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Biomedical subjects

Vivian Fonseca

Publications and source records attributed to Vivian Fonseca.

At least 37 records · Page 2Linked to original sources
PubMed2004

The metabolic syndrome and chronic kidney disease in U.S. adults.

BACKGROUND: The metabolic syndrome is a common risk factor for cardiovascular disease. OBJECTIVE: To examine the association between the metabolic syndrome and risk for chronic kidney disease and microalbuminuria. DESIGN: Cross-sectional study. SETTING: The Third National Health and Nutrition Examination Survey. PATIENTS: Participants 20 years of age or older were studied in the chronic kidney disease (n = 6217) and microalbuminuria (n = 6125) analyses. MEASUREMENTS: The metabolic syndrome was defined as the presence of 3 or more of the following risk factors: elevated blood pressure, low high-density lipoprotein cholesterol level, high triglyceride level, elevated glucose level, and abdominal obesity. Chronic kidney disease was defined as a glomerular filtration rate less than 60 mL/min per 1.73 m2, and microalbuminuria was defined as a urinary albumin-creatinine ratio of 30 to 300 mg/g. RESULTS: The multivariate-adjusted odds ratios of chronic kidney disease and microalbuminuria in participants with the metabolic syndrome compared with participants without the metabolic syndrome were 2.60 (95% CI, 1.68 to 4.03) and 1.89 (CI, 1.34 to 2.67), respectively. Compared with participants with 0 or 1 component of the metabolic syndrome, participants with 2, 3, 4, and 5 components of chronic kidney disease had multivariate-adjusted odds ratios of 2.21 (CI, 1.16 to 4.24), 3.38 (CI, 1.48 to 7.69), 4.23 (CI, 2.06 to 8.63), and 5.85 (CI, 3.11 to 11.0), respectively. The corresponding multivariate-adjusted odds ratios of microalbuminuria for participants with 3, 4, and 5 components were 1.62 (CI, 1.10 to 2.38), 2.45 (CI, 1.55 to 3.85), and 3.19 (CI, 1.96 to 5.19), respectively. CONCLUSIONS: These findings suggest that the metabolic syndrome might be an important factor in the cause of chronic kidney disease.

Adult↗
PubMed2004

Differential association of birth weight with cardiovascular risk variables in African-Americans and Whites: the Bogalusa heart study.

PURPOSE: To study the relationship between low birth weight and the subsequent development of cardiovascular risk factors and to compare this relationship between African-Americans and whites at 7 to 21 years of age. METHODS: The relationship of birth weight with cardiovascular risk factors, namely, systolic and diastolic blood pressure (BP), BMI, HDL, LDL, triglycerides, and HOMA insulin resistance (HOMA-IR) was examined retrospectively using information on 1155 participants (730 whites and 425 African-Americans) from two cohorts of the Bogalusa Heart Study. RESULTS: Participants with lower birth weight had higher systolic BP, HOMA-IR, triglycerides, and LDL. The association of birth weight with LDL, triglycerides, and HOMA-IR was stronger in African-Americans, while the association with systolic BP was stronger in whites. Subjects with birth weight <2500 g were at increased risk of having values of HOMA-IR and LDL in the upper quartile of the observed range compared with those with birth weight >2500 g. CONCLUSIONS: These results support a relationship between low birth weight and the later development of important cardiovascular risk factors in young African-Americans and white individuals. This relationship tends to be stronger in African-Americans than in whites, except for systolic blood pressure.

Adolescent↗
PubMed2004

Prevalence of non-traditional cardiovascular disease risk factors among persons with impaired fasting glucose, impaired glucose tolerance, diabetes, and the metabolic syndrome: analysis of the Third National Health and Nutrition Examination Survey (NHANES III).

