Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sexuality is an important component of emotional and physical intimacy that men and women experience through their lives. Male erectile dysfunction (ED) and female sexual dysfunction increase with age. About a third of the elderly population has at least one complaint with their sexual function. However, about 60% of the elderly population expresses their interest for maintaining sexual activity. Although aging and functional decline may affect sexual function, when sexual dysfunction is diagnosed, physicians should rule out disease or side effects of medications. Common disorders related to sexual dysfunction include cardiovascular disease, diabetes, lower urinary tract symptoms and depression. Early control of cardiovascular risk factors may improve endothelial function and reduce the occurrence of ED. Treating those disorders or modifying lifestyle-related risk factors (eg obesity) may help prevent sexual dysfunction in the elderly. Sexuality is important for older adults, but interest in discussing aspects of sexual life is variable. Physicians should give their patient's opportunity to voice their concerns with sexual function and offer them alternatives for evaluation and treatment.
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PMID:Sexual dysfunction in the elderly: age or disease? 1639 44

Adrenocorticotrophic hormone (ACTH(1-39)) and the melanocortins (alpha, beta and gamma-melanocyte-stimulating hormone [MSH]) are derived from a larger precursor molecule known as the pro-opiomelanocortin (POMC) protein. They exert their numerous biological effects by activating 7 transmembrane G-protein coupled receptors (GPCR), leading to adenylyl cyclase activation and subsequent cAMP accumulation within the target cell. To date, 5 melanocortin receptors (MCR) have been identified and termed MC1R to MC5R, they have been shown to have a wide and varied distribution throughout the body, being found in the central nervous system (CNS), periphery and immune cells. Melanocortins have a multitude of actions including: (i) modulating disease pathologies including arthritis, asthma, obesity; (ii) affecting functions, for example erectile dysfunction, skin tanning; and (iii) organ systems, for example cardiovascular system. Recently a mechanistic approach has been identified with alpha-MSH preventing NF-kappaB activation via the preservation and expression of IkappaBalphaprotein. This leads to a reduction of pro-inflammatory mediators including cytokines and inhibition of adhesion molecule expression, with subsequent reduction in leukocyte emigration. Development of selective ligands with an appropriate pharmacokinetic profile will enable a pharmacological evaluation of the potential beneficial effects of the melanocortins. In this review I have discussed the potential mechanistic action for the melanocortins and some of the disease pathologies shown to be modulated. This review proposes targeting the MCR with the ultimate aim of controlling many of the diseases that we face today.
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PMID:Targeting melanocortin receptors as potential novel therapeutics. 1648 18

There is ample evidence from many epidemiological studies that lower urinary tract symptoms (LUTS) and sexual dysfunction are strongly linked, independently of age and comorbidities such as hypertension, diabetes, dyslipidaemia and coronary heart disease. However, a causal link between both conditions is not yet established. Four pathophysiological mechanisms currently support the relationship between LUTS and erectile dysfunction (ED): (i) The nitric oxide synthase (NOS)/NO theory; there is a reduction in NOS-containing nerves in the prostate and bladder/urethra in patients with bladder outlet obstruction (BOO), and that lack of NO or loss of protein kinase G causes ED; (ii) The autonomic hyperactivity and metabolic syndrome hypothesis: benign prostatic hyperplasia (BPH) may be part of the metabolic syndrome, which includes cardiovascular diseases (e.g. hypertension, ischaemic heart disease) and diabetes mellitus, known risk factors for ED. Hypertension, obesity, and hyperinsulinaemia have all been claimed to be associated with an increased sympathetic activity. Increased sympathetic activity is involved in LUTS/BPH and may have a role in ED/sexual dysfunction, with noradrenaline and alpha1-adrenoceptors representing a common link; (iii) the Rho-kinase activation/endothelin pathway; there can be increased Rho-kinase activity, and consequently calcium sensitivity of the contractile machinery, in prostate smooth muscle in BPH, the detrusor in BOO, corpora cavernosa in ED, and in the resistance vessels in hypertension. The actions of several factors beside noradrenaline (e.g. endothelin-1, angiotensin II), possibly involved in the increased smooth muscle activity found in both LUTS/BPH and sexual dysfunction, are dependent on Rho-kinase activity. Thus increased Rho-kinase activity might represent a common link between LUTS and sexual dysfunction; (iv) Pelvic atherosclerosis; animal models mimicking pelvic ischaemia and hypercholesterolaemia show similar smooth muscle alterations of the detrusor and corpora. Pelvic ischaemia may induce the biological modifications described above and may thus represent as well a common link between LUTS and sexual dysfunction. Studies treating one condition (e.g. ED) and measuring the impact on the other (e.g. LUTS) should further contribute to support this common link.
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PMID:Lower urinary tract symptoms and sexual dysfunction: epidemiology and pathophysiology. 1650 50

