbon dioxide (CO2) during laparoscopy are not yet well defined. Changes in brain oxygenation have been reported as a possible cause of cerebral hypotension and perfusion. The side effects of anaesthesia could also be involved in these changes, especially in children. To date, no data have been reported on brain oxygenation during routine laparoscopy in paediatric patients. PATIENTS AND METHODS: Brain and peripheral oxygenation were investigated in 10 children (8 male, 2 female) who underwent elective minimally invasive surgery for inguinal hernia repair. Intraoperative transcranial near-infrared spectroscopy to assess regional cerebral oxygen saturation (rScO2), peripheral oxygen saturation using pulse oximetry and heart rate (HR) were monitored at five surgical intervals: Induction of anaesthesia (baseline T1); before CO2insufflation induced pneumoperitoneum (PP) (T2); CO2PP insufflation (T3); cessation of CO2PP (T4); before extubation (T5). RESULTS: rScO2decreases were recorded immediately after T1 and became significant after insufflation (P = 0.006; rScO2decreased 3.6 ± 0.38%); restoration of rScO2was achieved after PP cessation (P = 0.007). The changes in rScO2were primarily due to IAP increases (P = 0.06). The HR changes were correlated to PP pressure (P < 0.001) and CO2flow rate (P = 0.001). No significant peripheral effects were noted. CONCLUSIONS: The increase in IAP is a critical determinant in cerebral oxygenation stability during laparoscopic procedures. However, the impact of anaesthesia on adaptive changes should not be underestimated. Close monitoring and close collaboration between the members of the multidisciplinary paediatric team are essential to guarantee the patient's safety during minimally invasive surgical procedures.

Integrated Cardio-Respiratory Control: Insight in Diabetes.

Autonomic dysfunction is a frequent and relevant complication of diabetes mellitus, as it is associated with increased morbidity and mortality. In addition, it is today considered as predictive of the most severe diabetic complications, like nephropathy and retinopathy. The classical methods of screening are the cardiovascular reflex tests and were originally interpreted as evidence of nerve damage. A more modern approach, based on the integrated control of cardiovascular and respiratory function, reveals that these abnormalities are to a great extent functional, at least in the early stage of the disease, thus suggesting new potential interventions. Therefore, this review aims to go further investigating how the imbalance of the autonomic nervous system is altered and can be influenced in many chronic pathologies through a global view of cardio-respiratory and metabolic interactions and how the same mechanisms are applicable to diabetes.

The effects of canrenone on inflammatory markers in patients with metabolic syndrome.

AIM: To evaluate the effects of canrenone compared to placebo on blood pressure control, some non-conventional biomarkers in cardiovascular stratification, and on metalloproteinases in patients affected by metabolic syndrome. METHODS: A total of 156 Caucasian patients were treated with placebo or canrenone, 50 mg once a day, for 3 months and then 50 mg twice a day, till the end of the study. We evaluated: systolic (SBP) and diastolic blood pressure (DBP), body weight, body mass index (BMI), fasting plasma glucose (FPG), lipid profile, plasma aldosterone, creatinine, potassium, brain natriuretic peptide (BNP), metalloproteinases 2 and 9 (MMP-2 and -9), lipoprotein (a) (Lp(a)), and serum myeloperoxidase (MPO). RESULTS: We observed a significant decrease of SBP and DBP in the canrenone group compared to baseline. Canrenone gave a significant decrease of MMP-2 and -9, Lp(a), and MPO compared to baseline, not observed with placebo. Plasma aldosterone, but not BNP, decreased with canrenone, both compared to baseline and to placebo. CONCLUSION: Canrenone seems to be effective in reducing blood pressure in patients with metabolic syndrome. Moreover, canrenone seems also to improve MPO, Lp(a), and metalloproteinases in these patients.

Metformin powder formulation compared to metformin tablets on glycemic control and on treatment satisfaction in subjects with type 2 diabetes mellitus.

