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

Evidence-based guidelines for the treatment of type 2 diabetes mellitus focus on three areas: intensive lifestyle intervention that includes at least 150 minutes per week of physical activity, weight loss with an initial goal of 7 percent of baseline weight, and a low-fat, reduced-calorie diet; aggressive management of cardiovascular risk factors (i.e., hypertension, dyslipidemia, and microalbuminuria) with the use of aspirin, statins, and angiotensin-converting enzyme inhibitors; and normalization of blood glucose levels (hemoglobin A1C level less than 7 percent). Insulin resistance, decreased insulin secretion, and increased hepatic glucose output are the hallmarks of type 2 diabetes, and each class of medication targets one or more of these defects. Metformin, which decreases hepatic glucose output and sensitizes peripheral tissues to insulin, has been shown to decrease mortality rates in patients with type 2 diabetes and is considered a first-line agent. Other medications include sulfonylureas and nonsulfonylurea secretagogues, alpha glucosidase inhibitors, and thiazolidinediones. Insulin can be used acutely in patients newly diagnosed with type 2 diabetes to normalize blood glucose, or it can be added to a regimen of oral medication to improve glycemic control. Except in patients taking multiple insulin injections, home monitoring of blood glucose levels has questionable utility, especially in relatively well-controlled patients. Its use should be tailored to the needs of the individual patient.
 ...
PMID:Management of blood glucose in type 2 diabetes mellitus. 2064 60

Hyperglycaemia is a typical feature of metabolic syndrome (MeTS) and one of its independent diagnostic criteria. The term includes impaired glucose homeostasis (impaired fasting glucose and impaired glucose tolerance) and type 2 diabetes mellitus. Although glycaemic control has been shown to lower the risk of microvascular events, the effect of intensive glycaemic control on macrovascular outcomes is less clear. Epidemiological studies show hyperglycaemia, particularly the postprandial one, to be a clear risk factor for cardiovascular (CV) mortality and morbidity. However, the intervention studies are less conclusive. The large interventional studies published in 2008 and 2009 (UKPDS, VADT, ACCORD, ADVANCE, RECORD) advocate the controlling of nonglycemic risk factors (through blood pressure control, lipid lowering with statin therapy, aspirin therapy, and lifestyle modifications) as the primary strategies for reducing the burden of CV disease in people with diabetes, and demonstrated the need for individualized approach to the patients' care in terms of blood glucose control. The patients with shorter duration of type 2 diabetes and without established atherosclerosis might reap CV benefit from intensive glycemic control. Conversely, it is possible that potential risks of intensive glycaemic control (hypoglycaemia) may outweigh its benefits in other patients, such as those with a very long duration ofdiabetes, known history of severe hypoglycemia, advanced atherosclerosis, and advanced age/frailty. According to the latest recommendations of the Czech Diabetes Society that are in line with the European and US standards the best way to protect type 2 diabetic patients against coronary and cerebrovascular disease is to target all cardiovascular risk factors (blood pressure treatment, including lipid-lowering with statins, aspirin prophylaxis, smoking cessation, and healthy lifestyle behaviors hypertension, dyslipidemia, obesity and other symptoms of metabolic syndrome. The target HbA1c levels in patients with the low CV risk shoul be below 4.5%. Less strict goals (HbA1c below 6%) may be appropriate for patients with a history of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, or extensive comorbid conditions or those with long-standing diabetes. The individual targets should be achieved safely (without hypoglycaemias). Slow advancing in diabetes compensation is preferred. Lifestyle changes are the cornerstone of therapy. Metformin is the drug of choice; its administration, together with lifestyle changes, should be initiated immediately after the diagnoses of diabetes. If monotherapy does not provide satisfactory glucose control, other oral antidiabetic agents or insulin are added to the combination. Since it is not known which hypoglycaemic agents are beneficial from the perspective of long-term patient prognosis, the selection is liberal. Contraindication of the various farmaceuticals must be respected. It is possible to use a range of different combinations, metformin is administered with a glitazone (zero risk of hypoglycaemias is the advantage) with sulphonylurea derivatives (low price is the advantage) with glinides, with incretins, acarbose, antiobesity agents or insulin. The next step is a triple combination of hypoglycaemic agents with different mechanisms of action. Therapy also includes education focusing on changes to dietary and lifestyle habits, including smoking cessation, and education related to the prevention of complications, with particular regard to prevention of diabetic foot and atherosclerosis.
 ...
PMID:[Treatment of diabetes in metabolic syndrome]. 1973 68

