Polyphenols Rich Diets and Risk of Type 2 Diabetes.

Type 2 diabetes is an increasing health concern worldwide. Both genetic and environmental risk factors as improper dietary habits or physical inactivity are known to be crucial in the pathogenesis of type 2 diabetes. Polyphenols are a group of plant-derived compounds with anti-inflammatory and antioxidant properties that are associated with a low prevalence of metabolic conditions characterized by insulin resistance, including obesity, diabetes, and hypertension. Moreover, there is now full awareness that foods that are rich in phytochemicals and polyphenols could play an important role in preserving human cardiovascular health and substantial clinical evidence indicates that regular dietary consumption of such foods affects favorably carbohydrate metabolism. This review briefly summarizes the evidence relating dietary patterns rich in polyphenols with glucose metabolism and highlights the potential benefits of these compounds in the prevention of type 2 diabetes.

Dulaglutide reduces binge episodes in type 2 diabetic patients with binge eating disorder: A pilot study.

AIMS: Binge eating disorder (BED) is the most common eating disorder in the United States and Europe and is associated with obesity and type 2 diabetes (T2D). Presence and severity of BED have been associated with worse metabolic control and greater BMI in T2D patients. Glucagon Like Peptide-1 (GLP1) receptors are present in central nervous system areas involved in appetite regulation and treatment with GLP-1 receptor agonists modulates appetite and reward-related brain areas in humans. We evaluated the effects of treatment with dulaglutide on eating behavior in T2D outpatients with BED. METHODS: This was a pilot open label, prospective controlled study. Inclusion criteria were: Age ≤65, HbA1c between 7.5 and 9% on metformin therapy alone, normal renal function and diagnosis of BED. Patients were randomly assigned to receive either Dulaglutide 1,5 mg/sett or Gliclazide 60 mg for 12 weeks. We evaluated baseline binge eating scale score (BES), weight, BMI, percentage fat mass, HbA1c and their changes after treatment. A multivariate linear regression model was used to verify the association between Δ BES from baseline with Δ Hba1c and variation of anthropometric parameters after treatment. RESULTS: After 12 weeks patients treated with dulaglutide had grater reduction of binge eating behaviour (p < 0.0001), body weight (p < 0,0001), BMI (p < 0.0001), percentage fat mass (p < 0.0001) and HbA1c (p = 0.009) than patients treated with gliclazide. Reduction in BES was associated with reduction in body weight (p < 0.0001) and HbA1c (p = 0.033). CONCLUSION: Dulaglutide treatment reduces binge eating behaviour in T2D patients with BED.

Sustained virologic response to direct-acting antiviral agents predicts better outcomes in hepatitis C virus-infected patients: A retrospective study.

BACKGROUND: Direct-acting antiviral agents (DAAs) are extremely effective in eradicating hepatitis C virus (HCV) in chronically infected patients. However, the protective role of the sustained virologic response (SVR) achieved by second- and third-generation DAAs against the onset of hepatocellular carcinoma (HCC) and mortality is less well established. AIM: To examine the occurrence of HCC or death from any cause in a retrospective-prospective study of patients treated with DAAs. METHODS: Patients were enrolled from a tertiary academic hospital center for liver disease management that collects subject data mainly from northeastern Italy. The study was conducted in 380 patients (age: 60 ± 13 years, 224 males, 32% with cirrhosis) treated with DAAs with or without SVR (95/5%), with a median follow up of 58 wk (interquartile range: 38-117). The baseline anthropometric features, HCV viral load, severity of liver disease, presence of extra-hepatic complications, coinfection with HIV and/or HBV, alcohol consumption, previous interferon use, alpha-fetoprotein levels, and renal function were considered to be confounders. RESULTS: The incidence rate of HCC in patients with and without SVR was 1.3 and 59 per 100 person-years, respectively (incidence rate ratio: 44, 95%CI: 15-136, P < 0.001). Considering the combined endpoint of HCC or death from any cause, the hazard ratio (HR) for the SVR patients was 0.070 (95%CI: 0.025-0.194, P < 0.001). Other independent predictors of HCC or death were low HCV viremia (HR: 0.808, P = 0.030), low platelet count (HR: 0.910, P = 0.041), and presence of mixed cryoglobulinemia (HR: 3.460, P = 0.044). Considering SVR in a multi-state model, the independent predictors of SVR achievement were absence of cirrhosis (HR: 0.521, P < 0.001) and high platelet count (HR: 1.019, P = 0.026). Mixed cryoglobulinemia predicted the combined endpoint in patients with and without SVR (HR: 5.982, P = 0.028 and HR: 5.633, P = 0.047, respectively). CONCLUSION: DAA treatment is effective in inducing SVR and protecting against HCC or death. A residual risk of HCC persists in patients with advanced liver disease or with complications, such as mixed cryoglobulinemia or renal failure.

Heart failure in the elderly: A geriatric syndrome. Picture of the modern situation.

Among the older patients' cohort, the aetiology of heart failure is peculiar and differs in many ways from the younger one, both in its epidemiology, diagnostic work-up and clinical presentation. Focusing on this population, we could assume that heart failure is a real geriatric syndrome, characterized by several features, which coexist with other comorbidities and require specific and targeted cares. It is therefore necessary to examine the global burden of heart failure and the patient's history rather than the causal cardiomyopathy - frequently more than one in the elderly - facing with the condition, bearing in mind the quality of life even before its duration.

