Metabolic Vascular Risk Research Articles

Effects of simultaneous pancreas-kidney transplantation and kidney transplantation alone on the outcome of peripheral vascular diseases

BackgroundThe effects of Simultaneous Pancreas Kidney Transplantation (SPKT) on Peripheral Vascular Disease (PVD) warrants additional study and more target focus, since little is known about the mid- and long-term effects on the progression of PVD after transplantation.Methods101 SPKT and 26 Kidney Transplantation Alone (KTA) recipients with insulin-dependent diabetes mellitus (IDDM) were retrospectively evaluated with regard to graft and metabolic outcome. Special subgroup analysis was directed towards the development and progression of peripheral vascular complications (PVC) (amputation, ischemic ulceration, lower extremity angioplasty/ bypass surgery) after transplantation.ResultsThe 10-year patient survival was significantly higher in the SPKT group (SPKT: 82% versus KTA 40%; P < 0.001). KTA recipients had a higher prevalence of atherosclerotic risk factors, including coronary artery disease (P < 0.001), higher serum triglyceride levels (P = 0.049), higher systolic (P = 0.03) and diastolic (P = 0.02) blood pressure levels. The incidence of PVD before transplantation was comparable between both groups (P = 0.114). Risk factor adjusted multivariate analysis revealed that patients with SPKT had a significant lower amount (32%) of PVCs (32 PVCs in 21 out of 101 SPKT; P < 0.001) when compared to the KTA patients who developed a significant increase in PVCs to 69% of cases (18 PVCs in 11 out of 26 KTA; P < 0.001). In line mean values of HbA1c (P < 0.01) and serum triglycerides (P < 0.01) were significantly lower in patients with SPKT > 8 years after transplantation.ConclusionSPKT favorably slows down development and progression of PVD by maintaining a superior metabolic vascular risk profile in patients with IDDM1.

Ernährungsempfehlungen beim metabolisch-vaskulären Syndrom

Cardiovascular disease is the number one cause of death globally. Poor diet constitutes a key factor in the initiation and progression of cardiovascular disease and has become the leading risk factor for disability and death worldwide. Therefore, addressing suboptimal nutrition is of key prognostic relevance in primary and secondary prevention of metabolic vascular syndrome. Metabolic vascular syndrome is a multidimensional network of acquired cardiometabolic risk factors closely related to insulin resistance (IR) and concomitant hyperinsulinemia. IR, being the underlying cause of metabolic vascular syndrome and certain types of cancer, should attract the attention of every clinician. As changes in lipoprotein metabolism are one of the earliest indicators of metabolic dysfunction, a relevant biomarker for identifying individuals with IR is the TAG/HDL-C ratio. IR – and concomitant metabolic vascular risk – can be effectively treated by lifestyle intervention. If IR is present, dietary carbohydrate restriction has consistently been shown to be superior to dietary fat restriction in reversing metabolic dysfunction. The beneficial effects of carbohydrate restricted diets on metabolic vascular risk are independent of BMI – diet quality therefore confers patient benefit beyond weight reduction. The effect of single nutrients on isolated lipid surrogate markers such as LDL-C does not capture their global effect on metabolic vascular risk. Targeting IR with a low glycemic load, real food diet will reduce overall energy density and will improve all risk factors of metabolic vascular syndrome. In particular, replacing refined carbohydrates with healthy fats in the context of a Mediterranean style-, low carbohydrate and calorie-unrestricted dietary pattern has been shown to significantly reduce burden of metabolic vascular disease.