The aim of this study was to evaluate if the new metformin powder formulation improves the treatment satisfaction in patients with type 2 diabetes, in a case-control clinical trial. We enrolled 602 subjects in therapy with metformin in tablets formulation and instructed them to take the same dose of metformin in the new powder formulation. At baseline, and after 6 months since the assumption of metformin powder, each patient answered the following questionnaires: the SF-36 Health Survey, the Diabetes Quality Of Life questionnaire Modified (DQOL/Mod), and the Diabetes Treatment Satisfaction Questionnaire (DTSQ). We also assessed the following at baseline, at 3 and 6 months: fasting plasma glucose (FPG) and postprandial glucose (PPG), glycated hemoglobin (HbA(1c)), fasting plasma insulin (FPI), and homeostasis model assessment index of insulin resistance (HOMA-IR). We observed a statistically significant reduction in HbA(1c), FPG, PPG, FPI, and HOMA-IR (P < .05 for all) with metformin powder. The DTSQ questionnaire showed a higher level of satisfaction linked to the assumption of metformin powder compared to the tablets formulation. In conclusion, metformin powder formulation seems to be more appropriate for the treatment of diabetic patients. The improvement of glycemic control suggests a better adherence to the powder formulation.

Vildagliptin compared to glimepiride on post-prandial lipemia and on insulin resistance in type 2 diabetic patients.

OBJECTIVES: To evaluate the effects of vildagliptin compared to glimepiride on glycemic control, insulin resistance and post-prandial lipemia. MATERIAL AND METHODS: 167 type 2 diabetic patients, not adequately controlled by metformin, were randomized to vildagliptin 50 mg twice a day or glimepiride 2 mg three times a day for 6 months, in a double blind, randomized clinical trial. We evaluated: body mass index (BMI), glycemic control, fasting plasma insulin (FPI), homeostasis model assessment insulin resistance index (HOMA-IR), fasting plasma proinsulin (FPPr), glucagon, lipid profile, resistin, retinol binding protein-4 (RBP-4), visfatin and vaspin. Furthermore, at the randomization and at the end of the study all patients underwent an euglycemic hyperinsulinemic clamp to evaluate M value and an oral fat load. RESULTS: Despite a similar decrease of glycated hemoglobin, there were an increase of body weight with glimepiride + metformin and a decrease with vildagliptin + metformin. Fasting plasma insulin increased with glimepiride + metformin, while it did not change with vildagliptin + metformin. Vildagliptin + metformin improved lipid profile. Regarding insulin sensitivity, vildagliptin + metformin increased M value. Resistin, RBP-4, vaspin and visfatin were decreased by vildagliptin + metformin, but in group to group comparison, only vaspin reduction resulted statistically significant. Vildagliptin + metformin reduced post-prandial lipemia and insulinemia compared to glimepiride + metformin. CONCLUSION: Vildagliptin, in addition to metformin, was more effective than glimepiride + metformin in reducing insulin resistance and post-prandial lipemia.

Enalapril/lercanidipine combination on markers of cardiovascular risk: a randomized study.

The aim of this study was to evaluate enalapril/lercanidipine combination effects on markers of cardiovascular risk stratification in hypertensive patients. A total of 359 patients were randomized to enalapril 20 mg, lercanidipine 10 mg, or enalapril/lercanidipine 20/10 mg fixed combination. We evaluated blood pressure (BP), fasting plasma glucose (FPG), lipid profile, lipoprotein(a) (Lp[a]), soluble receptor for advanced glycation end products (sRAGE), soluble CD40 ligand (sCD40 L), serum myeloperoxidase (MPO), high sensitivity C-reactive protein (Hs-CRP), and tumor necrosis factor-α (TNF-α). We recorded a decrease of BP in all groups, with the enalapril/lercanidipine combination being more effective in reducing BP compared with single monotherapies. Lipid profile or FPG were not affected by various treatments. Lercanidipine, but not enalapril, improved Lp(a) levels compared with baseline, with enalapril/lercanidipine having a greater effect on Lp(a) reduction. All treatments increased sRAGE levels, and decreased sCD40 L and MPO, even if enalapril/lercanidipine combination was more effective than single monotherapies. TNF-α and Hs-CRP were greater reduced by enalapril/lercanidipine combination compared with enalapril (P < .05 for both). The enalapril/lercanidipine fixed combination was more effective than single monotherapies in decreasing BP, but also in improving markers of cardiovascular risk stratification in hypertensive patients.

