leptin and Myocardial-Ischemia

Psychosocial factors, such as stress and vital exhaustion, are associated with an increased risk of cardiovascular events, and women report more psychosocial ill-being after an acute myocardial infarction than men. We have earlier shown that a cognitive-behavioural intervention in women with ischaemic heart disease (IHD) improved psychosocial well-being. In the present study, we tested the hypothesis that the improvement in psychosocial well-being is associated with an improvement in biochemical indicators of cardiovascular risk.. Randomized-controlled trial in northern Sweden.. Outpatient care.. Women with IHD were randomized to either a 1-year cognitive-behavioural stress management programme or usual care. Of the 159 women who completed the study, 77 were in the intervention group, and 82 in the control group.. A 1-year cognitive-behavioural stress management programme versus conventional care.. Group assignment was not found to be a determinant of waist circumference, high sensitive C-reactive protein (hs-CRP), fibrinogen, von Willebrand factor (vWF), plasminogen activator inhibitor type 1 (PAI-1) activity, tissue plasminogen activator (tPA) activity, tPA antigen, tPA-PAI-1 complex, leptin, or HOMA2 insulin resistance index (HOMA2-IR) at follow up. Changes in psychosocial variables were not associated with changes in any of the biological risk indicators.. Even if our cognitive-behavioural stress management programme had effects on proximal targets, such as stress behaviour and vital exhaustion, we found no improvement in intermediate biochemical targets related to the metabolic syndrome and IHD. Our results challenge the proposition that the relationship between psychological well-being and biological cardiovascular risk indicators is a direct cause-effect phenomenon.

Topics: Biomarkers; C-Reactive Protein; Cognitive Behavioral Therapy; Female; Fibrinogen; Humans; Insulin Resistance; Leptin; Middle Aged; Myocardial Ischemia; Plasminogen Activator Inhibitor 1; Prospective Studies; Risk Factors; Stress, Psychological; Tissue Plasminogen Activator; von Willebrand Factor

Topics: Animals; Central Nervous System; Female; Ischemia; Leptin; Male; Myocardial Ischemia; Myocardial Reperfusion Injury; Rats; Rats, Wistar; Reperfusion; Sex Characteristics

Leptin, an adipocyte-derived satiety hormone, has been previously linked to cardioprotection. We have shown before that leptin conferred resistance to ischemic damage in the heart in long-lived transgenic αMUPA mice overexpressing leptin compared to the wild type (WT) FVB/N control mice. To better understand the contribution of leptin to the ischemic heart, we measured here the expression of genes encoding leptin and ischemia-related proteins in αMUPA and WT mice in the heart vs adipose tissue after MI. In addition, we investigated gene expression in neonatal rat cardiomyocytes under hypoxia in the absence and presence of exogenously added leptin or a leptin antagonist. We used real time RT-PCR and ELISA or Western blot assays to measure, respectively, mRNA and protein levels. The results have shown that circulating leptin levels and mRNA levels of leptin and heme oxygenase-1 (HO-1) in the heart were elevated in both mouse genotypes after 24 h myocardial infarction (MI), reaching higher values in αMUPA mice. In contrast, leptin gene expression in the adipose tissue was significantly increased only in WT mice, but reaching lower levels compared to the heart. Expression of the proinflammatory genes encoding TNFα and IL-1β was also largely increased after MI in the heart in both mouse types, however reaching considerably lower levels in αMUPA mice indicating a mitigated inflammatory state. In cardiomyocytes, mRNA levels of all aforementioned genes as well as HIF-1α and SOD2 genes were elevated after hypoxia. Pretreatment with exogenous leptin largely reduced the mRNA levels of TNFα and IL-1β after hypoxia, while enhancing expression of all other genes and reducing ROS levels. Pretreating the cells with a leptin antagonist increased solely the levels of leptin mRNA, suggesting a negative regulation of the hormone on the expression of its own gene. Overall, the results have shown that leptin affects expression of genes in cardiomyocytes under hypoxia in a manner that could mitigate inflammation and oxidative stress, suggesting a similar influence by endogenous leptin in αMUPA mice. Furthermore, leptin is likely to function in the ischemic murine heart more effectively in an autocrine compared to paracrine manner. These results suggest that leptin can reduce ischemic damage by modulating gene expression in the heart.

