Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several lines of evidence suggest that a subset of women may be at increased risk of cardiovascular disease because of unfavorable alterations in insulin action and/or production, accompanying altered apolipoprotein metabolism and altered androgenicity and/or estrogenicity. A number of cardiovascular disease risk factors, including central obesity, insulin resistance (with associated hyperinsulinemia), dyslipidemia, and/or diabetes mellitus, tend to cluster in these women. Another common ovarian morphology in women with hyperandrogenism is polycystic ovaries, which cluster with hirsutism, anovulation, infertility, gonadotropin secretion abnormalities, android fat distribution, and many important cardiovascular disease risk factors. Studies indicate that androgen excess may be a signal of increased risk for coronary artery disease, even in younger women. If androgenicity and insulin resistance are early warning signs of increasing risk of morbidity and mortality, these patients are prime candidates for preventive medicine. It is important that primary care providers begin to recognize these androgen disorders as a clue to the existence of a complex, lifelong pattern potentially placing women at risk for premature morbidity and mortality and initiate preventive treatment before irreversible thresholds are crossed.
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PMID:Obesity, lipids, cardiovascular risk, and androgen excess. 782 38

The high prevalence of obesity and its well documented association with the cardiovascular risk factors diabetes mellitus, dyslipidemia and hypertension represents a major problem for the general health status of industrialized societies. Although numerous studies have shown that genetic factors have a major influence on the regulation of energy homeostasis and the susceptibility to obesity, the genes and predisposing mutations involved are insufficiently understood. Among several known rodent models of obesity due to single gene mutations, mice homozygous for the obese (ob) gene exhibit massive early-onset obesity, hyperphagia, non-insulin-dependent diabetes mellitus, defective thermoregulation and infertility. Recently the ob gene was identified by positional cloning and shown to be mutated in ob/ob mice. Leptin, the product of the ob gene, is a 167-amino acid secreted protein that is synthesized exclusively in adipose tissue. With the exception of ob/ob mice, circulating plasma leptin is elevated in obesity. Administration of recombinant leptin to ob/ob mice reduces fat mass, food intake, hyperglycemia and hyperinsulinemia. The various effects of the hormone are mediated by leptin receptors expressed at high levels in the hypothalamus, but also in several other non-neuronal tissues. A mutation in the leptin receptor gene is responsible for the obese phenotype of db/db mice. Plasma leptin in humans is positively correlated with body fat mass, suggesting that leptin resistance rather than leptin deficiency is a common feature of human obesity. This review briefly summarizes the current status of the rapidly growing evidence that leptin plays an important role in the regulation of body weight and fat deposition.
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PMID:Regulation of energy balance by leptin. 888 45

Women with polycystic ovary syndrome come to the gynecologist with a variety of symptoms, including menstrual irregularities, hirsutism, acne, weight gain, obesity, and infertility. An accurate diagnosis requires both confirmation of signs and symptoms of polycystic ovary syndrome and exclusion of other disorders. Once the diagnosis of polycystic ovary syndrome has been established, the presence of concomitant conditions, such as hypertension, dyslipidemia, and diabetes, must be assessed. Because the cause of polycystic ovary syndrome is not clear, treatment options have focused on symptom management. Such treatment options include oral contraceptives, gonadotropin-releasing hormone analogs with "add-back" hormone regimens, antiandrogens, ovulation-inducing agents, electrolysis, nutritional and weight loss counseling, exercise, laparoscopic ovarian drilling, and glucocorticoids. Pathogenic considerations, risk factor assessments, and treatment objectives combine to determine the choice of therapies. It is not clear whether insulin resistance is clinically important or causal in polycystic ovary syndrome symptom complex in all affected women. Polycystic ovary syndrome may be the final common expression of a variety of metabolic or neuroendocrine perturbations. If insulin resistance is a universal feature, it would make sense to treat with an insulin-sensitizing agent in the expectation that symptoms would resolve or improve. If insulin resistance is not the main etiologic factor, however, then insulin-sensitizing agents would be useful as adjunctive agents only for women with clinically important insulin resistance (eg, patients with polycystic ovary syndrome in whom insulin resistance causes hyperglycemia). In such cases an insulin-sensitizing agent could be instituted along with a program of weight loss and exercise.
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PMID:The obstetrician-gynecologist's role in the practical management of polycystic ovary syndrome. 985 17

Polycystic ovary syndrome is a complex endocrine disorder of hypothalamic-pituitary dysfunction that presents with anovulation, hirsutism and infertility. Women with PCOS have increased risk for developing NIDDM, dyslipidemia and premature cardiovascular disease. Because of its vague presentation and potential for numerous complications, PCOS should be evaluated carefully. Unfortunately, there is no cure for PCOS, and the treatment has numerous limitations. Weight loss in an obese patient may greatly improve the patient's response to treatment and should be encouraged.
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PMID:Polycystic ovary syndrome. 1103 90

The peroxisome proliferator-activated receptors (PPARs) are a group of three nuclear receptor isoforms, PPAR gamma, PPAR alpha, and PPAR delta, encoded by different genes. PPARs are ligand-regulated transcription factors that control gene expression by binding to specific response elements (PPREs) within promoters. PPARs bind as heterodimers with a retinoid X receptor and, upon binding agonist, interact with cofactors such that the rate of transcription initiation is increased. The PPARs play a critical physiological role as lipid sensors and regulators of lipid metabolism. Fatty acids and eicosanoids have been identified as natural ligands for the PPARs. More potent synthetic PPAR ligands, including the fibrates and thiazolidinediones, have proven effective in the treatment of dyslipidemia and diabetes. Use of such ligands has allowed researchers to unveil many potential roles for the PPARs in pathological states including atherosclerosis, inflammation, cancer, infertility, and demyelination. Here, we present the current state of knowledge regarding the molecular mechanisms of PPAR action and the involvement of the PPARs in the etiology and treatment of several chronic diseases.
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PMID:The mechanisms of action of PPARs. 1181 83