Insulin sensitivity in patients with primary aldosteronism: a follow-up study.

CONTEXT: The relationship between aldosterone and glucose metabolism is poorly understood, and there is substantial disparity among findings of studies that have examined glucose tolerance and insulin sensitivity in patients with primary aldosteronism. OBJECTIVE: The objective of the study was to determine the outcome of glucose tolerance and insulin sensitivity in patients with primary aldosteronism after treatment. DESIGN: This was a prospective study of patients who received a diagnosis of primary aldosteronism and were followed up for an average period of 5.7 yr (range, 3-9 yr). SETTING: The study was conducted at a university referral center. PATIENTS: A consecutive sample of 47 patients with tumoral or idiopathic aldosteronism was followed up after either surgical or medical treatment. Patients with primary aldosteronism were compared with 247 patients with essential hypertension with the same severity and duration of disease and 102 normotensive subjects. MAIN OUTCOME MEASURES: Short- and long-term changes in glucose tolerance and insulin sensitivity were measured. RESULTS: After adjustment for age, gender, and body mass index, patients with primary aldosteronism had greater homeostasis model assessment index (P < 0.05) and plasma insulin response to an oral glucose load (P < 0.05) and lower quantitative insulin sensitivity check index (P < 0.01) than normotensive controls. Changes in insulin sensitivity were significantly greater in essential hypertension than primary aldosteronism, and this difference was confirmed by assessment with the hyperinsulinemic-euglycemic clamp (P < 0.01). Treatment of primary aldosteronism decreased blood pressure significantly, and during the initial 6 months of follow-up, parameters of insulin sensitivity were restored to normal. Analysis of subsequent follow-up showed nonsignificant changes in glucose metabolism parameters in both adrenalectomized and spironolactone-treated patients. CONCLUSIONS: Insulin resistance is present in patients with tumoral and idiopathic aldosteronism, but the defect appears less severe than in patients with essential hypertension. Treatment with surgery or aldosterone antagonists restores rapidly and persistently normal sensitivity to insulin.

Rho-kinase inhibition blunts renal vasoconstriction induced by distinct signaling pathways in vivo.

In addition to intracellular calcium, which activates myosin light chain (MLC) kinase, MLC phosphorylation and hence contraction is importantly regulated by MLC phosphatase (MLCP). Recent evidence suggests that distinct signaling cascades of vasoactive hormones interact with the Rho/Rho kinase (ROK) pathway, affecting the activity of MLCP. The present study measured the impact of ROK inhibition on vascular F-actin distribution and on vasoconstriction induced by activation/inhibition of distinct signaling pathways in vivo in the microcirculation of the split hydronephrotic rat kidney. Local application of the ROK inhibitors Y-27632 or HA-1077 induced marked dilation of pre- and postglomerular vessels. Activation of phospholipase C with the endothelin ET B agonist IRL 1620, inhibition of soluble guanylyl cyclase with 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), or inhibition of adenylyl cyclase with the adenosine A1 agonist N6-cyclopentyladenosine (CPA) reduced glomerular blood flow (GBF) by about 50% through vasoconstriction at different vascular levels. ROK inhibition with Y-27632 or HA-1077, but not protein kinase C inhibition with Ro 31-8220, blunted ET B-induced vasoconstriction. Furthermore, the reduction of GBF and of vascular diameters in response to ODQ or CPA were abolished by pretreatment with Y-27632. ROK inhibitors prevented constriction of preglomerular vessels and of efferent arterioles with equal effectiveness. Confocal microscopy demonstrated that Y-27632 did not change F-actin content and distribution in renal vessels. The results suggest that ROK inhibition might be considered as a potent treatment of renal vasoconstriction, because it interferes with constriction induced by distinct signaling pathways in renal vessels without affecting F-actin structure.

The emerging risk factors for cardiovascular disease: a review of the epidemiologic evidence for lipoprotein(a), homocysteine, and fibrinogen.

Appropriate correction of cardiovascular risk factors is a mainstay of the treatment of patients that have developed or might develop cardiovascular disease. In addition to classical risk factors, such as hypertension, smoking, dyslipidemia, diabetes, obesity, and sedentary life, epidemiological research has identified a number of additional conditions that are associated with a greater risk of cardiovascular disease. In fact, a substantial percentage of patients who develop cardiovascular events do not have any of the classical risk factors. Over the past thirty years, effective intervention in the treatment of hypertension, dyslipidemia, and diabetes has reduced remarkably cardiovascular morbidity and mortality, but the incidence of coronary artery disease and stroke remains unacceptably high and cardiovascular diseases are still the leading cause of death in the Western world. New cardiovascular risk factors are likely to give substantial contribution to this scenario and it could be easily anticipated that this contribution will become more evident in the upcoming years. This is why physicians who operate in the field of cardiovascular medicine and deal with problems related to cardiovascular prevention should be aware of these emergent risk factors, evaluate them accurately in their patients, and treat them appropriately. This review will summarize the literature supporting the role of lipoprotein(a), homocysteine, and fibrinogen as cardiovascular risk factors.