Topics: Animals; Biomarkers; Female; Gene Expression Profiling; Gene Expression Regulation; Leptin; Mice; Mice, Transgenic; Myocardial Ischemia; Myocytes, Cardiac; Oxidative Stress; Rats

Leptin is a peptide hormone produced by adipose tissue whose basic function is regulating energy balance and sympathetic outflow. Previous studies have shown that increased nerve activity of the left stellate ganglion (LSG) promotes ventricular arrhythmia (VA).. The purpose of this study was to investigate whether leptin could facilitate VA through activation of the LSG.. Sixteen pentobarbital-anesthetized dogs were divided into a control group (saline; n = 8) and a leptin group (leptin; n = 8). Microinjections of either 0.1 mL saline or leptin (18 μg) were injected into the LSG. Action potential duration (APD) of the myocyte and the function and neural activity of the LSG were measured at different time points. VA induced by occlusion of the left anterior descending branch was continuously measured for 1 hour. At the end of the experiment, the LSG tissues were collected for molecular detections.. Compared with the control group, leptin microinjection resulted in (1) significant enhancement in the incidence of VA; (2) significant decrease in APD and increase in APD dispersion; and (3) significant increase in the function and neural activity of the LSG. Mechanistically, the leptin receptor was found in the LSG, and its signaling was significantly activated in the leptin-injected group. Additionally, leptin microinjection markedly increased the expression of proinflammatory cytokines.. LSG activation induced by leptin microinjection promotes ischemia-induced VAs. Activated leptin receptor signaling and up-regulation of proinflammatory cytokines in the LSG may be responsible for these effects.

Topics: Action Potentials; Animals; Disease Models, Animal; Dogs; Electrocardiography; Injections; Leptin; Male; Myocardial Ischemia; Stellate Ganglion; Sympathetic Nervous System; Tachycardia, Ventricular

Moderate alcohol consumption is cardioprotective but the mechanism of action remains unclear. Nuclear factor κ-B regulates the expression of genes involved in inflammation, stress, and apoptosis. We used a swine model of diet-induced metabolic syndrome to investigate the effects of red wine and vodka on nuclear factor κ-B signaling and cytokine activity in chronically ischemic myocardium.. Yorkshire swine were given a high-fat diet for 4 weeks; an ameroid constrictor was then placed on the left circumflex artery. The high-fat diet was continued and the swine were divided into 3 groups for 7 weeks: hypercholesterolemic diet alone (control, n = 8), hypercholesterolemic diet with vodka (vodka, n = 8), and hypercholesterolemic diet with wine (wine, n = 8). Ischemic myocardium was analyzed by Western blot and cytokine array.. Administration of alcohol was associated with decreased expression of inhibitor of κ-B kinase complex α, inhibitor of κ-B kinase complex β, and phosphorylated inhibitor of κ-B β in the ischemic myocardium compared with the control group. Alcohol administration demonstrated an increase in nuclear factor κ-B in the ischemic myocardium. Both wine and vodka demonstrated a significant decrease in leptin, interleukin-1α, IL-13, IL-15, and interferon-γ. Vodka demonstrated a significant decrease in phosphorylated BCL-2 and caspase-9.. In ischemic myocardium, alcohol modulates the nuclear factor κ-B pathway, which may contribute to the adaptive response of tissues to the stress of ischemia. Furthermore, both wine and vodka decreased multiple proinflammatory cytokines. This study provides a mechanism by which alcohol may be cardioprotective in ischemic myocardium.