PURPOSE: To calculate the prevalence of non-traditional cardiovascular disease (CVD) risk factors across diabetes status and for persons with and without the metabolic syndrome. METHODS: Data were analyzed from the Third National Health and Nutrition Examination Survey for normal plasma glucose [<100 mg/dl, n=4589]; impaired fasting glucose [IFG, 100-125 mg/dl, n=2008], diabetes [fasting glucose #10878; 126 mg/dl or diabetes medication, n=750]; and participants with and without the metabolic syndrome, n=1938 and n=5409, respectively. RESULTS: After adjustment for age, race, sex, body mass index, physical inactivity, cigarette smoking and alcohol consumption, a higher odds (p-trend < 0.01) of the metabolic syndrome, an elevated HOMA-insulin resistance index, chronic kidney disease, elevated C-reactive protein, high fibrinogen, and high white blood cell count was observed across diabetes status. After similar adjustment, the metabolic syndrome was associated with (odds ratio; 95% confidence interval) low apolipoprotein A1 (2.27: 1.30,3.96), high apolipoprotein-B (2.97: 2.03,4.34), a higher HOMA insulin resistance index (5.25: 4.16, 6.63), chronic kidney disease (2.27: 1.42, 3.63), and elevated markers of inflammation [high white blood cell count (1.55: 1.14, 2.10), and elevated C-reactive protein (1.46: 1.06, 2.00)]. Among participants with IFG, the presence of impaired glucose tolerance (IGT) was associated with a higher prevalence of the HOMA insulin reistance index, 32.3%, high fibrinogen, 18.5%, and elevated C-reactive protein, 13.2%, compared to persons with IFG alone, 19.7%, 13.3% and 5.7%, respectively (each p <== 0.05). CONCLUSIONS: In this representative of the US population, an increased prevalence of non-traditional CVD risk factors was present among persons with diabetes, IGT and IFG compared to IFG alone, and the metabolic syndrome.

Adult↗
PubMed2004

Effect of intensive treatment on vascular and other complications of diabetes mellitus.

Diabetes mellitus (DM) is a growing health problem in the United States afflicting over 18.2 million Americans. Before developing type 2 DM patients almost always have pre-diabetes. At least 20.1 million people in the United States ages > or =40 to < or =74 years have pre-diabetes. Research has shown that controlling blood glucose can delay or prevent type 2 DM from ever developing. Morbidity and mortality from DM most commonly result from the long-term complications of the disease. Data from several studies suggest that aggressive management of DM and its associated risk factors will lead to a reduction in these long-term complications. The term "intensive therapy" is being used for whatever strategy keeps blood sugar near normal, as well as for aggressive management of other associated risk factors such as lipid abnormalities and blood pressure. Intensive management of glycemia may have long-lasting benefits over conventional therapy. New clinical trials are being carried out to determine whether goals for intensive therapy should be lower than current goals while testing is being carried out on a variety of therapeutic strategies to determine the optimum methods to prevent diabetes complications.

Blood Glucose↗
PubMed2004

A comparison of bedtime insulin glargine with bedtime neutral protamine hagedorn insulin in patients with type 2 diabetes: subgroup analysis of patients taking once-daily insulin in a multicenter, randomized, parallel group study.

BACKGROUND: Basal insulin is frequently administered once daily. This subgroup analysis of a multicenter, randomized, parallel study compared insulin glargine (Lantus Aventis Pharmaceuticals, Bridgewater, NJ) with neutral protamine Hagedorn (NPH) insulin in patients with type 2 diabetes, evaluating only patients treated previously with once-daily NPH insulin. METHODS: Patients received bedtime insulin glargine or NPH insulin, with preprandial regular insulin. One hundred patients (mean age, 57.9 years; mean glycohemoglobin, 8.4%; mean fasting blood glucose, 167 mg/dL) were treated for up to 28 weeks. RESULTS: Patients treated with insulin glargine (n = 52) and NPH insulin (n = 48) achieved similar reductions from baseline in glycohemoglobin (-0.41% versus -0.46%) and fasting blood glucose (-22 mg/dL versus -22 mg/dL) at week 28. The proportion of patients reaching target fasting blood glucose (<120 mg/dL) at 28 weeks was 34.2% with insulin glargine and 24.4% with NPH insulin. Similar proportions of patients achieved glycohemoglobin less than 7% and less than 8% in both groups. Baseline and week-28 mean daily doses of insulin glargine (27.3 IU versus 36.4 IU) were similar to NPH insulin doses (25.5 IU versus 30.2 IU). However, significantly fewer patients reported one or more episodes of hypoglycemia with insulin glargine (46.2%) versus NPH insulin (60.4%; P < 0.05). Significantly fewer patients also reported one or more symptomatic episodes confirmed by blood glucose less than 50 mg/dL with insulin glargine (17.3%) versus NPH insulin (31.3%; P < 0.005). CONCLUSION: Bedtime insulin glargine is as effective as bedtime NPH insulin in improving glycemic control, with significantly less hypoglycemia.

