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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Excessive fat (adiposity) and dysfunctional fat (adiposopathy) constitute the most common worldwide epidemics of our time -- and perhaps of all time. Ongoing efforts to explain how the micro (adipocyte) and macro (body organ) biologic systems interact through function and dysfunction in promoting Type 2 diabetes mellitus, hypertension and dyslipidemia are not unlike the mechanistic and philosophical thinking processes involved in reconciling the micro (quantum physics) and macro (general relativity) theories in physics. Currently, the term metabolic syndrome refers to a constellation of consequences often associated with excess body fat and is an attempt to unify the associations known to exist between the four fundamental metabolic diseases of obesity, hyperglycemia (including Type 2 diabetes mellitus), hypertension and dyslipidemia. However, the association of adiposity with these metabolic disorders is not absolute and the metabolic syndrome does not describe underlying causality, nor does the metabolic syndrome necessarily reflect any reasonably related pathophysiologic process. Just as with quantum physics, general relativity and the four fundamental forces of the universe, the lack of an adequate unifying theory of micro causality and macro consequence is unsatisfying, and in medicine, impairs the development of agents that may globally improve both obesity and obesity-related metabolic disease. Emerging scientific and clinical evidence strongly supports the novel concept that it is not adiposity alone, but rather it is adiposopathy that is the underlying cause of most cases of Type 2 diabetes mellitus, hypertension and dyslipidemia. Adiposopathy is a plausible Theory of Everything for mankind's greatest metabolic epidemics.
Expert Rev Cardiovasc Ther 2005 May
PMID:Adiposopathy, metabolic syndrome, quantum physics, general relativity, chaos and the Theory of Everything. 1588 67

The objective of this trial was to compare the metabolic effects of long-term treatment with doxazosin to those of irbesartan in patients with type 2 diabetes and hypertension. We evaluated 96 hypertensive diabetic patients who were randomized to 12 months of double-blind treatment with doxazosin 4 mg/d or irbesartan 300 mg/d. At the end of the study, systolic and diastolic blood pressure (SBP and DBP) were significantly reduced from 152 to 140 mm Hg and from 97 to 87 mm Hg, respectively, with doxazosin (P < 0.01). SBP and DBP were reduced from 150 to 134 mm Hg and from 94 to 83 mm Hg, respectively, with irbesartan (P < 0.01). Irbesartan had significantly better antihypertensive efficacy than doxazosin (P < 0.05). Doxazosin had the greatest effect on glucose metabolism and lipid parameters, with significant (P </= 0.05) reductions observed at study end compared with baseline in glycosylated hemoglobin, fasting plasma glucose, fasting plasma insulin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, and Homeostasis Model Assessment Index. In conclusion, both doxazosin and irbesartan reduced BP during long-term treatment, but not to recommended levels, and doxazosin had the more beneficial effect on glucose metabolism and lipid profile.
J Cardiovasc Pharmacol 2005 Jun
PMID:Effects of doxazosin and irbesartan on blood pressure and metabolic control in patients with type 2 diabetes and hypertension. 1589 88

Patients with type 2 diabetes mellitus have a greater risk of cardiovascular disease than nondiabetic individuals. These patients are often insulin resistant and have an associated clustering of risk factors that contribute to cardiovascular disease. The risk factors include dyslipidemia, hypertension, altered hemostasis, and chronic inflammation. A primary objective in the management of type 2 diabetes mellitus is normalization of blood glucose levels; however, some of the oral drugs used to control blood glucose levels have significant effects on these risk factors. In this article, we review the current data involving the modification of these cardiovascular risk factors by the biguanide (metformin), the thiazolidinediones (troglitazone, rosiglitazone, and pioglitazone), the alpha-glucosidase inhibitors (miglitol, acarbose), and the insulin secretagogs (glyburide [glibenclamide], glipizide, chlorpropamide, tolbutamide, tolazamide, glimepiride, repaglinide, and nateglinide). Generally, the thiazolidinediones improve hemostasis and endothelial function and reduce blood pressure, while having variable effects on dyslipidemia. Metformin improves dyslipidemia and altered hemostasis and decreases plasma C-reactive protein levels with little or no effect on blood pressure. Data on the effects of the alpha-glucosidase inhibitors and insulin secretagogs are sparse; however, these drugs appear to have little or no effect on cardiovascular risk factors.
Am J Cardiovasc Drugs 2005
PMID:Cardiovascular risk factors associated with insulin resistance: effects of oral antidiabetic agents. 1590 Dec 7