Topics: Animals; Biomarkers; Biopsy, Needle; Blotting, Western; Chemokines; Diet, High-Fat; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Ethanol; Immunohistochemistry; Interleukins; Leptin; Male; Myocardial Ischemia; NF-kappaB-Inducing Kinase; Protein Serine-Threonine Kinases; Random Allocation; Sensitivity and Specificity; Swine; Wine

New and clinically useful markers of cardiovascular risk are of essence in type 2 diabetes since ischemic heart disease is a major cause of death in these patients.. We analyzed baseline data from 476 men and 244 women who participated in "Cardiovascular Risk factors in Patients with Diabetes -a Prospective study in Primary care" study. All participants had type 2 diabetes and were 55-66 years old at recruitment during year 2005 to 2008. Except for established traditional risk markers for vascular disease, we also estimated vascular complications non-invasively by performance of carotid-femoral pulse-wave velocity (PWV, with applanation-tonometry) and intima-media thickness of carotid arteries (IMT, with B-mode ultrasound). Patients were followed for incidence of ischemic heart disease mortality and morbidity until end of the year 2012, using the national Swedish Cause of Death and Hospitalization Registries.. During the follow-up period of a median of 6 years 47 men and 10 women died or were hospitalized for ischemic heart disease including myocardial infarction. Leptin levels were positively related to the hazard ratio (HR) in men (HR for each log 10 unit 4.9, CI 1.99 to 11.8) and women (HR 11.5, CI 1.47 to 89.7). Leptin predicted ischemic heart disease independently of age, HbA1c, BMI, systolic blood pressure and LDL-cholesterol/HDL-cholesterol ratio (men: HR 12.9 CI 3.2-53, women: HR 19.9, CI 1.2-327) This finding of increased risk related to high leptin levels was also statistically significant when carotid-femoral PWV and IMT were both added to the equations in men (hazard ratio 9.2 CI 2.1-41).. Our data support the use of serum leptin in type 2 diabetes to add independent prognostic information in terms of ischemic heart disease when compared with traditional cardiovascular risk factors. In the men of the cohort this prognostic information was in addition also to data on IMT and PWV, two non-invasive measurements of the extent of vascular disease. The power to detect a similar relationship in women was less strong due to lower incidence of cardiovascular disease.. ClinicalTrials.gov: NCT01049737.

Topics: Carotid Arteries; Carotid Intima-Media Thickness; Cohort Studies; Diabetes Mellitus, Type 2; Female; Humans; Incidence; Leptin; Longitudinal Studies; Male; Middle Aged; Myocardial Infarction; Myocardial Ischemia; Prognosis; Proportional Hazards Models; Prospective Studies; Pulse Wave Analysis

Diabetic patients often exhibit severe, asymptomatic coronary artery disease (CAD). The relationship between osteoprotegerin (OPG), inflammatory markers and silent myocardial ischemia remains to be elucidated.. We recruited 45 type 2 diabetic patients and 33 healthy controls and assessed them for silent myocardial ischemia (SMI) by myocardial perfusion imaging. Patient blood was tested for OPG, IL-6 and leptin concentrations.. OPG, leptin and IL-6 levels were found significantly elevated in diabetic patients (p < 0.001, p < 0.01, p < 0.05). Based on our classification of presence/absence of SMI in our diabetic group, we found that there was a significant association between SMI and the biomarkers IL-6 (p < 0.001), leptin (p < 0.001) and OPG (p < 0.05). In multivariate regression analyses, OPG was found to be significantly related to diabetes mellitus and to SMI. Age, sex and smoking increased the association between OPG and SMI.. High OPG, leptin and IL-6 levels are associated with the presence and severity of SMI in type 2 diabetic patients.

Topics: Adult; Biomarkers; Case-Control Studies; Coronary Artery Disease; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Exercise Test; Female; Humans; Interleukin-6; Leptin; Male; Middle Aged; Multivariate Analysis; Myocardial Ischemia; Myocardial Perfusion Imaging; Osteoprotegerin; Regression Analysis