Body Mass Index↗
PubMed2003

Effect of thiazolidinediones on body weight in patients with diabetes mellitus.

Treatment of diabetes mellitus with medications, including insulin, sulfonylureas, and thiazolidinediones (TZDs), often leads to weight gain through a variety of mechanisms. Weight gain can have adverse consequences for patients with type 2 diabetes, many of whom are overweight or obese, because obesity is linked to insulin resistance and other medical consequences such as cardiovascular disease. TZDs improve glycemic control and insulin sensitivity in patients with type 2 diabetes, despite their potential to cause weight gain. Studies have attempted to elucidate the mechanisms behind the apparent paradox of TZDs improving insulin sensitivity while causing weight gain. Data indicate that with TZD treatment, there is a favorable shift in fat distribution from visceral to subcutaneous adipose depots that is associated with improvements in hepatic and peripheral tissue sensitivity to insulin. Although weight gain may occur with TZD therapy, it is not inevitable. A weight-management program combining a low-calorie, low-sodium diet with education and behavior modification has been shown to be effective in patients with type 2 diabetes being treated with TZDs. Further research is needed to define the optimal dietary modifications that can be used universally in TZD-treated patients to minimize weight gain while effectively treating insulin resistance and hyperglycemia.

Adipose Tissue↗
PubMed2003

Insulin resistance and risk of chronic kidney disease in nondiabetic US adults.

This study examined the relationship of fasting serum glucose, insulin, C-peptide, glycosylated hemoglobin A (HbA1c), and Homeostasis Model Assessment (HOMA)-insulin resistance to risk of chronic kidney disease (CKD) among 6453 persons without diabetes (fasting glucose <126 mg/dl and not taking diabetes medication) who participated in the Third National Health and Nutrition Examination Survey and were aged 20 yr or older. CKD was defined as an estimated GFR <60 ml/min per 1.73 m(2). The prevalence of CKD was significantly and progressively higher with increasing levels of serum insulin, C-peptide, HbA1c, and HOMA-insulin resistance. After adjustment for potential confounding variables, the odds ratio of CKD for the highest compared with the lowest quartile was 4.03 (95% confidence interval [CI], 1.81 to 8.95; P = 0.001), 11.4 (95% CI, 4.07 to 32.1; P < 0.001), 2.67 (95% CI, 1.31 to 5.46; P = 0.002), and 2.65 (95% CI, 1.25 to 5.62; P = 0.008) for serum insulin, C-peptide, HbA1c levels, and HOMA-insulin resistance, respectively. For a one SD higher level of serum insulin (7.14 micro U/ml), C-peptide (0.45 Deltamol/ml), HbA1c (0.52%), and HOMA-insulin resistance (1.93), the odds ratio (95% CI) of CKD was 1.35 (1.16 to 1.57), 2.78 (2.25 to 3.42), 1.69 (1.28 to 2.23), and 1.30 (1.13 to 1.50), respectively. These findings combined with knowledge from previous studies suggest that the insulin resistance and concomitant hyperinsulinemia are presented in CKD patients without clinical diabetes. Further studies into the causality between insulin resistance and CKD are warranted.

Blood Glucose↗
PubMed2003

Is weight loss possible in patients treated with thiazolidinediones? Experience with a low-calorie diet.

BACKGROUND: Weight gain is a frequent side-effect of thiazolidinediones, possibly related to fluid retention and stimulation of pre-adipocyte differentiation. METHODS: We report our experience with a low-calorie diet (800 cal, sodium content 1500 mmol/day) combined with behavior modification on eight patients treated with thiazolidinediones (six pioglitazone and two rosiglitazone). RESULTS: All patients had reported previous weight gain following treatment with thiazolidinediones. All patients lost weight over 12 weeks in the program with their mean +/- SD body weight falling from 270 +/- 54 lbs (123 +/- 25 kg) to 244 +/- 61 lbs (111 +/- 28 kg) (p < 0.01). The weight loss observed was no different from that observed in 16 age- and gender-matched patients with type 2 diabetes not treated with thiazolidinediones (from 263 +/- 54 lbs (120 +/- 25 kg) to 239 +/- 52 lbs (109 +/- 24 kg); p < 0.01). Glycemic control improved while reducing insulin treatment. Blood pressure control also improved and antihypertensive medications were decreased. The degree and time course of weight loss is no different from that in patients treated with other diabetic therapies and is associated with improved glycemic and blood pressure control. CONCLUSIONS: We conclude that a program of caloric restriction and behavior modification is effective in leading to weight loss in patients treated with thiazolidinediones. This effect is reassuring, since thiazolidinediones stimulate adipogenesis.