Sitagliptin added to previously taken antidiabetic agents on insulin resistance and lipid profile: a 2-year study evaluation.

The aim of this study was to evaluate whether the positive effects of sitagliptin on glycemic control and insulin resistance were maintained also after 2 years of therapy and whether sitagliptin could be effective also in improving lipid profile. In this randomized, double-blind, placebo-controlled trial, 205 patients with type 2 diabetes in therapy with different antidiabetic drugs were randomized to add sitagliptin 100 mg once a day or placebo to their current therapy. We evaluated at the baseline and after 6, 12, 18, and 24 months the following parameters: body mass index, glycated hemoglobin (HbA1c ), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), fasting plasma insulin (FPI), homeostasis model assessment insulin resistance index (HOMA-IR), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (Tg). Sitagliptin, added to previously taken antidiabetic agents, proved to be effective in improving glycemic profile, reducing HbA1c by -17.5%, FPG by -12.7%, PPG by -20.5%. Regarding insulin resistance, sitagliptin decreased FPI by -8.3% and HOMA-IR by -20.0%, confirming that what have been already reported in short-term studies can be applied also after 2 years of treatment. Sitagliptin also reduced body weight by -4.3%. Our study also showed the positive effect of sitagliptin on lipid profile; in particular, sitagliptin decreased TC by -13.3%, LDL-C by -20.4%, and Tg by -32.3%, and also increased HDL-C by + 13.6%. Sitagliptin proved to be effective on glycemic profile and insulin resistance even after 2 years of therapy and to be effective in improving body weight and lipid profile.

Berberis aristata/Silybum marianum fixed combination on lipid profile and insulin secretion in dyslipidemic patients.

BACKGROUND: Relatively large number of dietary supplements and nutraceuticals have been studied for their supposed or demonstrated ability to reduce cholesterolemia in humans. OBJECTIVES: The aim of this study was to evaluate the efficacy as antihypercholesterolemic and insulin-sensitizing agent of a combination of Berberis aristata/Silybum marianum extract (Berberol®) in a sample of dyslipidemic patients. A total of 102 dyslipidemic subjects were enrolled. After a 6 months run-in period of diet and physical activity, the patients were randomized to placebo or Berberis aristata/Silybum marianum extract 588 mg/105 mg, twice a day for 3 months. Berberis aristata/Silybum marianum and placebo were then interrupted for 2 months (washout period), and then restarted for further 3 months. Anthropometric and metabolic parameters were assessed; moreover, all patients underwent a glucagon stimulation test. RESULTS: Berberis aristata/Silybum marianum reduced total cholesterol, triglycerides and low-density lipoprotein cholesterol and increased high-density lipoprotein cholesterol after 3 months from randomization and compared to placebo group. When Berberis aristata/Silybum marianum was interrupted, lipid profile worsened, and it improved again when nutraceutical combination was reintroduced. During the glucagon stimulation test, a higher increase of C-peptide levels and a lower increase in glycemia after the test with Berberis aristata/Silybum marianum compared to placebo, to baseline and to randomization were recorded. No patients had serious adverse events in both groups. CONCLUSION: Berberis aristata/Silybum marianum is effective and safe in improving lipid profile and insulin secretion in euglycemic dyslipidemic patients.

Effects of canrenone in patients with metabolic syndrome.