Although circumstantial evidence supports raising high-density lipoprotein cholesterol (HDLC) in patients with low levels of HDLC, the scarcity of event-based trials has led to uncertainty with regard to the benefit of high-density lipoprotein (HDL)-raising therapy. Based on the National Cholesterol Education Program guidelines, therapy for dyslipidemia is focused initially on targeting low-density lipoprotein cholesterol (LDLC), and in patients with hypertriglyceridemia, secondarily on targeting non-HDLC. When HDLC remains low, the decision to target HDLC depends on the assessment of risk of cardiovascular events. We often consider drug therapy specifically to raise HDLC in high-risk patients, such as those with established atherosclerotic vascular disease, type 2 diabetes, or a Framingham risk score of 20% or above. The majority of high-risk patients require drug therapy, usually a statin, to achieve aggressive LDLC and non-HDLC goals, and thus many patients with low HDLC are candidates for statin therapy. However, a second drug is often required to achieve substantial HDL raising. Although no formal goals for HDLC exist, reasonable goals are HDLC greater than 40 mg/dL in men and greater than 50 mg/dL in women. We often add either niacin or a fibrate to a statin in high-risk patients with low HDLC levels. Targeting HDLC with pharmacologic therapy is a more difficult decision in moderate-risk patients, in whom therapy must be highly individualized.
Curr Treat Options Cardiovasc Med 2005 May
PMID:Current Drug Options for Raising HDL Cholesterol. 1591

Both genetic and environmental factors are involved in the pathogenesis of obesity and type 2 diabetes. Most of the genetic studies on common obesity are confined to the links between a given gene polymorphism or gene loci and different phenotypes of obesity or anthropometric measures. Some studies indicate that genetic factors modify the weight reduction response to energy restriction or weight gain in the long-term. Only a few studies have focused on gene-diet interaction in the development of type 2 diabetes. The Finnish Diabetes Prevention Study shows (DPS) that the success of a lifestyle intervention depends also on the polymorphisms of those genes, which are suggested to play a role in energy metabolism, lipid metabolism, insulin resistance or insulin secretion. This review deals with selected genes examined so far in the DPS.
Nutr Metab Cardiovasc Dis 2005 Jun
PMID:Gene-diet interaction in relation to the prevention of obesity and type 2 diabetes: evidence from the Finnish Diabetes Prevention Study. 1595 72

Cardiovascular disease (CVD) and diabetes are growing public health burdens and remain one of the leading causes of morbidity and mortality in Canada (Heart and Stroke Foundation, 2003). It has become increasingly evident that individuals who present with a cluster of metabolic disorders, known as the metabolic syndrome, are at an increased risk of developing both CVD and type 2 diabetes (Ng, 2003). Due to the increased risk of morbidity and mortality associated with the metabolic syndrome, it is imperative for health care professionals to become familiar with the diagnostic criteria for this disorder. This will enable nurses to provide the appropriate primary and secondary prevention strategies in order to help reduce individual risk. With the help of a case study, this article will define metabolic syndrome, review its prevalence and risk factors, and discuss therapeutic interventions for this disorder.
Can J Cardiovasc Nurs 2005
PMID:Metabolic syndrome. 1597 60

