Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective in this study was to determine whether there was any relation between leptin and vascular endothelial growth factor (VEGF) in children with cyanotic and acyanotic heart anomalies. The study group consisted of 18 children with cyanotic congenital heart disease (CHD) and 20 age-adjusted children with acyanotic CHD as controls. Serum VEGF and leptin levels were determined by enzyme-linked immunosorbent assay (ELISA). The mean VEGF level was 149.25+/-42.93 pg/ml (range 80.66-217.00) in the cyanotic group and 88.18+/-20.94 pg/ml (range 48.44-112.71) in the acyanotic group (p<0.001). The mean leptin level was 7.55+/-1.46 ng/ml (range 4.08-10.25) in the cyanotic group and 6.89+/-1.43 ng/ml (range 2.67-8.57) in the acyanotic group (p=0.168). There was a significant positive correlation (r=0.723, p<0.001) between VEGF and leptin levels in the cyanotic group while there was no correlation (r=0.235, p=0.348) in the acyanotic group. Arterial oxygen saturation (SaO2) was negatively correlated (r=-0.625, p<0.001) with VEGF, but not correlated with leptin (r=-0.207, p=0.211) in the cyanotic group. There was no correlation between VEGF, leptin and SaO2 in the acyanotic group. We conclude that it is likely that both VEGF and leptin have a role in the pathogenesis of angiogenesis in cyanotic CHD.
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PMID:Correlation between vascular endothelial growth factor and leptin in children with cyanotic congenital heart disease. 1824 35

Adipokines represent a family of proteins released by adipocytes that affect various biological processes including metabolism, satiety, inflammation, and cardiovascular function. The first adipokine to be identified is leptin, a product of the obesity gene whose primary function is to act as a satiety factor. However, it is now recognized that leptin and many of the newly discovered adipokines produce effects on numerous organ systems including the heart. Indeed, various adipokines including leptin, adiponectin, and apelin exert potent and diverse cardiovascular effects which are mediated by their specific receptors and involve complex and multifaceted cell-signalling pathways. Among these are effects on the heart as well as blood pressure where leptin has been proposed to potentially contribute to obesity-related hypertension. In this review, we focus primarily on the diverse effects of adipokines on the heart and discuss the potential cell-signalling mechanisms underlying their actions. The potential role of adipokines in the regulation of cardiac metabolism and function is discussed. Discussion is also presented on the emerging role, both deleterious and salutary, of various adipokines in heart disease with an examination of the possible underlying mechanisms which contribute to these effects.
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PMID:Signalling mechanisms underlying the metabolic and other effects of adipokines on the heart. 1847 23

Obestatin, derived from the same gene as the hunger hormone ghrelin, may reduce food intake in animals. The role of obestatin in human physiology is unclear. We evaluated cross-sectional associations between participant characteristics and fasting levels of obestatin as well two other hormones associated with energy balance, ghrelin and leptin. Data are from the baseline visit of the Optimal Macronutrient Intake Trial to Prevent Heart Disease (OMNI-Heart) Trial that enrolled adults with elevated blood pressure (systolic 120-159 mm Hg or a diastolic of 80-99 mm Hg) but who were otherwise healthy. Partial Spearman's correlations and linear regression models estimated the association between age, gender, BMI, physical activity, and smoking with fasting hormones. Obestatin was directly associated with ghrelin (r = 0.45, P < 0.05). On average, overweight (BMI 25-30) and obese (BMI > 30) individuals had obestatin concentrations that were 12.6 (s.d. 8.8) and 25.4 (s.d. 8.4) pg/ml lower compared to normal weight (BMI < 25) individuals, respectively (P for trend = 0.002). Overweight (BMI 25-30) and obese (BMI > 30) individuals had ghrelin concentrations that were 161.7 (s.d. 69.6) and 284.7 (s.d. 66.5) pg/ml lower compared to normal weight (BMI < 25) individuals, respectively (P for trend <0.0001). A 5 unit increase in BMI was associated with 41.3% (s.d. 4.3%) (P < 0.0001) higher leptin. Obestatin and ghrelin are directly correlated and share the same patterns of association with participant characteristics. Modifiable risk factors for chronic diseases, such as BMI, are associated with fasting levels of leptin, obestatin, and ghrelin.
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PMID:Characteristics associated with fasting appetite hormones (obestatin, ghrelin, and leptin). 1905 26