Depression in Type 2 diabetes is associated with obesity, cardiovascular disease, and mortality. Leptin is a plausible mediating factor because it has been related to obesity, depression, and cardiovascular disease in nondiabetic populations. We sought to assess whether leptin is related to depressive symptoms in people with Type 2 diabetes.. One thousand fifty-seven subjects (48.5% women, mean [standard deviation] age = 67.9 [4.2] years) with Type 2 diabetes were assessed for depressive symptoms using the Hospital Anxiety and Depression Scale and other clinical variables by interview and physical examination. Plasma leptin was determined by radioimmunoassay. Multiple linear regression was performed to assess the relationship between depressive symptoms and ln leptin while adjusting for other covariates. A mediation analysis was performed to test whether depressive symptoms mediated the relationship between obesity and leptin.. In univariate analyses, symptoms of depression were related to leptin in men (r = 0.214, p < .001) and women (r = 0.146, p = .007). When adjusting for other covariates including body mass index, ischemic heart disease, glycated hemoglobin, duration of diabetes, and treatment with antidepressants, insulin, or glucocorticoids, using a hierarchical multiple linear regression, depressive symptoms (ln Hospital Anxiety and Depression Scale-depression score) were significant only in men (B = 0.083, standard error = 0.037, p = .03). In the mediation analysis, depressive symptoms partially mediated the effect of obesity (body mass index) on leptin in men but not in women.. There is a sex difference in the relationship between depressive symptoms and leptin in people with Type 2 diabetes, with a positive association in men but not in women. Adipocyte-derived factors are associated with depressive symptoms in Type 2 diabetes.

Topics: Adipose Tissue; Aged; Body Mass Index; Comorbidity; Depression; Diabetes Mellitus, Type 2; Female; Humans; Leptin; Male; Middle Aged; Myocardial Ischemia; Obesity; Prospective Studies; Psychiatric Status Rating Scales; Radioimmunoassay; Regression Analysis; Scotland; Sex Characteristics; Sex Factors

Obesity and diabetes contribute to cardiovascular disease and alter cytokine profile. The cytokine, tumour necrosis factor alpha (TNFα), activates a protective signalling cascade during ischaemic postconditioning (IPostC). However, most successful clinical studies with IPostC have not included obese and/or diabetic patients. We aimed to investigate the influence of TNFα on the outcome of IPostC in obese or diabetic mice. TNF knockout or wildtype mice were fed for 11 weeks with a high carbohydrate diet (HCD) to induce modest obesity. Diabetes was induced in a separate group by administration of a single intraperitoneal injection of streptozotocin. Hearts were then isolated and subjected to ischaemia (35 min of global ischaemia) followed by 45 min of reperfusion. HCD increased body weight, plasma insulin and leptin levels while the glucose level was unchanged. In streptozotocin-treated mice, blood glucose, plasma leptin and insulin were altered. Control, obese or diabetic mice were protected with IPostC in wiltype animals. In TNF knockout mice, IPostC failed to protect control and diabetic hearts while a slight protection was observed in obese hearts. Our data confirm a bidirectional role for TNFα associated with the severity of concomitant comorbidities and suggest that diabetic and/or modestly obese patients may still benefit from IPostC.

Topics: Animals; Cardiomegaly; Diabetes Mellitus, Type 1; Dietary Carbohydrates; Disease Susceptibility; Heart; Hyperglycemia; Hyperinsulinism; In Vitro Techniques; Ischemic Postconditioning; Leptin; Mice; Mice, Knockout; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Obesity; Organ Size; Severity of Illness Index; Streptozocin; Tumor Necrosis Factor-alpha

Leptin and interleukin-6 (IL-6) are inversely correlated and associated with decreased survival in critically ill patients. We investigated changes in leptin, IL-6, and troponin in children undergoing open-heart surgery, hypothesizing that IL-6 and troponin will increase after cardiopulmonary bypass (CPB) and will be negatively correlated with leptin.. Serial blood samples were collected from 21 patients 24 hours before and up to 48 hours after surgery.. Leptin levels decreased by 50% during CPB (P < .001), then gradually increased, reaching baseline levels 12 hours after surgery. The IL-6 levels increased (P < .001) during CPB, peaking 2 hours after surgery and remaining slightly elevated at 24 hours after surgery (P < .001). Leptin and IL-6 were negatively correlated (R = -0.448, P < .001). Troponin levels increased during CPB (P < .001). Postoperative leptin and troponin were inversely correlated (r = -0.535, P < .001). Patients with modest elevations in troponin levels (<20 microg/L) had a shorter aortic clamp and CPB time (P < .01), lower IL-6 peak levels (P = .03), and shorter duration of ventilation and inotropic support compared with patients with peak troponin levels greater than 20 microg/L.. Lower leptin and higher IL-6 levels correlated with troponin, a marker of myocardial injury. Because leptin may have cardioprotective effects, the postoperative drop in its levels may further contribute to myocardial dysfunction.