In both sexes, obesity, particularly the abdominal obesity phenotype, may impair fertility. This adverse effect appears to be mainly related to disorders of sex hormone secretion and/or metabolism, leading in turn to a condition of relative hyperandrogenism in obese women and of hypotestosteronemia (and, in some cases, a true hypogonadotropic hypogonadism) in obese men. In women, obesity can also play a relevant role in the pathophysiology of hyperandrogenism and metabolic abnormalities which characterize the polycystic ovary syndrome. These hormonal alterations may also play an important role in the pathophysiology of different obesity phenotypes and associated metabolic and cardiovascular comorbidities. Weight loss can improve hormonal abnormalities and fertility rates in both women and men. Erectile dysfunction, which is very common in obese males, can also be improved by lifestyle intervention strategies favouring weight loss.
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PMID:Obesity, fat distribution and infertility. 1672 87

We attempted in this study to investigate the prevalence of Peyronie's disease (PD) among diabetic patients with erectile dysfunction (ED). Two-hundred and six diabetic patients were further evaluated in this study. Forty-two (20.3%) patients had PD. There were significant associations between PD and risk factors of age, obesity and smoking. All patients with PD had also ED. Penile curvature was present in 82.1% of all patients with PD. Of the patients with PD, 25.4% had pain with or without erection. Significant associations between PD and ED and ED duration were detected. This study confirmed the high prevalence of PD among diabetic patients with ED. Further work is needed probing the mechanisms through which diabetes affects the pathogenesis of ED and PD.
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PMID:The prevalence of Peyronie's disease in diabetic patients with erectile dysfunction. 1691 4

Erectile dysfunction (ED) is associated with clinical atherosclerosis and several atherosclerotic risk factors including smoking, hypertension, dyslipidemia, diabetes mellitus, obesity and sedentary lifestyle. Clinical atherosclerosis is also associated with these same risk factors and with biomarkers of inflammation, thrombosis, endothelial cell activation. We evaluated the cross-sectional association between the degree of ED and levels of atherosclerotic biomarkers. A subcohort of 988 US male health professionals between the ages 46 and 81 years as part of an ongoing epidemiologic study had atherosclerotic biomarkers measured from blood collected in 1994-1995. These same men had in 2000, been retrospectively asked about erectile function in 1995 and in 2000. Biennial questionnaires since 1986 assessed medical conditions, medications, smoking, physical activity, body mass index, alcohol intake. The retrospective assessment of erectile function in 2000 for 1995 in these 988 men ranged from very good - 28.2%, good - 25.1%, fair - 19.2%, poor - 13.6%, to very poor - 13.9%. Men with poor to very poor erectile function compared to men with good and very good erectile function had 2.9 the odds of having elevated Factor VII levels (P=0.03), 1.9 times the odds of having elevated vascular cell adhesion molecule (P=0.13) and 2.0 times the odds of having elevated intracellular adhesion molecule (P=0.06) and 2.1 times the odds of having elevated total cholesterol/high-density lipoprotein ratio (P=0.02) comparing the top to bottom quintiles for each atherosclerotic biomarker after multivariate adjustment. Lipoprotein(a), homocysteine, interleukin-6 and tumor necrosis factor receptor, C-reactive protein and fibrinogen were not associated with the degree of erectile function after adjustment. We conclude that selected biomarkers for endothelial function, thrombosis and dyslipidemia but not inflammation are associated with the degree of ED in this cross-sectional analysis. Future studies evaluating the prospective association of ED, endothelial function and cardiovascular disease appear warranted.
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PMID:A retrospective study of the relationship between biomarkers of atherosclerosis and erectile dysfunction in 988 men. 1691 3