Adult↗
PubMed2003

Clinical significance of targeting postprandial and fasting hyperglycemia in managing type 2 diabetes mellitus.

Measurement of glycosylated hemoglobin (HbA1c) remains the gold standard for the assessment of glycemic control in patients with type 2 diabetes. Recent investigations have studied the correlations between HbA1c levels and other aspects of glucose metabolism, specifically, postprandial glucose (PPG) and fasting plasma glucose (FPG). The results suggest that PPG is also important to overall glycemic control and may be a better index of glucose regulation than FPG. Further, elevated PPG values have been associated with cardiovascular complications and cardiovascular mortality. Such evidence has led to recommendations that PPG levels be monitored as part of type 2 diabetes management, in addition to HbA1c and FPG. These glycemic parameters are differentially affected by the various classes of oral antidiabetic agents used in the treatment of type 2 diabetes--sulfonylureas, meglitinides, insulin sensitizers and alpha-glucosidase inhibitors. The sulfonylureas, for example, lower HbA1c, PPG and FPG, while the meglitinides have virtually no effect on FPG. The insulin sensitizer metformin, on the other hand, does not affect PPG levels, whereas the alpha-glucosidase inhibitors, in the presence of a high-carbohydrate diet, can effectively lower PPG. Many patients receive combination therapy, thereby benefiting from multiple mechanisms of glucose control, although in most cases insulin must later be added to the regimen in order to effectively suppress FPG. Thus, all aspects of glucose metabolism appear to be clinically relevant and should be monitored for effective diabetes management. Further study will more precisely define the clinical significance of PPG.

Administration, Oral↗
PubMed2003

Association of hypoglycemia and cardiac ischemia: a study based on continuous monitoring.

OBJECTIVE: In some studies intensive diabetes treatment in patients with type 2 diabetes may be associated with increased cardiovascular events. It is not clear whether these events are related to hypoglycemic episodes. To determine whether episodes of hypoglycemia were more likely to be associated with cardiac ischemia than normoglycemia or hyperglycemia, we carried out a study in 21 patients with coronary artery disease (CAD) and type 2 diabetes treated with insulin who had good glycemic control. RESEARCH DESIGN AND METHODS: We carried out 72-h continuous glucose monitoring along with simultaneous cardiac Holter monitoring for ischemia. Patients also recorded symptoms of cardiac ischemia (chest pain) and symptoms of hypoglycemia. RESULTS: Satisfactory continuous glucose monitoring system recordings were obtained in 19 patients. We recorded 54 episodes of hypoglycemia (blood glucose <70 mg/dl; 26 of these were symptomatic) and 59 episodes of hyperglycemia (blood glucose >200 mg/dl; none symptomatic). Of the 54 episodes of hypoglycemia, 10 were associated with symptoms of chest pain, during 4 of which electrocardiographic abnormalities were documented. In contrast, only 1 episode of chest pain occurred during 59 episodes of hyperglycemia. No chest pain or electrocardiographic abnormalities occurred when the blood glucose was within the normal range. The difference between the frequency of ischemia during hypoglycemia and the frequency during both hyperglycemia and normoglycemia was statistically significant (P < 0.01). There were 50 episodes during which the blood glucose changed by >100 mg over a 60-min period, and ischemic symptoms occurred during 9 of these episodes (P < 0.01 compared with stable normoglycemia or hyperglycemia). CONCLUSIONS: Hypoglycemia is more likely to be associated with cardiac ischemia and symptoms than normoglycemia and hyperglycemia, and it is particularly common in patients who experience considerable swings in blood glucose. These data may be important in the institution of insulin treatment and attempting near-normal glycemia in patients with known CAD. Further research is needed to determine strategies to prevent ischemia associated with hypoglycemia.

Blood Glucose↗
PubMed2003

Addition of nateglinide to rosiglitazone monotherapy suppresses mealtime hyperglycemia and improves overall glycemic control.

