Jose Maria Pou

Relationship Between Adiponectin and Left Atrium Size in Uncomplicated Obese Patients: Adiponectin, a Link Between Fat and Heart

BackgroundIt is well known that obesity is a risk factor for severe cardiovascular complications, such as coronary heart disease, heart failure, stroke, venous thromboembolic disease, and atrial fibrillation. Left ventricle (LV) and left atrium (LA) enlargement is a characteristic feature of these patients with the consequent cardiovascular risk. Factors other than hemodynamic may influence LA remodeling. The aim of the study is to evaluate the relationship between adiponectin and LA size in uncomplicated obese patients.MethodsSeventy-four asymptomatic obese patients and an age- and sex-matched control group (N = 70) were recruited. A detailed clinical, echocardiographic, and analytical study was performed. Insulin resistance was assessed using the homeostasis model assessment for insulin resistance (HOMA-IR) method. Insulin sensitivity was assessed measuring serum total adiponectin concentrations.ResultsAdiponectin levels were lower in the obese group (P < 0.001) and particularly so in those obese participants with enlarged LA (32%; P < 0.0005). LA sizes were higher in the obese group (P < 0.0005). Adiponectin displayed significant correlations with body mass index, glucose, insulin, high-density lipoprotein cholesterol, and triglyceride concentrations as well as HOMA-IR (P < 0.001 for all). Adiponectin displayed significant correlations with LV mass and LA size, diastolic and systolic cardiac volumes and diameters, and cardiac output (P < 0.001 for all). Adiponectin correlations with LA size (r = −0.429; P < 0.001) persisted after adjustment for HOMA-IR, age, sex, and LV mass.ConclusionsA novel inverse relationship between adiponectin and LA size independent of age, sex, insulin resistance, and LV mass appears in our series. Adiponectin could be a link between adipose tissue and the heart, having an influence on cardiac remodeling.

Physical training decreases plasma thrombomodulin in type I and type II diabetic patients.

Aims/hypothesis. Endothelial damage is an early step in the pathogenesis of atherosclerosis and its improvement through physical training can contribute to the known reduction of cardiovascular risk associated with exercise. An increase in some endothelium-dependent haemostatic parameters, considered as markers of endothelial damage, has been observed in diabetic patients. Methods. The effect of a three-month physical exercise programme on thrombomodulin, tissue factor pathway inhibitor, plasminogen activator inhibitor, tissue-type plasminogen activator and von-Willebrand factor was evaluated in 14 well-controlled patients with Type I (insulin-dependent) diabetes mellitus and 13 patients with Type II (non-insulin-dependent) diabetes mellitus (HbA1 c 6.5 ± 0.8 and 7.4 ± 0.8 %, respectively). A matched control group was also studied. Results. Thrombomodulin at baseline was higher in both Type I and Type II diabetic patients than in their respective matched control subjects (50.0 ± 16 vs 31.1 ± 8.7 μg/l, p < 0.05; 51.0 ± 10 vs 28.5 ± 11 μg/l, p < 0.05, respectively). After the exercise programme, thrombomodulin plasma concentrations had decreased (p < 0.05) in both groups of patients, with final thrombomodulin values being similar to those observed in their control groups (38.2 ± 11 μg/l for Type I and 34.6 ± 12 μg/l for Type II patients). The thrombomodulin decrement correlated with baseline thrombomodulin and VO2max increase in Type I diabetic patients. A decrease in tissue factor pathway inhibitor was also observed in Type II diabetic patients. Conclusion/interpretation. We conclude that the normalisation of plasma thrombomodulin concentrations in Type I and Type II diabetic patients after physical training might reflect the improvement in endothelial function associated with physical exercise. [Diabetologia (2001) 44: 693–699]

Clinical screening and diagnosis of diabetic polyneuropathy: the North Catalonia Diabetes Study

Background  To evaluate the prevalence of diabetic polyneuropathy (DPN) and develop a simple and accurate method for the evaluation of DPN risk in primary care settings.

A novel truncated form of apolipoprotein A-I transported by dense LDL is increased in diabetic patients.

Diabetic (DM) patients have exacerbated atherosclerosis and high CVD burden. Changes in lipid metabolism, lipoprotein structure, and dysfunctional HDL are characteristics of diabetes. Our aim was to investigate whether serum ApoA-I, the main protein in HDL, was biochemically modified in DM patients. By using proteomic technologies, we have identified a 26 kDa ApoA-I form in serum. MS analysis revealed this 26 kDa form as a novel truncated variant lacking amino acids 1-38, ApoA-IΔ(1-38). DM patients show a 2-fold increase in ApoA-IΔ(1-38) over nondiabetic individuals. ApoA-IΔ(1-38) is found in LDL, but not in VLDL or HDL, with an increase in LDL3 and LDL4 subfractions. To identify candidate mechanisms of ApoA-I truncation, we investigated potentially involved enzymes by in silico data mining, and tested the most probable molecule in an established animal model of diabetes. We have found increased hepatic cathepsin D activity as one of the potential proteases involved in ApoA-I truncation. Cathepsin D-cleaved ApoA-I exhibited increased LDL binding affinity and decreased antioxidant activity against LDL oxidation. In conclusion, we show for the first time: a) presence of a novel truncated ApoA-I form, ApoA-IΔ(1-38), in human serum; b) ApoA-IΔ(1-38) is transported by LDL; c) ApoA-IΔ(1-38) is increased in dense LDL fractions of DM patients; and d) cathepsin D-ApoA-I truncation may lead to ApoA-IΔ(1-38) binding to LDLs, increasing their susceptibility to oxidation and contributing to the high cardiovascular risk of DM patients.

Amino-Terminal Brain Natriuretic Peptide is Related to the Presence of Diabetic Polyneuropathy Independently of Cardiovascular Disease

Diabetic polineuropathy (DPN) is among the most common long-term complications of diabetes, affecting up to 50% of patients (1,2). Type 2 diabetes is considered by many to be a cardiovascular disease (CVD) (3). Plasma levels of the NH2-terminal fragment of the brain natriuretic peptide (NT-proBNP) have recently gained extreme importance as markers of myocardial dysfunction in type 2 diabetes. Excessive secretion of NT-proBNP is independently associated with coronary artery disease and overt nephropathy (4) in addition …

Effect of Melatonin on Insulin Secretion from Isolated Rat Islets of Langerhans

The aim of this paper was to evaluate the possible interaction between β-cells and some indolamines. The effects of melatonin (MEL) on insulin secretion from rat islets were evaluated. Rat islets were obtained by enzymatic degestion of the pancreas from Sprague-Dawley rats with collagenase (Boehringer).