1. Metformin is not efficient enough in order to regulate menstrual cycles. 2.Metformin is not efficient enough in order to treat hyperandrogenism. 3. Metformin should not be used as a first-line treatment in order to treat infertility. Clomiphene citrate (CC) is the reference treatment. 4. Metformin in addition to CC is not recommended as a second line treatment, after the failure of CC alone. 5. Metformin should not be used during pregnancy in non diabetic women with PCOS, in order to prevent the risk of gestational diabetes. 6. Metformin should be prescribed to PCOS women when they are diabetic, in order to prevent their cardiovascular risk, after lifestyle modification. 7. Metformin should not be used in PCOS non diabetic women in order to lose weight. Metformin should not be used in order to treat dyslipidemia in women with PCOS. 8. In PCOS women, without diabetes, but with fasting hyperglycemia or carbohydrate intolerance, metformin should be prescribed if: BMI>35.
 ...
PMID:Should physicians prescribe metformin to women with polycystic ovary syndrome PCOS? 2007 83

Patients with schizophrenia have a greater incidence of being overweight or obese compared with the general population. Such individuals are often treated with second-generation (atypical) antipsychotics (SGAs), which are associated with weight gain, dyslipidemia, and other metabolic derangements. As a result, frequent monitoring of weight and other metabolic parameters is recommended. In addition, several pharmacologic strategies to help prevent or reduce SGA-induced weight gain have been proposed. Despite this, clinicians often struggle to manage obesity and metabolic issues in such patients. Metformin has attracted attention as a potential treatment option because it is thought to result in weight reduction and improved glycemic control in obese patients with and without type 2 diabetes mellitus. This article focuses on relevant pharmacologic aspects of metformin and reviews currently available evidence on the use of metformin as an augmentation agent for the treatment or prevention of SGA-induced weight gain.
 ...
PMID:The adjunctive use of metformin to treat or prevent atypical antipsychotic-induced weight gain: a review. 2085 6

We shall open our overview of issues related to obesity and hyperlipoproteinemia (HLP) or dyslipidemia with a notoriously known truth (that some are still reluctant to accept): HLP/DLP is not obesity. It is certainly not possible to put an equal sign between subcutaneous fat and the level of plasma lipids and lipoproteins. On the other hand, it is obvious that there is a number of connecting links between HLP/DLP and obesity. These associations on one side and differences on the other are the focus of this review paper. (1) HLP/DLP as well as obesity represent a group of high incidence metabolic diseases (gradually evolving from epidemic to pandemic) that affect several tens of percent of inhabitants. (2) Both HLP/DLP and obesity often occur concurrently, often as a result of unhealthy lifestyle. However, genetic factors are also been studies and it is possible that mutual predispositions for the development of both diseases will be identified. At present, it is only possible to conclude that obesity worsens lipid metabolism in genetically-determined HLP. (3) Both these metabolic diseases represent a risk factor for other pathologies, cardiovascular diseases are the most important common complication of both conditions (central type of obesity only). Concurrent presence of HDL/DLP and obesity is often linked to other diagnoses, such as type 2 diabetes mellitus (DM2T), hypertension, pro-coagulation or pro-inflammatory states; all as part of so called metabolic syndrome. (4) Patients with metabolic syndrome and, mainly, central obesity usually have typical dyslipidemia with reduced HDL-cholesterol (HDL-C) and sometimes hypertriglyceridaemia. Current treatment of HDL/DLP aims to first impact on the primary aim, i.e. LDL-cholesterol (LDL-C), and than influence HDL-C. (5) It seems that the therapeutic efforts in HLP/DLP and obesity will go in the same direction. I will skip the trivial (and difficult to accept by patients) dietary changes. Pharmacotherapy, however, (very scarce with respect to obesity) may bring positive effects on lipids and BMI. Metformin used to be considered as a drug that could improve lipid profile and lead to body weight reduction. Even though larger studies did not provide an unambiguous evidence for this, metformin keeps its position as a first line oral antidiabetic (not only) in patients with T2DM, HLP and obesity. Positive effect on lipids, mainly HDL-C is reported with pioglitazone. This drug, unlike other glitazones, does not bring body weight reduction but at least does not have a negative effect. Other antidiabetics with a positive effect on lipids and body weight include incretins, liraglutid in particular. Liraglutid importantly decreases triglyceride levels and has anorectic effect. Furthermore, metabolic effects of bariatric surgery should not be overlooked. Bariatric surgery brings weight reduction as well as it improves lipid profile and compensation of diabetes mellitus (DM). It should be mentioned here that bariatric surgery has been used for the treatment of HLP as early as 1980s. The results of the 25-year follow up within the POSCH study (ideal bypass indicated for HLP), presented in 2010, confirm a decrease in overall as well as cardiovascular mortality in an operated group, even though patients who did not undergo surgery were significantly more frequently treated with statins.
 ...
PMID:[Dyslipidemia and obesity 2011. Similarities and differences]. 2149 5

