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)

Cigarette smoking has been associated with increased upper body fat deposition, as estimated by the waist to hip ratio, which has been shown to be associated with glucose intolerance and dyslipidemia in nonsmoking subjects. Whether smoking is at the origin of central adiposity and its related metabolic disturbances is unclear. Moreover, it is controversial whether smoking influences fuel metabolism. Therefore, young healthy male volunteers smoking more than 10 cigarettes/day for more than 5 yr (n = 14) were compared with nonsmokers (n = 13) matched for age, sex, body mass index, alcohol consumption, physical activity, as well as family history for hypertension, diabetes, obesity, and coronary heart disease. After an overnight fast, blood was drawn for chemistry, body composition was assessed by dual energy x-ray absorptiometry, and fuel metabolism was determined by indirect calorimetry. Nicotine uptake was estimated by 24-h urinary excretion of cotinine. Lean and fat body mass as well as their respective segmental distribution (i.e. arms, trunk, legs, and head), total bone mineral content, resting energy expenditure, and fat, carbohydrate, and protein oxidation were similar between smokers and nonsmokers. In contrast, 24-h urinary cotinine excretion (72.0 +/- 11.4 vs. 0.8 +/- 0.2 mumol/L.24 h; P < 0.001), plasma glucose (4.62 +/- 0.09 vs. 4.25 +/- 0.1 mmol/L; P < 0.01), total cholesterol (4.87 +/- 0.15 vs. 4.27 +/- 0.16 mmol/L; P < 0.02), low density lipoprotein cholesterol (3.05 +/- 0.19 vs. 2.43 +/- 0.16 mmol/L; P < 0.02), and apolipoprotein B concentrations (1.09 +/- 0.11 vs. 0.83 +/- 0.03 mmol/L; P < 0.03) were all higher in smokers than in nonsmokers. In smokers, 24-h urinary cotinine excretion positively correlated with the waist to hip ratio (r = 0.58; P = 0.03) and negatively with hip circumference (r = 0.87; P < 0.001). Moreover, 24-h cotinine excretion positively correlated with fat oxidation (r = 0.57; P = 0.03), but was independent of the other metabolic parameters studied. These results suggest that the dyslipidemia and glucose intolerance observed in smokers are not related to either central obesity or the amount of nicotine inhaled, but, rather, are due to some other component in cigarette smoke. In contrast, in smokers, fat oxidation increases with increasing nicotine uptake, a fact that might account for the often observed weight gain after cessation of smoking, thus suggesting different mechanisms of action of tobacco consumption on cholesterol and glucose metabolism on one side and fat oxidation on the other.
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PMID:Impact of chronic cigarette smoking on body composition and fuel metabolism. 760 76

Arterial hypertension is a chronic condition regarded as one of the main risk factors for development of coronary atherosclerosis. As dyslipidemia and reduced glucose tolerance are also risk factors for coronary disease, it is considered important to use antihypertensive drugs having no negative effects on lipid and glucose metabolism when diabetic patients are treated for hypertension. Lacidipine, a new dihydropyridine-like calcium antagonist, has been shown in in vivo and in vitro preclinical studies to possess potent, long-lasting antihypertensive activity. The present study compared the efficacy and safety of once-daily treatment with lacidipine versus nifedipine SR given twice-daily in non-insulin-dependent diabetic patients. Results have shown a similar efficacy of the two treatments: 6 months later, both drugs had reduced blood pressure values [lacidipine from 184.8/105.2 mm Hg to 144.4/87.1 mm Hg; nifedipine slow-release (SR) from 182.3/106.8 mm Hg to 143.6/89.4 mmHg]. However, lacidipine exhibited a lower incidence of adverse events (particularly ankle edema and tachycardia) than nifedipine SR. Finally, both treatments showed no negative effect on metabolic parameters (total cholesterol, high-density lipoprotein cholesterol, triglycerides, and blood glucose).
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PMID:Calcium antagonist antihypertensive treatment of non-insulin-dependent diabetics: efficacy and safety of lacidipine versus nifedipine SR. 760 94