BACKGROUND: Metabolic syndrome is becoming a common disease due to a rise in obesity rates among adults. OBJECTIVES: The aim was to evaluate the effects of canrenone compared to placebo on metabolic and inflammatory parameters in patients affected by metabolic syndrome. A total of 145 patients were treated with placebo or canrenone, 50 mg/day, for 3 months and then 50 mg b.i.d. till the end of the study. Blood pressure, body weight, body mass index, fasting plasma glucose (FPG), fasting plasma insulin, HOMA-IR, lipid profile, plasma aldosterone, brain natriuretic peptide, high-sensitivity C-reactive protein (Hs-CRP), tumor necrosis factor-α (TNF-α) and M value were evaluated. RESULTS: A decrease of blood pressure was observed in canrenone group compared to baseline; moreover, systolic blood pressure value recorded after 6 months of canrenone therapy was lower than the one recorded with placebo. Canrenone gave a significant decrease of FPI and HOMA index, and an increase of M value both compared to baseline and to placebo. Canrenone also decreased triglycerides and FPG was not observed with placebo. Canrenone also decreased plasma aldosterone, Hs-CRP and TNF-α compared to baseline and to placebo. CONCLUSION: Canrenone seems to be effective in reducing some factors involved in metabolic syndrome and in improving insulin-resistance and the inflammatory state observed in these patients.

Adipocytokine levels in obese and non-obese subjects: an observational study.

We evaluated the levels of some inflammatory adipocytokines in 363 obese and 365 non-obese subjects. We measured: body mass index (BMI), waist circumference (WC), fasting plasma glucose, fasting plasma insulin (FPI), homeostasis model assessment (HOMA) index, blood pressure, lipid profile, retinol binding protein-4 (RBP-4), vaspin, omentin-1, leptin, interleukin-6 (IL-6), visfatin, resistin, adiponectin (ADN), adipsin, tumor necrosis factor-α (TNF-α), and high sensitivity C-reactive protein (Hs-CRP). We observed higher BMI, WC, FPI, HOMA index, TC, LDL-C, RBP-4, leptin, IL-6, adipsin, Hs-CRP, vaspin, resistin and TNF-α levels, and lower visfatin, and ADN levels in obese compared to non-obese subjects. Higher WC correlated with lower ADN and visfatin levels, and higher vaspin levels. Higher HOMA index correlated with higher resistin, adipsin, RBP-4, and leptin concentrations, while higher leptin levels correlated with higher TNF-α, Hs-CRP, and IL-6 concentration, and lower ADN values. We confirmed obese subjects' predisposition to develop dysmetabolic disease and hormonal dysfunctions.

Effects of berberine on lipid profile in subjects with low cardiovascular risk.

OBJECTIVE: To evaluate the efficacy as antihypercholesterolemic agent of berberine in patients with low cardiovascular risk. RESEARCH DESIGN AND METHODS: 144 Caucasian subjects were enrolled. After a 6-month run-in period following diet and practicing physical activity, patients were randomized to take placebo or berberine 500 mg twice a day, for 3 months, in a double-blind, placebo-controlled design. Berberine and placebo were then interrupted for 2 months (washout period), and all patients continued with only diet and physical activity. At the end of the washout period, patients restarted berberine or placebo twice a day for further 3 months. Anthropometric and metabolic parameters were assessed during the run-in period, at randomization, before and after the washout period. RESULTS: A decrease of body weight and BMI was observed after the run-in period. Berberine reduced total cholesterol, triglycerides and LDL cholesterol and increased HDL cholesterol after 3 months from randomization and compared with placebo. After the washout period, lipid profile worsened; afterward, when berberine was reintroduced, lipid profile improved again both compared with the washout period, and with placebo. CONCLUSIONS: Berberine is effective and safe to mildly improve lipid profile in subjects with low risk for cardiovascular disease.

Effects of a combination of sitagliptin plus metformin vs metformin monotherapy on glycemic control, ß-cell function and insulin resistance in type 2 diabetic patients.