Topics: Biomarkers; Cardiopulmonary Bypass; Critical Illness; Female; Heart Defects, Congenital; Hospital Mortality; Humans; Infant; Inflammation; Interleukin-6; Leptin; Male; Myocardial Ischemia; Postoperative Complications; Prognosis; Survival Analysis; Time Factors; Troponin

Cardiac myocytes depend on a delicate balance of glucose and free fatty acids as energy sources, a balance that is disrupted in pathological states such as diabetic cardiomyopathy and myocardial ischaemia. There are two families of cellular glucose transporters: the facilitated-diffusion glucose transporters (GLUT); and the sodium-dependent glucose transporters (SGLT). It has long been thought that only the GLUT isoforms, GLUT1 and GLUT4, are responsible for cardiac myocyte glucose uptake. However, we discovered that one SGLT isoform, SGLT1, is also an important glucose transporter in heart. In this study, we aimed to determine the human and murine cardiac expression pattern of SGLT1 in health and disease and to determine its regulation.. SGLT1 was largely localized to the cardiac myocyte sarcolemma. Changes in SGLT1 expression were observed in disease states in both humans and mouse models. SGLT1 expression was upregulated two- to three-fold in type 2 diabetes mellitus and myocardial ischaemia (P < 0.05). In humans with severe heart failure, functional improvement following implantation of left ventricular assist devices led to a two-fold increase in SGLT1 mRNA (P < 0.05). Acute administration of leptin to wildtype mice increased cardiac SGLT1 expression approximately seven-fold (P < 0.05). Insulin- and leptin-stimulated cardiac glucose uptake was significantly (P < 0.05) inhibited by phlorizin, a specific SGLT1 inhibitor.. Our data suggest that cardiac SGLT1 expression and/or function are regulated by insulin and leptin, and are perturbed in disease. This is the first study to examine the regulation of cardiac SGLT1 expression by insulin and leptin and to determine changes in SGLT1 expression in cardiac disease.

Topics: Adult; Aged; Animals; Cardiomyopathies; Female; Glucose; Glucose Transporter Type 1; Glucose Transporter Type 4; Humans; Insulin; Leptin; Male; Mice; Mice, Inbred C57BL; Middle Aged; Myocardial Ischemia; Myocardium; Myocytes, Cardiac; RNA, Messenger; Sodium-Glucose Transporter 1

Low Carbohydrate Diets (LCD) are a popular intervention for weight loss, but the effect of such diets on myocardial ischemia is not known. Myocardial energy substrates and insulin signaling pathways may be affected by these diets, and both may play a role in protection of ischemic myocardium. We investigated whether LCD increases susceptibility to cardiac injury during ischemia and reperfusion in the isolated rat heart.. Rats were fed LCD (60% kcal from fat/30% protein/10% carbohydrate) or a control diet (CONT; 16%/19%/65%) for 2 weeks. Hearts from rats fed with LCD or CONT were isolated and subjected to normal perfusion in Langendorff mode, with 30 min global low flow ischemia (LFI; 0.3 ml/min) followed by 60 min reperfusion, or 60 min LFI followed by 120 min reperfusion.. LCD diet led to an increase in 3-hydroxybutyrate and lower circulating insulin. LCD diet also resulted in impaired left ventricular performance during LFI, reduced recovery of function following LFI and reperfusion, and 10- to 20-fold increased injury as measured by lactate dehydrogenase release and histologic infarct area. LCD diet also led to lower myocardial glycogen stores and glycogen utilization during LFI, and lower insulin signaling as assessed by Akt phosphorylation at the end of LFI and reperfusion, but no differences in ERK 1/2 phosphorylation.. These results demonstrate that LCD affects myocardial energy substrates, affects insulin signaling, and increases myocardial injury following ischemia-reperfusion in the isolated heart.