Several risk factors for the development of microalbuminuria such as: blood glucose unbalance, high blood pressure, dyslipidemia, genetic susceptibility have been described and discussed. The object of this study was to ascertain the importance of these factors. To this end albuminuria was measured using MICRAL-test in two groups of subjects: 100 diabetics (43 type I (insulin-dependent) and 57 type II (non insulin-dependent), and 54 controls. According to diabetes duration, the cases were divided into four sub-groups (less than 5 years; 5-9 yrs; 10-19 yrs; over 20 yrs). The mean values of albuminuria were assessed in the two groups (diabetics and controls) and also for each subgroup of diabetes duration. It was found that in insulin-dependent diabetes mellitus (IDDM), the duration of the disease is an important determinant of albuminuria, a significant increase in its values being observed after 10 yrs of diabetes evolution. The importance of diabetes duration, glucose unbalance and high blood pressure (BP) as possible determinants of microalbuminuria was assessed by comparing the micro- and normoalbuminuric diabetics. Our results are similar to those reported by many other authors, showing that these are important risk factors for microalbuminuria, especially in IDDM.
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PMID:Determinants of microalbuminuria in diabetics. 761 2

Upper-body obesity (UBO) in white women is associated with increased fatty acid turnover and resistance to the effects of insulin on systemic glucose metabolism. The present study determined whether the abilities of insulin to stimulate glucose transport and suppress lipolysis are impaired in adipocytes from white UBO (W-UBO) women. Because the clinical risks associated with UBO are attenuated in black women, the effects of race on adipocyte insulin sensitivity were assessed. Forty-two healthy, equally obese women were selected for study on the basis of race (black or white) and body fat distribution (UBO or lower-body obesity [LBO]). In white women, both abdominal and gluteal fat cells from the UBO versus LBO group were less responsive to the stimulatory effects of insulin on glucose uptake and less sensitive to the antilipolytic effects of insulin and the adenosine analog, phenylisopropyladenosine (PIA). In contrast, in black women, fat cells from UBO and LBO groups were equally sensitive to the stimulatory effects of insulin on glucose transport and the suppressive effects of insulin and PIA on lipolysis. These in vitro data correlate well with previous clinical findings that UBO in white women but not in black women is associated with insulin resistance and dyslipidemia. Thus, resistance to the antilipolytic effects of insulin and adenosine at the level of adipose tissue may increase systemic lipolysis and play a role in the development or maintenance of peripheral insulin resistance associated with UBO in white women, but not in black women.
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PMID:Insulin resistance in adipocytes of obese women: effects of body fat distribution and race. 763 56

The study was undertaken to evaluate the development and association of parameters related to the metabolic syndrome during celiprolol treatment. Hyperinsulinemic euglycemic clamp and independent oral glucose tolerance tests (OGTT) were performed on 25 nondiabetic patients with controlled hypertension and dyslipidemia. The tests were carried out during the patients' previous antihypertensive monotherapy (beta- or Ca-blocker, or an ACE inhibitor), and after 6 and 12 months of celiprolol treatment. About one third of patients were randomized to a control group in which treatment was kept unchanged. Insulin sensitivity index (ISI), measured by the euglycemic clamp test, increased 35% in the celiprolol group at 6 months and remained at that level at 12 months, independent of the previous treatment (p = 0.03, compared to the change in the control group). During a 2 hour OGTT, incremental glucose area under the curve (AUC) decreased from 4.5 to 1.9 hr x mmol/l during 6 months of celiprolol treatment, and decreased further to 1.5 hr x mmol/l at 12 months (p < 0.001). Insulin AUC decreased from 113 to 72 hr x mU/l, and decreased further to 68 hr x mU/l (p < 0.01). All insulin parameters in OGTT were highly significant (p < 0.0001) and inversely associated with ISI. Insulin AUC had the best linear correlation with ISI (r = -0.682, p < 0.0001). Glucose parameters in OGTT correlated only weakly and inversely with insulin sensitivity. From the fasting serum lipids, triglycerides showed an inverse (p < 0.001) and HDL a weak (p < 0.05) positive association with ISI. Four out of 20 metabolic, clinical, and demographic parameters proved to be independently significant predictors for ISI in multiple regression analysis. These were insulin AUC, fasting insulin levels, triglyceride values, and age. The coefficient of determination in this four-parameter linear model was 69%. In this preliminary, observer-masked trial with a limited control group, celiprolol improved the impaired insulin sensitivity and glucose tolerance of dyslipidemic hypertensive patients. A fairly predictive model can be formulated to evaluate the peripheral insulin sensitivity of hypertensive patients with suspected metabolic syndrome using OGTT with serum insulin determinations.
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PMID:Association between serum lipids, glucose tolerance, and insulin sensitivity during 12 months of celiprolol treatment. 766 96