Because of increasingly sedentary lifestyles and diets higher in saturated fats, obesity and dyslipidemias are common and increasing in prevalence in Westernized countries. Longitudinal population-based studies clearly demonstrate that dyslipidemias and obesity, as well as factors such as hypertension, diabetes, and smoking, are major risk factors for atherosclerosis. Both clinical and animal models of endothelial dysfunction confirm that atherosclerosis leads to increased cerebrovascular and cardiovascular morbidity. Clinical studies with hypolipidemic agents demonstrate that hydroxy-3-methylglutaryl coenzyme A reductase inhibitors can decrease the risk of vascular morbidity. An increasing body of evidence from animal models demonstrates that hypercholesterolemia and atherosclerosis are risk factors for the development of erectile dysfunction (ED). This causal relationship between obesity and dyslipidemias with the development of ED in humans still needs further definition with convincing peer-reviewed scientific studies. The challenge for the future will be to define the benefit of controlling obesity and dyslipidemias on the development of ED and improvement of erectile function.
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PMID:Obesity, dyslipidemias and erectile dysfunction: a report of a subcommittee of the sexual medicine society of North America. 1694 22

Erectile dysfunction (ED) has been linked increasingly to cardiovascular risk factors and comorbidities. Considering the potential risk associated with sexual activity, guidelines were developed (Princeton I) for assessment and management of patients with varying degrees of cardiac risk. These guidelines were recently updated (Princeton II) based on new data concerning the link between ED and cardiovascular disease and the availability of additional phosphodiesterase type 5 inhibitors (vardenafil, tadalafil). Despite the need for careful risk assessment in all cases, sexual activity remains safe for the large majority of patients. However, all patients presenting with complaints of ED should be carefully assessed for the presence of cardiovascular risk factors (eg, obesity, hypertension, hyperlipidemia). Risk-factor modification, including lifestyle interventions (eg, exercise, weight loss) is strongly encouraged. Guidelines are presented for the management of acute coronary syndromes in patients taking phosphodiesterase type 5 inhibitors, including alternatives to the use of nitrates for these patients. Other drug interactions and the cardiovascular safety of testosterone replacement therapy are considered.
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PMID:Erectile dysfunction and cardiac disease: recommendations of the Second Princeton Conference. 1705 47

There are few discoveries with the magnitude of the impact that NO has had on biology during the 25 years since its discovery. There is hardly a disease today not associated with altered NO homeostasis. In fact, despite numerous other endothelial functions, endothelial dysfunction has become synonymous with reduced biological activity of NO. Translating the preclinical discoveries in NO biology to new modalities for disease management has not been as impressive. Beyond the success of drugs for erectile dysfunction, clinical trials of nitric oxide synthase inhibitor have been proven either ineffective or wrought with side effects. NO donors (e.g., nitroglycerine) remain frequently used cardiovascular agents, but were discovered before 1980. Gene therapy studies have yet to become clinically useful. There is no doubt that endothelial- and NO-dysfunction is a hallmark of cardiovascular disease, including diseases which are considered as major current public health concerns: hypertension, obesity, diabetes, malnutrition. In many cases, cardiovascular disease (CVD) can be prevented by identifying and controlling modifiable risk factors. One conceivable approach to the management of multiple risk factors in CVD could be to treat endothelial dysfunction (e.g., by enhancing eNOS expression), since many CVD risk factors are related to endothelial dysfunction. In this regard one goal may include optimizing eNOS function. This can be realized by supplementing co-factors, e.g., BH4, or substrate, L-arginine, by increasing cGMP availability via phosphodiesterase inhibitors or sGC activators or by increasing NO bioavailability via antioxidants. The association of other proteins with the nitric oxide synthase (NOS) isoforms and sGC could also serve as experimental and potentially therapeutic targets to modulate NO bioactivity. There is tremendous promise behind NO itself as well as the numerous other molecules and processes associated with the L-arginine-NO-cGMP pathway. Collaborative efforts among bench scientists, clinical investigators and epidemiologists are the key in realizing this promise.
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PMID:Nitric oxide and the endothelium: history and impact on cardiovascular disease. 1705 61

There is abundant evidence for the association between erectile dysfunction (ED) and the traditional atherosclerotic risk factors, such as dyslipidemia, hypertension, glucose intolerance, and obesity, that make up the metabolic syndrome. Recent findings have demonstrated a linear relationship between the number of these risk factors and the prevalence of ED. There is also growing evidence that endothelial dysfunction characterized by decreased bioavailability of nitrogen monoxide (NO) and a proinflammatory, prothrombotic, and proliferative phenotype is the common pathogenetic pathway linking ED to peripheral vascular diseases. Since ED often occurs several years before any clinical manifestation of systemic cardiovascular disease, ED should be seen as a warning of early atherosclerotic disease and an opportunity for doctor and patient to initiate preventive measures.
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PMID:[Metabolic syndrome and erectile dysfunction. Epidemiologic associations and pathogenetic links]. 1716 Jun 68


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