Ernährungsempfehlungen beim metabolisch-vaskulären Syndrom

Cardiovascular disease is the number one cause of death globally. Poor diet constitutes a key factor in the initiation and progression of cardiovascular disease and has become the leading risk factor for disability and death worldwide. Therefore, addressing suboptimal nutrition is of key prognostic relevance in primary and secondary prevention of metabolic vascular syndrome.Metabolic vascular syndrome is a multidimensional network of acquired cardiometabolic risk factors closely related to insulin resistance (IR) and concomitant hyperinsulinemia. IR, being the underlying cause of metabolic vascular syndrome and certain types of cancer, should attract the attention of every clinician. As changes in lipoprotein metabolism are one of the earliest indicators of metabolic dysfunction, a relevant biomarker for identifying individuals with IR is the TAG/HDL-C ratio.IR - and concomitant metabolic vascular risk - can be effectively treated by lifestyle intervention. If IR is present, dietary carbohydrate restriction has consistently been shown to be superior to dietary fat restriction in reversing metabolic dysfunction. The beneficial effects of carbohydrate restricted diets on metabolic vascular risk are independent of BMI - diet quality therefore confers patient benefit beyond weight reduction.The effect of single nutrients on isolated lipid surrogate markers such as LDL-C does not capture their global effect on metabolic vascular risk.Targeting IR with a low glycemic load, real food diet will reduce overall energy density and will improve all risk factors of metabolic vascular syndrome. In particular, replacing refined carbohydrates with healthy fats in the context of a Mediterranean style-, low carbohydrate and calorie-unrestricted dietary pattern has been shown to significantly reduce burden of metabolic vascular disease.

Cigarette smoking/cessation and metabolic syndrome

AbstractThe metabolic syndrome (MetS) is a common cluster of pre-morbid, modified metabolic–vascular risk factors/diseases (visceral obesity, hyperglycaemia, dyslipidaemia and hypertension) associated with increased cardiovascular (CV) morbidity, fatty liver and risk of cancer. Several studies reported a higher incidence of MetS in smokers. Cigarette smoking plays a substantial role in the pathogenesis of numerous chronic diseases such as CV disease (CVD), cancer, lung disease and others. However, due to the existence of the so-called “smoking paradox”, the impact of this risk factor on CVD mortality is still not clear. Smoking cigarettes may increase risk of MetS or worsen it by numerous mechanisms. Furthermore, individuals who quit smoking tend to increase their body weight. The possibility of gaining weight can stop smokers from quitting and increases the risk of relapse, particularly in women. Herein, we review the cigarette smoking status (active/cessation) in relation to the MetS.

Homoarginine supplementation improves blood glucose in diet-induced obese mice

L-Homoarginine (hArg) is an endogenous amino acid which has emerged as a novel biomarker for stroke and cardiovascular disease. Low circulating hArg levels are associated with increased mortality and vascular events, whereas recent data have revealed positive correlations between circulating hArg and metabolic vascular risk factors like obesity or blood glucose levels. However, it is unclear whether hArg levels are causally linked to metabolic parameters. Therefore, the aim of our study was to investigate whether hArg directly influences body weight, blood glucose, glucose tolerance or insulin sensitivity. Here, we show that hArg supplementation (14 and 28 mg/mL orally per drinking water) ameliorates blood glucose levels in mice on high-fat diet (HFD) by a reduction of 7.3 ± 3.7 or 13.4 ± 3.8 %, respectively. Fasting insulin concentrations were slightly, yet significantly affected (63.8 ± 11.3 or 162.1 ± 39.5 % of control animals, respectively), whereas body weight and glucose tolerance were unaltered. The substantial augmentation of hArg plasma concentrations in supplemented animals (327.5 ± 40.4 or 627.5 ± 60.3 % of control animals, respectively) diminished profoundly after the animals became obese (129.9 ± 16.6 % in control animals after HFD vs. 140.1 ± 8.5 or 206.3 ± 13.6 %, respectively). This hArg-lowering effect may contribute to the discrepancy between the inverse correlation of plasma hArg levels with stroke and cardiovascular outcome, on the one hand, and the direct correlation with cardiovascular risk factors like obesity and blood glucose, on the other hand, that has been observed in human studies. Our results suggest that the glucose-lowering effects of hArg may reflect a compensatory mechanism of blood glucose reduction by hArg upregulation in obese individuals, without directly influencing body weight or glucose tolerance.