Microalbuminuria in diabetic patients is associated with ischemic heart disease and insulin resistance. We previously found a 9% prevalence of microalbuminuria in a nondiabetic population that we have reassessed, investigating associations of microalbuminuria with hypertension, dyslipidemia, hyperinsulinemia, and sodium-lithium countertransport. Of 125 subjects reexamined, 42 had been microalbuminuric 3 years previously. Twelve of these (29%) were microalbuminuric on at least one sample at follow-up, and 30 (76%) were normoalbuminuric on two. Of the 79 previously normoalbuminuric subjects, 12 (15%) became microalbuminuric on one sample, while 67 (85%) remained normoalbuminuric. Subjects who were microalbuminuric at both screening and recall were older (mean +/- SD, 65.9 +/- 11 versus 59.1 +/- 10.2 years, P = .04), with a higher waist-to-hip ratio (0.93 +/- 0.09 versus 0.86 +/- 0.08, P = .008) and at recall, on univariate analysis, had higher specific insulin (44.2 [range, 16.9 to 157.0] versus 28.4 [7.4 to 129.0] pmol/L, P = .005), intact proinsulin (5.1 [1.5 to 11.0] versus 3.0 [0.8 to 14.6] pmol/L, P = .003), and des-31,32-proinsulin (5.0 [0.5 to 9.8] versus 1.0 [0.5 to 12.2] pmol/L, P = .004) concentrations. There was also a significant difference in des-31,32-proinsulin concentration, after adjustment for covariates (P = .013), between subjects classified either as microalbuminuric or as normoalbuminuric at screening. There was no difference in body mass index; fasting blood glucose; systolic or diastolic blood pressure; total, HDL, or LDL cholesterol; triglycerides; plasminogen activator inhibitor-1; or sodium-lithium countertransport activity between consistently normoalbuminuric and persistently microalbuminuric subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Longitudinal study of associations of microalbuminuria with the insulin resistance syndrome and sodium-lithium countertransport in nondiabetic subjects. 767 Sep 46

Epidemiologic studies have demonstrated hypertension is one of the risk factors of atherosclerosis, but the underlying mechanism is complex and still controversial. Salt-sensitivity is an important characteristic demonstrated in a subgroup of hypertension, since the factors relating to salt-sensitivity also influence smooth muscle hypertrophy and proliferation which are essential processes of atherosclerosis. Insulin resistance is also involved in the causal relationship between hypertension and atherosclerosis, because accumulating data indicate a central role of insulin resistance in patients with hypertension, glucose-intolerance and dyslipidemia. Vasoacting substances give direct effects on not only the tension but also the growth of smooth muscle cells, namely vasodilators, such as nitric oxide and atrial natriuretic peptides inhibit the proliferation of smooth muscle cells. On the other hand, vasoconstrictors such as angiotensin II, vasopressin and endothelin promote the proliferation of smooth muscle cells. The factors which influence both tension and proliferation of smooth muscle cells may play a central role in the relationship between hypertension and atherosclerosis.
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PMID:[The role of hypertension as a risk factor of atherosclerosis]. 769 22