AIMS: To evaluate the impact on glycemic control, insulin resistance, and insulin secretion of sitagliptin+metformin compared to metformin in type 2 diabetic patients. METHODS: Patients were instructed to take metformin for 8 ± 2 months, then they were randomly assigned to sitaglipin 100 mg or placebo for 12 months. We evaluated at 3, 6, 9, and 12 months: body mass index (BMI), glycemic control, fasting plasma insulin (FPI), HOMA-IR, HOMA-ß, fasting plasma proinsulin (FPPr), proinsulin/fasting plasma insulin ratio (Pr/FPI ratio), C-peptide, glucagon, adiponectin (ADN), and high sensitivity-C reactive protein (Hs-CRP). Before, and after 12 months since the addition of sitagliptin, patients underwent a combined euglycemic hyperinsulinemic and hyperglycemic clamp, with subsequent arginine stimulation. RESULTS: Both treatments similarly decreased body weight, and BMI; on the other hand, they both improved glycemic control, glucagon and HOMA-IR, but sitagliptin+metformin were more effective in reducing these parameters. Sitagliptin+metformin, but not placebo+metformin, decreased FPPr, FPPR/FPI ratio, and increased C-peptide values, even if no differences between the groups were recorded. Sitaglitin+metformin gave also a greater increase of HOMA-ß, M value, C-peptide response to arginine and disposition index compared to placebo+metformin group. CONCLUSIONS: Other than improving glycemic control, sitagliptin+metformin also improved ß-cell function better than metformin alone.

Glyco-metabolic profile among type 2 diabetic patients with erectile dysfunction.

The aim of this study was to evaluate the glyco-metabolic profile among type 2 diabetic patients with erectile dysfunction (ED). We evaluated 88 type 2 diabetic males, aged 62.78 ± 9.26 years. We administered patients the IIEF (International Index of Erectile Function) questionnaire to assess erectile function, organ function, sexual desire, and satisfaction level during and after the sexual intercourse and the SAS (self-rating anxiety scale) and SDS (self-rating depression scale) questionnaires to evaluate anxiety and depression. We evaluated: BMI, abdominal circumference, glycated hemoglobin (HbA(1c)), fasting plasma glucose (FPG), fasting plasma insulin (FPI), HOMA index, lipid profile, testosterone, free testosterone, dihydrotestosterone, and sex hormone binding globulin (SHBG). The IIEF questionnaire showed that in the examined sample there were 50 patients (56.8%) affected by ED, and 38 patients (43.2%) without ED. Comparing the two groups, 57.9% of patients without ED, and 70.0% of patients with ED were smokers, and the difference between the two groups was significant (p<0.05). Furthermore, 23.7% of patients without ED, and 38.0% of patients with ED had a history of chronic ischemic heart disease (p<0.05 between the two groups). Patients with ED were older, and, surprisingly, had lower levels of HbA(1c). Furthermore, patients with ED had higher levels of FPI, and lower levels of testosterone and dihydrotestosterone. The prevalence of ED in Italian type 2 diabetic males with mean age of 62 years is about 56% and it is linked to higher levels of FPI, but lower levels of HbA(1c), free testosterone and dihydrotestosterone.

Vildagliptin added to metformin on ß-cell function after a euglycemic hyperinsulinemic and hyperglycemic clamp in type 2 diabetes patients.