Excess lipid accumulation resulting from an elevated supply of plasma fatty acids is linked to the pathogenesis of the metabolic syndrome and heart disease. The term 'lipotoxicity' was coined to describe how lipid accumulation leads to cellular dysfunction and death in non-adipose tissues including the heart, pancreas and liver. While lipotoxicity has been shown in cultured skeletal muscle cells, the degree of lipotoxicity in vivo and the functional consequences are unresolved. We studied three models of fatty acid overload in male mice: 5 h Intralipid((R)) and heparin infusion, prolonged high fat feeding (HFF) and genetic obesity induced by leptin deficiency (ob/ob mice). Markers of apoptosis, proteolysis and autophagy were assessed as readouts of lipotoxicity. The Intralipid((R)) infusion increased caspase 3 activity in skeletal muscle, demonstrating that enhancing fatty acid flux activates pro-apoptotic pathways. HFF and genetic obesity increased tissue lipid content but did not influence apoptosis. Gene array analysis revealed that HFF reduced the expression of 31 pro-apoptotic genes. Markers of autophagy (LC3beta and beclin-1 expression) were unaffected by HFF and were associated with enhanced Bcl(2) protein expression. Proteolytic activity was similarly unaffected by HFF or in ob/ob mice. Thus, contrary to our previous findings in muscle culture in vitro and in other non-adipose tissues in vivo, lipid overload did not induce apoptosis, autophagy or proteolysis in skeletal muscle. A broad transcriptional suppression of pro-apoptotic proteins may explain this resistance to lipid-induced cell death in skeletal muscle.
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PMID:Examination of 'lipotoxicity' in skeletal muscle of high-fat fed and ob/ob mice. 1920 53

The authors compared effects of macronutrients on self-reported appetite and selected fasting hormone levels. The Optimal Macronutrient Intake Trial to Prevent Heart Disease (OMNI-Heart) (2003-2005) was a randomized, 3-period, crossover feeding trial (n = 164) comparing the effects of 3 diets, each rich in a different macronutrient. Percentages of kilocalories of carbohydrate, fat, and protein were 48, 27, and 25, respectively, for the protein-rich diet; 58, 27, and 15, for the carbohydrate-rich diet; and 48, 37, and 15 for the diet rich in unsaturated fat. Food and drink were provided for each isocaloric 6-week period. Appetite was measured by visual analog scales. Pairwise differences between diets were estimated using generalized estimating equations. Compared with the protein diet, premeal appetite was 14% higher on the carbohydrate (P = 0.01) and unsaturated-fat (P = 0.003) diets. Geometric mean leptin was 8% lower on the protein diet than on the carbohydrate diet (P = 0.003). Obestatin levels were 7% and 6% lower on the protein diet than on the carbohydrate (P = 0.02) and unsaturated-fat (P = 0.004) diets, respectively. There were no between-diet differences for ghrelin. A diet rich in protein from lean meat and vegetables reduces self-reported appetite compared with diets rich in carbohydrate and unsaturated fat and can be recommended in a weight-stable setting. The observed pattern of hormone changes does not explain the inverse association between protein intake and appetite.
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PMID:Associations between macronutrient intake and self-reported appetite and fasting levels of appetite hormones: results from the Optimal Macronutrient Intake Trial to Prevent Heart Disease. 1922 77