The use of atypical antipsychotics in the clinical management of schizophrenia and schizoaffective disorders has been associated with the development of insulin resistance. The present study evaluates the possible individual ameliorating effect of single daily oral treatments with 20 mg/kg/day of metformin and 0.1 mg/kg of glibenclamide in two groups of Wistar rats pretreated with 0.2 mg/kg of risperidone for 60 days. Two additional groups of rats were only treated with 0.2 mg/kg of risperidone and 10 mL/kg of distilled water, respectively, also for 60 days. Results showed that oral pre-treatment with metformin significantly attenuated increases in the weight gain pattern, fasting glucose, fasting plasma insulin, serum triglyceride and total cholesterol levels that were elevated by risperidone treatment. Metformin also significantly reduced glycosylated hemoglobin concentration, fasting insulin-glucose ratio and fasting insulin resistance index. Conversely, oral pre-treatment with glibenclamide for 60 days did not significantly reduce any of the measured parameters except for glycosylated hemoglobin concentrations. Thus, results of this study showed that 20 mg/kg of metformin effectively ameliorated the development of risperidone-induced insulin resistance and dyslipidemia which was mediated via improvement in insulin resistance. This study provides insight into the therapeutic potential of metformin in preventing risperidone-induced insulin resistance diabetes mellitus and dyslipidaemia.
 ...
PMID:Metformin: an effective attenuator of risperidone-induced insulin resistance hyperglycemia and dyslipidemia in rats. 2161 56

Diabetes accounts for millions of office visits each year to primary care offices in the United States. Successful care of the patient with type 2 diabetes requires not only focus on glucose management but also on comorbidities such as hypertension, dyslipidemia and obesity which are closely linked to microvascular and macrovascular complications. Primary care clinicians must stay abreast of frequently published diabetes literature and new treatments to care for these increasingly complex patients. Metformin and its effect on B12 absorption continues to be an issue encountered by clinicians in daily clinical practice. There has also been recent discussion regarding the increased risk of diabetes with statins; data to date on this issue have been conflicting. Rosiglitazone continues to face public scrutiny and there are now Food and Drug Administration regulations regarding its increased risk of cardiovascular disease. Liraglutide and saxagliptin represent new treatment options for type 2 diabetes, increasing the available options for treating this complex disease. A review of the primary literature involving these topics is provided.
 ...
PMID:Recent diabetes issues affecting the primary care clinician. 2188 36