The metabolic syndrome usually goes along with abdominal obesity: diabetes type II, hypertension, dyslipidemia, and gout are often associated. The common characteristic is the resistance to insulin action. Reasons for the metabolic syndrome are--besides a genetic determination--overnutrition, physical inactivity, and alcohol consumption. Therefore, a causal therapy aims at the elimination of these factors. Consequently, the non-pharmacological therapy of the metabolic syndrome should be emphasized. The most important treatment is the reduction of body weight in the presence of obesity which is relevant for almost 90% of the patients. Body weight can rapidly be diminished by hypocaloric diets. Both, conventional reducing diets or formula diets may be used for weight reduction. Total fasting should not be performed for several reasons. For minor weight reduction or weight maintenance following a period of rapid weight loss with a hypocaloric diet, increased physical activity also lowers weight or prevents relapsing. Aims of therapeutical procedures are the elimination or amelioration of insulin resistance and subsequently the diseases of the metabolic syndrome. Both methods, reducing diet and physical training, act on various factors related to insulin resistance. For example, hypocaloric diets activate thyroxine kinase of the insulin receptor and reduce glucose and insulin in plasma. Physical training reduces not only insulin and glucose in plasma but also free fatty acids in addition and increases capillary density in skeletal muscle. Using the glucose clamp technique, diets and training are equally effective in improving glucose metabolism. Compared to these non-pharmacological methods drugs are less convincing. Since the non-pharmacological treatment implies behavioral changes with regard to nutrition, physical activity and alcohol consumption, simple instructions are not sufficient. Usually long-lasting changes in life style are necessary in order to achieve health improvement. Therefore, health care programs on individual or social basis are required in order to improve nutrition and increase physical activity. However, long-acting effects are difficult to achieve in adults; more promising is the prevention of insulin resistance.
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PMID:[Non-pharmacological therapy of metabolic syndrome]. 771 78

In addition to high blood pressure, patients with hypertension often have insulin resistance, dyslipidemia and increased sympathetic tone. An increased sympathetic tone can negatively affect glucose utilization through three distinct mechanisms; a direct beta-adrenoreceptor-mediated insulin resistance, through conversion to more insulin resistant fast twitch fibers and through alpha-adrenergic vasoconstriction which may decrease the delivery of insulin and glucose to the skeletal muscle cells. The insulin resistance in turn may be responsible for the observed dyslipidemia in hypertension. The sympathetic overactivity in hypertension reflects a chronic activation of defense/vigilance reaction. The increase of cardiac output, blood pressure and insulin resistance in the course of the defense reaction are viewed as an appropriate preparatory response to facilitate muscular exercise (through higher cardiac output and increased pressure) and preserve (through insulin resistance) the optimal supply of glucose to the brain. The defense reaction may have been useful in evolution and may have offered survival advantage. In modern times with prolonged life expectancy the previously useful response (in evolutionary terms) contributes to a faster and deleterious wear and tear of the cardiovascular system.
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PMID:The defense reaction: a common denominator of coronary risk and blood pressure in neurogenic hypertension? 773 82

Recent reports have shown that the frequency of the homozygous deletion genotype (DD) of the angiotensin-converting enzyme (ACE) gene is highly associated with myocardial infarction and cardiomyopathy, particularly in those considered to be at low risk for coronary heart disease (CHD) on the basis of their apoB or LDL cholesterol concentrations. The present study was initiated to extend this inquiry by exploring the possibility that the ACE/DD genotype might be associated with risk factors not evaluated in the initial reports. Consequently, we determined the ACE genotype in 181 subjects, 124 with normal glucose tolerance and 57 with noninsulin-dependent-diabetes mellitus (NIDDM), and compared various aspects of glucose, insulin, and lipoprotein metabolism in the three ACE genotypes. In general, normal subjects with the DD genotype had a lower body mass index, were more insulin sensitive (as assessed by the insulin suppression test), and had lower plasma glucose and insulin responses to oral glucose. In addition, plasma triglyceride and cholesterol concentrations were lowest and HDL cholesterol concentrations highest in the DD group. However, the only statistically significant differences were between the ID and DD groups; the latter had lower values for body mass index, was more insulin sensitive, and had a lower plasma insulin response to oral glucose. Similar but insignificant trends were noted in the patients with NIDDM. The present results show that subjects with the ACE/DD genotype are not at increased risk for CHD because of insulin resistance, relative hyperglycemia and hyperinsulinemia, or a dyslipidemia characterized by a high triglyceride and low HDL cholesterol concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between deletion polymorphism of the angiotensin-converting enzyme gene and insulin resistance, glucose intolerance, hyperinsulinemia, and dyslipidemia. 777 33


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