The vascular endothelial basement membrane and extra cellular matrix is a compilation of different macromolecules organized by physical entanglements, opposing ionic charges, chemical covalent bonding, and cross-linking into a biomechanically active polymer. These matrices provide a gel-like form and scaffolding structure with regional tensile strength provided by collagens, elasticity by elastins, adhesiveness by structural glycoproteins, compressibility by proteoglycans--hyaluronans, and communicability by a family of integrins, which exchanges information between cells and between cells and the extracellular matrix of vascular tissues. Each component of the extracellular matrix and specifically the capillary basement membrane possesses unique structural properties and interactions with one another, which determine the separate and combined roles in the multiple diabetic complications or diabetic opathies. Metabolic syndrome, prediabetes, type 2 diabetes mellitus, and their parallel companion (atheroscleropathy) are associated with multiple metabolic toxicities and chronic injurious stimuli. The adaptable quality of a matrix or form genetically preloaded with the necessary information to communicate and respond to an ever-changing environment, which supports the interstitium, capillary and arterial vessel wall is individually examined.
Cardiovasc Diabetol 2005 Jun 28
PMID:The central role of vascular extracellular matrix and basement membrane remodeling in metabolic syndrome and type 2 diabetes: the matrix preloaded. 1598 57

Cardiovascular disease (especially coronary heart disease ) is the most common complication and cause of death in patients with type 2 diabetes. CHD prevention should be the major focus in preventive care of diabetes patients. There is a solid evidence base from which to recommend aggressive control of elevated blood pressure and lipids to reduce CHD events in diabetes. Aggressive glycemic control alone will not reduce CHD events, but will prevent diabetes-specific microvascular complications. Blood pressure should be treated to a goal of at least 130/80 mm Hg, and possibly lower, using angiotensin-converting enzyme inhibitors, thiazide diuretics, or beta blockers as first-line agents. Low-density lipoprotein cholesterol should be treated with a statin to reduce the level by 30% to 40%, regardless of pretreatment level, to a goal of less than 100 mg/dL for most patients or a goal of less than 70 mg/dL in diabetes patients with CHD. Patients with high-density lipoprotein levels less than 40 mg/dL may benefit from fibrate therapy. Cigarette smoking should be actively discouraged, and prophylactic aspirin therapy should be prescribed for most patients. A regular program of physical activity and weight control should be prescribed to improve insulin sensitivity. Use of thiazolidinediones may be considered early in the course of hypoglycemic therapy, but additional research is needed to define the role of insulin sensitization as a primary means to reduce CHD risk in type 2 diabetes.
Curr Treat Options Cardiovasc Med 2005 Aug
PMID:Prevention of coronary heart disease in diabetes. 1600 57

Obesity has long been recognized as a significant risk factor for type 2 diabetes. Both obesity and type 2 diabetes are associated with an increase in cardiovascular risk. As cardiovascular disease continues to be the number one killer in the USA and western adult populations, the rise in prevalence of obesity and type 2 diabetes is alarming. This is especially disturbing in the tripling of overweight children and adolescents, accompanied by the increase in prevalence of pediatric type 2 diabetes. Optimal strategies for long-term diabetes management aim at effectively controlling, reducing and ultimately preventing obesity. This review explores the clinical recommendations in place, new clinical investigations, diet therapy, medical nutrition therapy, meal replacements, behavior therapy, exercise therapy, pharmacotherapy and surgical therapy as strategies to achieve weight-loss success in diabetic patients and ultimately reduce cardiovascular disease.
Expert Rev Cardiovasc Ther 2005 Jul
PMID:Optimal diabetes management during medical weight loss for cardiovascular risk reduction. 1607 84

Studies published before the introduction of highly active antiretroviral therapy (HAART) have tracked the incidence and course of human immunodeficiency virus (HIV) infection in relation to cardiac disease.The introduction of HAART regimens, by preventing opportunistic infections and reducing the incidence of myocarditis, has reduced the prevalence of HIV-associated cardiomyopathy of about 30% and the prevalence of cardiac involvement of AIDS-associated malignancies of about 50%. However, HAART regimens, especially those including protease inhibitors have been shown to cause, in a high proportion of HIV-infected patients, a metabolic syndrome (lipodystrophy/lipoatrophy, dyslipidemia, type 2 diabetes mellitus, insulin resistance) that may be associated with an increased risk of cardiovascular disease (approximately 1.4 cardiac events per 1000 years of therapy according to the Framingham score). A careful stratification of the cardiovascular risk and cardiovascular monitoring of patients under HAART according to the most recent clinical guidelines is needed.
Curr Drug Targets Cardiovasc Haematol Disord 2005 Aug
PMID:Reviewing the cardiovascular complications of HIV infection after the introduction of highly active antiretroviral therapy. 1610 66


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