Obesity is one of the most important known preventable causes of cancer, accounting for up to 20% of cancer deaths in women. Obese women have increased risk of dying from breast cancer as well as an increased risk of distant metastasis. Metabolic Syndrome (MetSyn) is a group of metabolic conditions that include 1) abdominal obesity, 2) atherogenic dyslipidemia, 3) elevated blood pressure, and 4) insulin resistance. MetSyn is known to promote the development of cardiovascular disease and diabetes and may be associated with increased breast cancer risk. Emerging evidence supports an association between mammary adipocytes and their secreted adipocytokines and breast cancer initiation and progression. Metformin (1,1-dimethylbiguanide hydrochloride) is a drug used to treat type 2 diabetes and MetSyn. We review the potential association between MetSyn in promoting breast cancer and emerging evidence for the use of metformin in cancer prevention.
 ...
PMID:Metabolic Syndrome and Breast Cancer Risk: Is There a Role for Metformin? 2194 68

The Metabolic Syndrome (MetS) confers a greater risk for both diabetes and cardiovascular diseases. Both insulin resistance and low grade inflammation appear to be pivotal in the pathogenesis of this disorder. The cornerstone of treatment presently is therapeutic lifestyle change with the emphasis on weight loss by diet and exercise. It appears that the evidence base will support statins as first line therapy for the dyslipidemia. Also, there is a limited role for both bile acid sequestrants and fibrates in certain subgroup of patients. It would appear that the Angiotensin converting enzyme inhibitors (ACEs) and angiotensin II receptor blockers (ARBs) are the preferred therapies for hypertension but invariably a combination therapy with additional drugs is required keeping in mind that certain drugs can exacerbate the dyslipidemia and or glycemia of MetS. Whilst metformin appears to be the drug of choice for the dysglycemia, thiazolidinediones (TZDs) like pioglitazone can also be beneficial but recent concern about bladder cancer has resulted in its discontinuation in certain countries in Europe. Metformin therapy has been shown to prevent new onset MetS. Modulating the incretin axis can prove very fruitful. A drug targeting all 3 disorders would be ideal but to date does not exist.
 ...
PMID:Pharmacotherapy for the metabolic syndrome. 2202 73

Polycystic ovary syndrome (PCOS) is associated with metabolic derangements including insulin resistance, dyslipidemia, systemic inflammation and endothelial dysfunction. There is a growing need to develop pharmacologic interventions to improve metabolic function in women with PCOS. Medications that have been tested in patients with PCOS include metformin, thiazolidinediones, acarbose, naltrexone, orlistat, vitamin D and statins. Metformin decreases hepatic gluconeogenesis and free fatty acid oxidation while increasing peripheral glucose uptake. Early studies in PCOS suggested that metformin indirectly reduces insulin level, dyslipidemia and systemic inflammation; however, recent placebo-controlled trials failed to demonstrate significant metabolic benefit. Thiazolidinediones act primarily by increasing peripheral glucose uptake. Most studies in PCOS have demonstrated that thiazolidinediones reduce insulin resistance; however, effects on dyslipidemia were disappointing. Use of thiazolidinediones is associated with weight gain and major complications. Acarbose reduces digestion of polysaccharides. Studies in PCOS yielded inconsistent effects of acarbose on insulin sensitivity and no significant improvement of dyslipidemia. Naltrexone reduces appetite and modulates insulin release; its use in PCOS may reduce hyperinsulinemia. Orlistat decreases absorption of dietary fats; studies in PCOS suggest beneficial effects on insulin sensitivity. Vitamin D may improve insulin sensitivity but mixed results on lipid profile in PCOS have been reported. Statins are competitive inhibitors of the key enzyme regulating the mevalonate pathway; their effects are related to reduced cholesterol production as well as anti-inflammatory and anti-oxidant properties. In women with PCOS, statins reduce hyperandrogenism, improve lipid profile and reduce systemic inflammation while the effects on insulin sensitivity are variable. Use of statins is contraindicated in pregnancy.
 ...
PMID:Medical management of metabolic dysfunction in PCOS. 2218 33


<< Previous 1 2 3 4 5 6 Next >>