Topics: Animals; Diet, Carbohydrate-Restricted; Energy Metabolism; Heart Function Tests; Insulin; Leptin; Male; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion; Myocardial Reperfusion Injury; Myocardium; Rats; Rats, Sprague-Dawley

Recent studies have provided evidence that leptin has significant effects on vascular development and repair. The aim was to determine the levels of leptin and lipid profile in diabetic postmenopausal women with and without the complication of ischemic heart disease and to develop correlation between them. Moreover, the relationship between leptin levels and extent of ischemic changes were determined.. One hundred twenty postmenopausal subjects between the ages of 45 and 60 years were included in the study. They were divided into three groups of forty subjects each. The first group comprised normal healthy controls, the second diabetic type 2 patients with no history of ischemic heart disease (I1ID), and the third diabetic patients with IHD. Serum leptin levels were determined by a Kit obtained from DRG and samples were analyzed on ELISA. Fasting and random blood glucose was determined by the glucose oxidase method, cholesterol, triglycerides, LDL cholesterol, and HDL cholesterol were also determined by kits obtained from Merck.. The results show that leptin and serum lipid levels increased significantly in diabetic patients with IHD compared with diabetic patients without IHD as well as normal subjects. Moreover; the sertum leptin level increased significantly in the diabetic patients with IHD who had positive findings in myocardial perfusion scan compared with those having negative findings.. Hyperleptinemia in diabetic patients shows that leptin contributes to the development of cardiovascular disease in diabetic patients.

Topics: Aged; Diabetes Mellitus, Type 2; Female; Humans; Hyperlipidemias; Leptin; Lipids; Middle Aged; Myocardial Ischemia; Postmenopause

Leptin, the 16-kDa peptide hormone product of the ob gene, is produced primarily by adipocytes and was initially thought to exert its effects exclusively through actions on the hypothalamus via distinct leptin receptors termed OB-R. However, recent data show that leptin is produced elsewhere and that receptors are present in many other tissues. Using real-time PCR, we determined whether leptin and its receptors are present in the rat heart and demonstrated regional distribution patterns and gender differences as well as the effect of ischemia and reperfusion. Gene expression of leptin and its receptors (OB-Ra, OB-Rb, and OB-Re) was identified in myocytes and whole heart homogenates from all regions of the heart of male and female rats, with the highest abundance in left and right atria of male and female rats, respectively. No differences in regional distribution of OB-R were evident in male rat hearts. In female rats, expression was highest in right atria for all three isoforms and was significantly greater than in male rats. Ischemia and reperfusion significantly downregulated leptin and OB-R expression, although this was more pronounced in male rat hearts. Leptin release in the coronary effluent was also detected using ELISA, although this was generally unaffected by global ischemia and reperfusion. Our results demonstrate for the first time the presence of the leptin system, including the peptide and its receptors, in all regions of the rat heart. In view of emerging evidence for cardiac effects of leptin, it is proposed that the heart is a target for leptin action and that the peptide modulates function through a paracrine- or autocrine-dependent manner.

Topics: Animals; Autocrine Communication; Female; Gene Expression; Heart; Leptin; Male; Myocardial Ischemia; Paracrine Communication; Polymerase Chain Reaction; Rats; Rats, Sprague-Dawley; Receptors, Cell Surface; Receptors, Leptin; Sex Characteristics

Patients with chronic heart failure (CHF) have metabolic abnormalities, leading to a catabolic syndrome, with progressive loss of skeletal muscle in advanced stages of the disease. Leptin, the product of an obesity gene, has been associated with energy expenditure and weight regulation. The aim of this study was to assess serum levels of leptin and its soluble receptor in relation to exercise intolerance and neurohumoral activation in patients with CHF. We investigated 53 patients with CHF left ventricular ejection fraction (LVEF) 25+/-1%, age 56.6+/-1.3 years, Maximal oxygen uptake (VO(2) max) 16.3+/-0.6 ml/min.kg) sub-classified according to peak oxygen consumption of > or 14 ml/min.kg and controls). Elevated levels of leptin correlated with an increased serum concentration of TNFalpha (r=0.749, P<0.01) in this subgroup of patients with CHF. We conclude that patients with advanced CHF show elevated serum levels of leptin and its soluble receptor. This finding indicates that leptin may participate in the catabolic state leading to the development of cardiac cachexia in the course of CHF.