Circulating miRNA Profiles in Patients with Metabolic Syndrome

Coordinated interplay of dysregulated microRNAs in isolated metabolic disorder is implicated in the pathogenesis of metabolic syndrome. The objective of the study was to characterize microRNA expression in the blood and exosomes of individuals with metabolic syndrome and compare them with those manifesting one of the metabolic vascular risk factors (type 2 diabetes, hypercholesterolemia, or hypertension). RESEARCH DESIGN/SETTING/PARTICIPANTS: A total of 265 participants were recruited in a health screening and characterized into distinct groups as follows: 1) healthy controls (n = 46); 2) metabolic syndrome (n = 50); 3) type 2 diabetes (n = 50); 4) hypercholesterolemia (n = 89); and 5) hypertension (n = 30). Total RNA was subjected to microRNA profiling, and a panel of significantly dysregulated microRNAs was validated using quantitative PCR. Analysis of profiling data characterized unique pools of miRNAs that could categorize the different risk factors of metabolic syndrome. We have identified miR-197, miR-23a, and miR-509-5p as potential contributors of dyslipidemia in metabolic syndrome (correlation with body mass index; P = 0.029, 0.021, and 0.042, respectively) and miR-130a and miR-195 as contributors of hypertension (correlation with blood pressure; P = 0.019 and 0.045, respectively). A plausible association of miR-27a and miR-320a with metabolic syndrome and type 2 diabetes patients has also been found because these miRNAs remained dysregulated in both cases (correlation with fasting glucose; P = 0.010 and 0.016, respectively). Significant dysregulation of seven candidate microRNAs has been found to be associated with risks involved in the manifestation of metabolic syndrome.

Moderate Dietary Salt Restriction Does Not Alter Insulin Resistance or Serum Lipids in Normal Men

Dietary salt restriction lowers blood pressure and has been advocated as a population-based strategy to reduce the cardiovascular morbidity associated with hypertension. However, the effect of lowering salt intake on metabolic vascular risk factors such as insulin resistance and levels of atherogenic lipids and fasting insulin is uncertain. We have studied the short-term effect of moderate dietary salt restriction on insulin resistance and serum lipids in 34 nonobese (body mass index [mean +/- SD] 23.4 +/- 1.8 kg/m2), normotensive young white men. Subjects were maintained on a low salt diet ( < 80 mmol/day) for the 2-week study period. In a randomized, cross-over, double-blind fashion, each subject also received 120 mmol of sodium chloride per day during one of the study weeks, and a matching placebo during the other. Insulin resistance, serum insulin, lipids, and blood pressure were measured in the fasting state at the end of each study week. Urinary sodium excretion (185 +/- 46 v 52 +/- 25 mmol/day, P < .001), serum sodium (141.2 +/- 1.2 v 140.1 +/- 1.3 mmol/L, P < .001) and body weight (75.4 +/- 9.1 v 75.0 +/- 9.3 kg, P < .05) were higher during the high salt than the low salt period. Serum creatinine was higher during the low salt period (100 +/- 8 v 90 +/- 9 mumols/L, P < .01). There was no difference in blood pressure, insulin resistance, serum insulin, C-peptide, total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol or its subfractions, triglycerides, apolipoprotein A1, or apolipoprotein B between the high salt and low salt periods. We conclude that short-term, moderate dietary salt restriction does not adversely affect insulin sensitivity or levels of atherogenic lipids in normotensive nonobese men.

Metformin treatment in elderly type II diabetic patients

Pharmacological treatment in elderly patients with type II, non-insulin dependent diabetes mellitus (NIDDM) is becoming a growing and complex problem in the clinical practice, since longevity in almost every population is increasing, and the prevalence of NIDDM also rises with age. It is generally indicated that age over 65-70 years represents a specific contraindication against the administration of the biguanides since the risk of the drug-associated lactic acidosis increases with age. However very few data exist in literature about the effect of biguanides, particularly metformin, in aging patients. Therefore, we aimed to evaluate the effects of adding metformin to poorly controlled sulfonylurea-treated elderly diabetic subjects for a one year period. Eighty-four type II diabetic patients aged more than 70 years and with a poor glycemic control were recruited after an informed consent. All diabetic patients were treated with various sulfonylureas at medium doses and presented renal and liver biochemical function tests within normal ranges and were free of severe macroangiopathy and respiratory or congestive heart failure. Metformin treatment was added to the previous sulfonylurea dosages in order to achieve a satisfactory glycemic control. All patients showed a marked improvement in the glycemic control with no significant modification in fasting blood lactate and a mild increase in the post-prandial lactate peak which, however, always felt largely within the normal ranges. Metformin also improved some metabolic vascular risk factors such as plasma cholesterol levels that were reduced, circulating HDL-cholesterol levels that mildly but significantly increased and uric acid that was lowered. In conclusion our data further support the opinion that metformin has not to be denied to diabetic patients on the sole basis of their age.