In addition to its role as an energy storage depot, adipose tissue is now recognized as a complex endocrine organ. Adipose tissue releases a variety of factors, termed adipokines, that regulate energy metabolism, cardiovascular function, reproductive status, and immune function. Some of the better-studied adipokines include leptin, adiponectin, and components of the renin-angiotensin system such as angiotensinogen. The function of more recently discovered adipokines such as resistin are under intense scrutiny. Abnormal production or regulation of adipokines occurs in obese individuals and is implicated in the development of a variety of associated co-morbidities including metabolic syndrome, type 2 diabetes, atherosclerosis, heart disease, and cancer in people, although evaluation in domestic species is just beginning. Adipokines are now being examined as potential biomarkers for risk assessment for development of complications related to obesity. This article summarizes the function and regulation of some better-characterized adipokines. It also reviews the current information on the characterization of adipokines in some domestic species in which rates of obesity and obesity-related disorders are increasing, such as the dog, cat, and horse.
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PMID:Adipokines: a review of biological and analytical principles and an update in dogs, cats, and horses. 1939 60

Classical non-insulin antihyperglycemic drugs currently approved for the treatment of type 2 diabetes mellitus (T2DM) comprise five groups: biguanides, sulfonylureas, meglitinides, glitazones and alpha-glucosidase inhibitors. Novel compounds are represented by the incretin mimetic drugs like glucagon like peptide-1 (GLP-1), the dipeptidyl peptidase 4 (DPP-4) inhibitors, dual peroxisome proliferator-activated receptors (PPAR) agonists (glitazars) and amylin mimetic drugs. We review the cardiovascular effects of these drugs in an attempt to improve knowledge regarding their potential risks when treating T2DM in cardiac patients. Metformin may lead to lethal lactic acidosis, especially in patients with clinical conditions that predispose to this complication, such as recent myocardial infarction, heart or renal failure. Sulfonylureas exert their effect by closing the ATP-dependent potassium channels. This prevents the opening of these channels during myocardial ischemia, impeding the necessary hyperpolarization that protects the cell. The combined sulfonylurea/metformin therapy reveals additive effects on mortality in patients with coronary artery disease (CAD). Meglitinides effects are similar to those of sulfonylureas, due to their almost analogous mechanism of action. Glitazones lower leptin levels, leading to weight gain and are unsafe in NYHA class III or IV. The long-term effects of alpha-glucosidase inhibitors on morbidity and mortality rates is yet unknown. The incretin GLP-1 is associated with reductions in body weight and appears to present positive inotropic effects. DPP-4 inhibitors influences on the cardiovascular system seem to be neutral and patients do not gain weight. The future of glitazars is presently uncertain following concerns about their safety. The amylin mimetic drug paramlintide, while a satisfactory adjuvant medication in insulin-dependent diabetes, is unlikely to play a major role in the management of T2DM. Summarizing the present information it can be stated that 1. Four out the five classical oral antidiabetic drug groups present proven or potential cardiac hazards; 2. These hazards are not mere 'side effects', but biochemical phenomena which are deeply rooted in the drugs' mechanism of action; 3. Current data indicate that the combined glibenclamide/metformin therapy seems to present special risk and should be avoided in the long-term management of T2DM with proven CAD; 4. Glitazones should be avoided in patients with overt heart failure; 5, The novel incretin mimetic drugs and DPP-4 inhibitors--while usually inadequate as monotherapy--appear to be satisfactory adjuvant drugs due to the lack of known undesirable cardiovascular effects; 6. Customized antihyperglycemic pharmacological approaches should be implemented for the achievement of optimal treatment of T2DM patients with heart disease. In this context, it should be carefully taken into consideration whether the leading clinical status is CAD or heart failure.
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PMID:A cardiologic approach to non-insulin antidiabetic pharmacotherapy in patients with heart disease. 1961 27