BACKGROUND: This study evaluated the effect of vildagliptin + metformin on glycemic control and ß-cell function in type 2 diabetes patients. SUBJECTS AND METHODS: One hundred seventy-one type 2 diabetes patients, naive to antidiabetes therapy and with poor glycemic control, were instructed to take metformin for 8±2 months up to a mean dosage of 2,500±500 mg/day; then they were randomly assigned to add vildaglipin 50 mg twice a day or placebo for 12 months. We evaluated at 3, 6, 9, and 12 months: body mass index, glycemic control, fasting plasma insulin, homeostasis model assessment insulin resistance index (HOMA-IR), homeostasis model assessment ß-cell function index (HOMA-ß), fasting plasma proinsulin, proinsulin/fasting plasma insulin ratio, C-peptide, glucagon, adiponectin, and high-sensitivity C-reactive protein. Before and at 12 months after the addition of vildagliptin, patients underwent a combined euglycemic hyperinsulinemic and hyperglycemic clamp, with subsequent arginine stimulation, to assess insulin sensitivity and insulin secretion. RESULTS: After 12 months of treatment, vildagliptin + metformin gave a better decrease of body weight, glycemic control, HOMA-IR, and glucagon and a better increase of HOMA-ß compared with placebo + metformin. Regarding the measures of ß-cell function, treatment-induced changes in M-value, first- and second-phase C-peptide response to glucose, and C-peptide response to arginine were significantly higher in the vildagliptin + metformin group compared with the placebo + metformin group. CONCLUSION: The addition of vildagliptin to metformin gave a better improvement of glycemic control, insulin resistance, and ß-cell function compared with metformin alone.

RETRACTED: Acarbose on insulin resistance after an oral fat load: a double-blind, placebo controlled study.

AIM: We evaluated the effects of acarbose on insulin resistance parameters in diabetic patients before and after a standardized oral fat load (OFL). MATERIALS AND METHODS: Patients were assigned to take acarbose 50 mg three times a day or placebo; after the first month, acarbose was titrated to 100 mg three times a day. We evaluated body mass index, glycemic control, fasting plasma insulin (FPI), post-prandial plasma insulin (PPI), homeostasis model assessment insulin resistance index (HOMA-IR), blood pressure, lipid profile, retinol binding protein-4 (RBP-4), adiponectin (ADN), tumor necrosis factor-α and resistin (r). Furthermore, at the baseline and at the end of the study, all patients underwent an OFL and an euglycemic hyperinsulinemic clamp. RESULTS: We observed that acarbose was better than placebo in improving glycemic control and HOMA-IR and that it was also more effective in improving lipid profile, RBP-4 and ADN. Regarding FPI, PPI and r, we did not obtain any significant differences between the two groups. During the second OFL, performed after 7 months of therapy with acarbose, we observed a significant decrease of blood glucose, lipid profile and all insulin resistance parameters peaks compared with the OFL administered at baseline with acarbose, but not with placebo. CONCLUSION: Acarbose was more effective than placebo in improving glycemic and lipid profile and in reducing the post-OFL peaks of the various parameters including the insulin resistance biomarkers.

Acarbose actions on insulin resistance and inflammatory parameters during an oral fat load.

The aim of this study was to evaluate the effects of acarbose on inflammatory biomarkers and insulin resistance in diabetic patients before and after a standardized oral fat load (OFL). Ninety six patients were assigned to take acarbose 50mg three times a day and 92 to take placebo; after the first month acarbose was titrated to 100mg three times a day. We evaluated the following parameters at the baseline, and after 1, 2 and 7months: body mass index (BMI), glycemic control, fasting plasma insulin, post-prandial plasma insulin, homeostasis model assessment insulin resistance index (HOMA-IR), blood pressure, lipid profile, soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6), high-sensitivity C reactive protein (Hs-CRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble E-selectin (sE-selectin). Furthermore, at the baseline and at the end of the study all patients underwent OFL, and an euglycemic hyperinsulinemic clamp to evaluate M value and total glucose requirement. Acarbose was better than placebo in improving glycemic and lipid profile, and HOMA-IR. Furthermore, acarbose gave a decrease of fasting plasma insulin, post-prandial insulin, s-ICAM-1, sVCAM-1, IL-6, and Hs-CRP, not observed with placebo, even if no significant differences between the two groups were observed. During the second OFL performed after the therapy with acarbose, we observed a significant decrease of all inflammatory parameters' peaks compared to the OFL administered at baseline. Acarbose was more effective than acarbose in reducing the post-OFL peaks of the various parameters included the inflammatory markers, after 7months of therapy.