OBJECTIVE: To determine the effects of nateglinide added to rosiglitazone monotherapy on glycemic control and on postprandial glucose and insulin levels in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: This 24-week, multicenter, double-blind, randomized study compared the efficacy of nateglinide (120 mg a.c.) and placebo added to rosiglitazone monotherapy (8 mg q.d.) in 402 patients with type 2 diabetes with HbA(1c) between 7 and 11% (inclusive). Efficacy parameters tested included HbA(1c) and plasma glucose and insulin levels in the fasting state and after a standardized meal challenge. Safety data were also collected. RESULTS: In placebo-treated patients, HbA(1c) did not change (Delta = 0.0 +/- 0.1%). In patients randomized to nateglinide, HbA(1c) decreased from 8.3 to 7.5% (Delta = -0.8 +/- 0.1%, P < 0.0001 vs. placebo). Target HbA(1c) (<7.0%) was achieved by 38% of patients treated with combination therapy and by 9% of patients remaining on rosiglitazone monotherapy. In nateglinide-treated patients, fasting plasma glucose levels decreased by 0.7 mmol/l, 2-h postprandial glucose levels decreased by 2.7 mmol/l, and 30-min insulin levels increased by 165 pmol/l compared with no changes from baseline of these parameters with placebo added to rosiglitazone (P < 0.001). CONCLUSIONS: By selectively augmenting early insulin release and decreasing prandial glucose excursions, nateglinide produced a clinically meaningful improvement in overall glycemic exposure in patients with type 2 diabetes inadequately controlled with rosiglitazone. Therefore, nateglinide substantially improves the likelihood of achieving a therapeutic target of HbA(1c) <7.0%.

Blood Glucose↗
PubMed2002

The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on oxidative enzymes in adipocytes and liver.

Reactive oxygen species are produced in response to environmental toxins, and previous studies have suggested that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) damages a number of target organs through the generation of oxygen free radicals and oxidative stress. Upon exposure, TCDD becomes concentrated in adipose tissue, and adversely affects many organs, including liver. This study examined whether oxidative stress was induced in adipocytes and liver that were exposed to TCDD. 3T3-F442A adipocyte cultures were treated with TCDD (5-200 nM) for up to 72 h, and the activity and mRNA levels of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) in adipocyte cell lysates were measured. The addition of 50 nM TCDD induced a two-fold increase in SOD activity after 48 h (P<0.05). In contrast, TCDD had no significant effect on the activity of catalase or GSH-Px in the adipocytes, and the increase in SOD activity was not accompanied by a change in SOD mRNA levels. To assess the effects of TCDD on oxidative stress enzymes in vivo, male Sprague-Dawley rats were injected weekly for 8 weeks with 30 ng/kg TCDD. In addition, the rats were fed either a low-fat complex-carbohydrate (LFCC) diet, or a high fat sucrose diet (HFS). The HFS diet has previously been shown to induce mild obesity and insulin resistance, without inducing diabetes. SOD, catalase, and GSH-Px activities were measured in the liver and adipose tissue of these rats. TCDD injection resulted in a 52% decrease in catalase activity in the adipose tissue of HFS rats (P<0.05). In contrast, SOD and GSH-Px activities were not altered in adipose tissue of TCDD-injected rats. In liver, however, there were significant decreases in GSH-Px activity in response to TCDD. This effect of TCDD was observed in both the LFCC and HFS dietary groups. In addition, GSH-Px activity in the HFS rats was significantly decreased when compared to GSH-Px activity in LFCC rats, in both TCDD-treated and control groups, suggesting that TCDD and a high fat diet may combine to exacerbate oxidative stress. Thus, TCDD induces complex changes in enzymes of oxidative stress in both adipocytes and liver. In adipocytes, these changes occurred post-transcriptionally, as there were no changes in mRNA levels. In addition, a high fat diet per se also resulted in a decrease in GSH-Px activity in liver.

Adipocytes↗
PubMed2002

The effect of troglitazone on plasma homocysteine, hepatic and red blood cell S-adenosyl methionine, and S-adenosyl homocysteine and enzymes in homocysteine metabolism in Zucker rats.