A detailed review of the literature was performed in a bid to identify the presence of a common link between specific hormone interactions and the increasing prevalence of global disease. The synergistic action of unopposed oestrogen and leptin, compounded by increasing insulin, cortisol and xeno-oestrogen exposure directly initiate, promote and exacerbate obesity, type 2 diabetes, uterine overgrowth, prostatic enlargement, prostate cancer and breast cancer. Furthermore these hormones significantly contribute to the incidence and intensity of anxiety and depression, Alzheimer's disease, heart disease and stroke. This review, in collaboration with hundreds of evidence-based clinical researchers, correlates the significant interactions these hormones exert upon the upregulation of p450 aromatase, oestrogen, leptin and insulin receptor function; the normal status quo of their binding globulins; and how adduct formation alters DNA sequencing to ultimately produce an array of metabolic conditions ranging from menopausal symptoms and obesity to Alzheimer's disease and breast and prostate cancer. It reveals the way that poor diet, increased stress, unopposed endogenous oestrogens, exogenous oestrogens, pesticides, xeno-oestrogens and leptin are associated with increased aromatase activity, and how its products, increased endogenous oestrogen and lowered testosterone, are associated with obesity, type 2 diabetes, Alzheimer's disease and oestrogenic disease. This controversial break-through represents a paradigm shift in medical thinking, which can prevent the raging pandemic of diabetes, obesity and cancer currently sweeping the world, and as such, it will reshape health initiatives, reduce suffering, prevent waste of government expenditure and effectively transform preventative medicine and global health care for decades.
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PMID:The role of oestrogen in the pathogenesis of obesity, type 2 diabetes, breast cancer and prostate disease. 2053 61

Obesity has been associated with increasing the risk for type 2 diabetes and heart disease, but its influence on the immune response to viral infection is understudied. Memory T cells generated during a primary influenza infection are important for protection against subsequent influenza exposures. Previously, we have demonstrated that diet-induced obese (DIO) mice have increased morbidity and mortality following secondary influenza infection compared with lean mice. To determine whether the problem resided in a failure to maintain functional, influenza-specific CD8(+) memory T cells, male DIO and lean mice were infected with influenza X-31. At 84 d postinfection, DIO mice had a 10% reduction in memory T cell numbers. This reduction may have resulted from significantly reduced memory T cell expression of interleukin 2 receptor beta (IL-2R beta, CD122), but not IL-7 receptor alpha (CD127), which are both required for memory cell maintenance. Peripheral leptin resistance in the DIO mice may be a contributing factor to the impairment. Indeed, leptin receptor mRNA expression was significantly reduced in the lungs of obese mice, whereas suppressor of cytokine signaling (Socs)1 and Socs3 mRNA expression were increased. It is imperative to understand how the obese state alters memory T cells, because impairment in maintenance of functional memory responses has important implications for vaccine efficacy in an obese population.
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PMID:Diet-induced obesity in mice reduces the maintenance of influenza-specific CD8+ memory T cells. 2059 5

This article examines the relationships between allergic rhinitis and hypertension, chronic sinusitis and hypertension, and asthma and hypertension. Previous studies have demonstrated that men reporting seasonal or chronic rhinitis had on average a 3.5 mm Hg higher systolic blood pressure than those without allergic rhinitis. Proposed mechanisms to the relationship between allergic rhinitis and sinusitis with hypertension may lie in the pathway of obstructive sleep apnea via neurohumoral responses to hypoxemia. Asthmatics were 1.4 times more likely to have heart disease, and 1.3 times more likely to have high blood pressure, than non-asthmatics. The commonality of immunological dysfunction and inflammation between diseases of allergy and those mediated by hypertension and other vascular disorders may explain the correlations observed. Interestingly, obese individuals have higher levels of circulating IL-6, leptin and TNF-alpha skewing the immune system toward the allergen-reactive type 2 helper T-cell. This would mean that obese individuals were predisposed to diseases of chronic inflammation. The implications of allergic rhinitis, chronic sinusitis, and asthma deserve closer attention, especially into the possibility of co-morbidity for hypertension. Although associations between allergic diseases and hypertension have been reported, more studies need to be performed to elucidate the mechanisms behind such associations.
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PMID:Allergic respiratory disease as a potential co-morbidity for hypertension. 2086 73


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