Polycystic ovary syndrome is a common premenopausal endocrino-metabolic disorder. In addition to hyperandrogenism, menstrual abnormalities, ovulatory disturbances and infertility, insulin resistance, dyslipidemia, and obesity may eventuate in long-term cardiovascular consequences.
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PMID:Polycystic ovary syndrome [PCOS]: comprehensive management in primary care. 1236 Jun 33

The prevalence of obesity is increasing worldwide. In the United States, in 1999, 27% of adults had a body mass index >30 kg/m(2), almost double the prevalence of 20 years earlier. The estimated mortality from obesity-related diseases in the United States is approximately 300,000 annually and growing. In the future, mortality related to obesity is expected to exceed that of smoking. Numerous diseases are caused or made worse by obesity. These include type 2 diabetes; hypertension; dyslipidemia; ischemic heart disease; stroke; obstructive sleep apnea; asthma; nonalcoholic steatohepatitis; gastroesophageal reflux disease; degenerative joint disease of the back, hips, knees, and feet; infertility and polycystic ovary syndrome; various malignancies; and depression. Type 2 diabetes is perhaps the most visible obesity-related problem. Present in at least 14 million Americans, it leads to serious complications and premature death. It is largely caused by obesity, and is generally cured by weight loss. The quality of life of the obese is markedly reduced, and the costs to health care systems are great. Preventive programs have yet to affect the rising prevalence. An effective solution is needed.
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PMID:The extent of the problem of obesity. 1252 43

The etiology of human female infertility is often uncertain. The sterility of high-density lipoprotein (HDL) receptor-negative (SR-BI(-/-)) female mice suggests a link between female infertility and abnormal lipoprotein metabolism. SR-BI(-/-) mice exhibit elevated plasma total cholesterol [with normal-sized and abnormally large HDL and high unesterified to total plasma cholesterol (UC:TC) ratio]. We explored the influence of hepatic SR-BI on female fertility by inducing hepatic SR-BI expression in SR-BI(-/-) animals by adenovirus transduction or stable transgenesis. For transgenes, we used both wild-type SR-BI and a double-point mutant, Q402R/Q418R (SR-BI-RR), which is unable to bind to and mediate lipid transfer from wild-type HDL normally, but retains virtually normal lipid transport activities with low-density lipoprotein. Essentially wild-type levels of hepatic SR-BI expression in SR-BI(-/-) mice restored to nearly normal the HDL size distribution and plasma UC:TC ratio, whereas approximately 7- to 40-fold overexpression dramatically lowered plasma TC and increased biliary cholesterol secretion. In contrast, SR-BI-RR overexpression had little effect on SR-BI(+/+) mice, but in SR-BI(-/-) mice, it substantially reduced levels of abnormally large HDL and normalized the UC:TC ratio. In all cases, hepatic transgenic expression restored female fertility. Overexpression in SR-BI(-/-) mice of lecithin:cholesterol acyl transferase, which esterifies plasma HDL cholesterol, did not normalize the UC:TC ratio, probably because the abnormal HDL was a poor substrate, and did not restore fertility. Thus, hepatic SR-BI-mediated lipoprotein metabolism influences murine female fertility, raising the possibility that dyslipidemia might contribute to human female infertility and that targeting lipoprotein metabolism might complement current assisted reproductive technologies.
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PMID:Effects of hepatic expression of the high-density lipoprotein receptor SR-BI on lipoprotein metabolism and female fertility. 1654 76

This article boldly challenges the dynamic psychiatrist to engage directly and vigorously into a matter that many would prefer to regard somewhat passively. That passivity is no longer acceptable. The metabolic syndrome has become a central medical concern because of the epidemic of obesity. It causes cardiovascular disease, diabetes, some cancers, sleep apnea, sexual dysfunction, and infertility. Obesity leads to depression, anxiety, and osteoarthritis. Some atypical antipsychotic medicines contribute to the metabolic syndrome, but the epidemic is widespread independent of atypicals. Practical steps by psychiatrists to monitor metabolic parameters are not as simple as they appear to be. Yet this is an area of clinical practice that cannot be ignored. Psychodynamic therapists need to awaken to the health of patients because the metabolic syndrome is more life-threatening than self-mutilation and many other self-destructive behaviors. The article discusses countertransference and transference issues stirred up when physicians begin to take responsibility for the total health of their patients. Freud oriented us to focus on both sides of the mind body relationship. Recent research on obesity, hypertension, diabetes, sleep, anxiety,depression, exercise and dyslipidemia is reviewed from the viewpoint of how it impinges on the office practice of a dynamic psychiatrist.
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PMID:A psychodynamic approach to screening for the metabolic syndrome. 1701 91

Male sexual dysfunction-a term that is commonly used to refer to erectile dysfunction, premature ejaculation, decreased libido and impaired orgasm-is the primary complaint encountered by many urologists. Despite the high prevalence and bothersome nature of these complaints, they are frequently neglected in clinical practice. This paper highlights clinical situations in which urologists should systematically evaluate male sexual functioning. These include men who present with several common urologic disorders, such as pelvic trauma, malignancies, and lower urinary tract symptoms associated with benign prostatic hyperplasia, neurologic disorders and infertility. Studies have shown that erectile dysfunction might be a clinical marker of endothelial dysfunction, and consequently of undetected diabetes, hypertension, dyslipidemia, coronary artery disease and depression. We also address the question of whether urologists should adopt wide-ranging screening regimens for sexual dysfunction.
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PMID:How, why and when should urologists evaluate male sexual function? 1647 Feb 7


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