We studied the effect of troglitazone on the plasma concentrations of homocysteine (tHcy), the erythrocyte and hepatic concentrations of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), and the hepatic activities of cystathionine-beta-synthase (C beta S) and methylenetetrahydrofolate reductase (MTHFR) in lean and fatty Zucker rats (a model of insulin resistance). Four groups of female Zucker rats were studied. Troglitazone (200 mg/kg) was administered by gavage daily for 3 weeks to lean and fatty Zucker rats. The other 2 groups served as controls. The blood parameters were determined at days 0, 10, and 21. The hepatic SAM and SAH concentrations and MTHFR and C beta S were measured in the 3-week liver samples. Plasma homocysteine fell significantly in all troglitazone-treated animals from a mean +/- SD of 7.6 +/- 1.5 micromol/L to 4.5 +/- 1.1 micromol/L (P <.02) but not in control animals (5.7 +/-1.8 micromol/L to 5.9 +/- 1.8 micromol/L). The decreases induced by troglitazone in homocysteine were seen in both the lean and the fatty Zucker rats. This was accompanied by significant rises in the hepatic concentrations of SAH and SAM + SAH. In addition, a significant decline in the hepatic SAM/SAH ratio was observed. The mean +/- SD hepatic C beta S (expressed as nmol of cystathionine formed at 37 degrees C) in the troglitazone-treated rats was 1,226 +/- 47 nmol/h/mg protein, which was significantly higher than that in the control group (964 +/- 64 nmol/h/mg protein; P =.03). We conclude that troglitazone lowers plasma homocysteine in insulin-resistant animals. The homocysteine-lowering effects of troglitazone may be mediated in part by a shift in the concentrations of tHcy and its related metabolites from the blood to the liver as well as by an upregulation of hepatic C beta S activity. These data support the hypothesis that insulin may regulate homocysteine metabolism through regulation of hepatic C beta S activity, although activity of other hepatic enzymes not studied here may also contribute to these observations.

Animals↗
PubMed2002

Drugs affecting homocysteine metabolism: impact on cardiovascular risk.

Elevated total plasma homocysteine has been established as an independent risk factor for thrombosis and cardiovascular disease. A strong relationship between plasma homocysteine levels and mortality has been reported in patients with angiographically confirmed coronary artery disease. Homocysteine is a thiol containing amino acid. It can be metabolised by different pathways, requiring various enzymes such as cystathionine beta-synthase and methylenetetrahydrofolate reductase. These reactions also require several co-factors such as vitamin B6 and folate. Medications may interfere with these pathways leading to an alteration of plasma homocysteine levels. Several drugs have been shown to effect homocysteine levels. Some drugs frequently used in patients at risk of cardiovascular disease, such as the fibric acid derivatives used in certain dyslipidaemias and metformin in type 2 (non-insulin-dependent) diabetes mellitus, also raise plasma homocysteine levels. This elevation poses a theoretical risk of negating some of the benefits of these drugs. The mechanisms by which drugs alter plasma homocysteine levels vary. Drugs such as cholestyramine and metformin interfere with vitamin absorption from the gut. Interference with folate and homocysteine metabolism by methotrexate, nicotinic acid (niacin) and fibric acid derivatives, may lead to increased plasma homocysteine levels. Treatment with folate or vitamins B6 and B12 lowers plasma homocysteine levels effectively and is relatively inexpensive. Although it still remains to be demonstrated that lowering plasma homocysteine levels reduces cardiovascular morbidity, surrogate markers for cardiovascular disease have been shown to improve with treatment of hyperhomocystenaemia. Would drugs like metformin, fibric acid derivatives and nicotinic acid be more effective in lowering cardiovascular morbidity and mortality, if the accompanying hyperhomocysteinaemia is treated? The purpose of this review is to highlight the importance of homocysteine as a risk factor, and examine the role and implications of drug induced modulation of homocysteine metabolism.

Anticonvulsants↗
PubMed2002

Effects of the thiazolidinediones on cardiovascular risk factors.

Rosiglitazone and pioglitazone are medications from the thiazolidinedione class of compounds currently available for the treatment of type 2 diabetes mellitus. Traditionally used to enhance insulin sensitivity and decrease plasma insulin levels, added applications have emerged beyond those involving glycemic control. Cardiovascular risk factors associated with insulin resistance such as elevated blood pressure, dyslipidemia, abnormal fibrinolysis, and endothelial and vascular dysfunction have been shown to improve after thiazolidinedione treatment. Therapy with rosiglitazone or pioglitazone has been found to modify vascular reactivity and other processes involved in atherosclerosis. There may be differences between the agents in their effects on plasma lipid characteristics and particle size. These agents serve as excellent adjuncts to oral and insulin therapy for patients with type 2 diabetes mellitus and hold promise for the prevention of cardiovascular disease associated with the insulin resistance syndrome. Clinical trials are in progress to determine whether such therapy will lead to a reduction in cardiovascular events.

Cardiovascular Diseases↗