Topics: Aged; Biomarkers; Blood Sedimentation; Body Mass Index; Case-Control Studies; Chronic Disease; Cytokines; Exercise Test; Exercise Tolerance; Heart Failure; Humans; Inflammation Mediators; Leptin; Male; Middle Aged; Myocardial Ischemia; Oxygen Consumption; Receptors, Cell Surface; Receptors, Leptin; Severity of Illness Index; Solubility; Statistics as Topic; Stroke Volume; Tumor Necrosis Factor-alpha

Topics: Humans; Leptin; Myocardial Ischemia; Myocardial Reperfusion Injury; Signal Transduction

The author exposes the present concept of metabolic syndrome X, which is a complex of Type II diabetes, obesity, hypertension and vascular problems. This syndrome has been known for many years, but it has been individualized as such only recently. This is due to the huge importance that obesity is reaching in developed countries, especially in the U.S.A. Today this is a very important health problem. In this work, in addition to the description of the syndrome, which is purely an internal medicine issue, its relation to some women-specific problems is also explained, especially to the so-called polycystic ovary.

Topics: Diabetes Mellitus; Diabetes Mellitus, Type 2; Female; Humans; Hyperlipidemias; Hypertension; Insulin Resistance; Leptin; Menopause; Myocardial Ischemia; Obesity; Phenotype; Polycystic Ovary Syndrome; Syndrome

To investigate the possibility that leptin levels may be predictive of the risk of ischemic heart disease (IHD) through the relationship of leptin to body fat.. The Quebec Cardiovascular Study cohort consisted of 2,103 French-Canadian men without IHD in 1985 who were followed until 1990, by which time 114 had experienced an IHD event. These 114 men were then individually matched for age, BMI, cigarette smoking, and alcohol intake with 114 subjects who were free of IHD at follow-up. After exclusion of diabetic patients and those in whom leptin levels could not be measured, we were able to compare the initial metabolic profiles of 86 men in the IHD group and of 95 control subjects.. Plasma leptin concentrations were positively correlated with BMI (r = 0.67, P < 0.0001) and with fasting insulin concentrations (r = 0.46, P < 0.0001) in the overall sample. These significant associations were also observed when men with IHD and the control subjects were examined separately (control subjects: r = 0.68 for BMI and r = 0.45 for insulin; IHD subjects: r = 0.65 for BMI and r = 0.50 for insulin). With the exception of plasma triglyceride (r = 0.25, P < 0.001), no significant association was found between leptin and plasma lipoprotein and lipid concentrations. Furthermore, plasma insulin remained significantly associated with leptin levels even after adjustment for BMI (r = 0.22, P < 0.005). There was no difference in baseline leptin levels among men who developed IHD versus men who remained IHD-free during the 5-year follow-up (5.56 +/- 3.12 vs. 5.36 +/- 2.90 ng/ml, respectively). Thus, although significantly correlated with the BMI and fasting insulin levels, plasma leptin concentration was not a significant predictor of the 5-year incidence of IHD. This lack of a relationship to IHD was noted when leptin levels were analyzed as tertiles and when leptin concentration was analyzed as a continuous variable.. These prospective results suggest that leptinemia, despite being a strong correlate of obesity, does not appear to be an independent risk factor for the development of IHD in men.

Topics: Aged; Apolipoproteins B; Body Mass Index; Canada; Case-Control Studies; Cholesterol; Cohort Studies; Fasting; Follow-Up Studies; France; Humans; Insulin; Leptin; Logistic Models; Male; Middle Aged; Myocardial Ischemia; Prospective Studies; Proteins; Risk Factors; Triglycerides