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Serum lipoproteins are important risk factor variables for coronary artery disease (CAD). Studies of a large population of young individuals show changes in lipoproteins in childhood are race- (black-white) and sex-specific and certain changes occur during growth phases. White boys show adverse changes in lipoprotein levels during sexual maturation that mark them at high risk for CAD. Further, low-density lipoprotein particles are relatively apolipoprotein B enriched in white children, especially boys, a characteristic associated with low levels of high-density lipoprotein cholesterol. The impact of apolipoprotein E genotype on serum lipoproteins seen in adults is already apparent in children, which may be helpful in identifying a high-risk group. Observations of child-parent associations in terms of parental myocardial infarction and levels of lipoprotein variables in the offspring suggest that childhood profiles of lipoprotein (a), apolipoprotein A-I, and apolipoprotein B may be helpful as markers of future CAD. Clustering of increased levels of truncal fat, insulin, and blood pressure is often seen in young adults with an adverse lipoprotein profile. This clustering is related to subtle abnormalities in carbohydrate and lipid metabolism and obesity in childhood. The fact that lipoprotein levels persist from childhood to young adulthood underscores the importance of detection and management of dyslipidemia early in life.
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PMID:Childhood lipoprotein profiles and implications for adult coronary artery disease: the Bogalusa Heart Study. 750 26

Reviewed herein are data supporting the hypothesis that insulin and the sympathoadrenal system are involved in the pathogenesis of hypertension in the obese. Data from the Normative Aging Study, a population-based cohort followed in Boston, confirm other epidemiologic reports of a direct relationship between upper-body obesity, hyperinsulinemia, and hypertension. Because insulin is known to stimulate the sympathetic nervous system (SNS), the possibility that insulin-mediated sympathetic stimulation contributed to hypertension in the obese was investigated by the analysis of 24-h urinary norepinephrine (NE) excretion in this group. Urinary NE was directly correlated with body mass index and waist/hip ratio, supporting increased SNS activity in the obese. Epinephrine excretion, an index of adrenal medullary activity, was inversely related to obesity, and both high insulin and low epinephrine levels were independently correlated with lower levels of high-density lipoprotein cholesterol and higher levels of triglycerides. These results are consistent with the hypothesis that insulin-mediated sympathetic stimulation results in hypertension from concomitant sympathetic stimulation of the heart, vessels, and kidney. Reciprocal changes in adrenal medullary function contribute to the associated dyslipidemia. Therapeutic strategies aimed at diminishing insulin resistance and lowering insulin levels, and antagonizing the effects of sympathetic stimulation on the heart, the vessels, and the kidneys, would appear to have a solid physiological rationale in the obese.
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PMID:Pathophysiology of obesity-related hypertension: role of insulin and the sympathetic nervous system. 751 90

Hypertension is associated with insulin resistance and dyslipidemia in a syndrome named X. Epidemiologic evidence also supports a link between hyperinsulinemia and blood pressure (BP), independent of obesity and non-insulin-dependent diabetes mellitus. To assess the possible role of insulin receptors in this syndrome, we studied insulin binding by erythrocyte ghosts in patients with moderate essential hypertension with or without fasting or postglucose hyperinsulinemia. We measured plasma glucose and insulin before and at 30, 60, and 120 min after administration of 75 g glucose in 62 hypertensive patients and 20 matched normotensive controls. Both groups had comparable age (mean 45 years) and waist/hip ratios (mean 0.88). Patients undergoing antihypertensive treatment did not receive antihypertensive medication for 3 weeks. Patients with fasting or postglucose hyperglycemia were excluded from the study. Insulin binding to erythrocyte ghosts was significantly decreased (p < 0.001) to almost half the values of controls (6.5% specific binding) in both patients with hyperinsulinemic (3.2% specific binding) and those with normoinsulinemic (3.9% specific binding) hypertension. Scatchard analysis demonstrated that this was due to a lesser number of insulin receptors. These data indicate that patients with essential hypertension can show decreased erythrocyte insulin receptors without detectable hyperinsulinemia.
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PMID:Diminished insulin receptors on erythrocyte ghosts in nonobese patients with essential hypertension independent of hyperinsulinemia. 752 93

The epidemic of coronary artery disease (CAD), the main cause of deaths in 'western' countries, could have been avoided through appropriate lifestyles of eating and activities. The dramatic decline in CAD in some countries is more difficult to attribute to changes that is the rapid rise in eastern European countries (high dietary saturated fat plus smoking). While CAD rates in Asian/Pacific countries are relatively low, subgroups, mainly through affluence, show high rates. Inappropriate eating patterns are superimposed on genetic factors (commonly diabetes in Asia) and on other lifestyle factors (smoking). Eventually the combination of dyslipidemia ('high triglyceride-low high density lipoprotein' in Asia Pacific rim), plus smoking plus hypertension (part salt related) may trigger a CAD epidemic. The challenge is better public health management including balancing the nature of the food supply with the nutritional needs for preventing CAD through national food and nutrition policies. Critical are the sources of fats (often key economic commodities), the amount of salt, preventing obesity especially of the central type, and provision of plant foods with a better understood mix of fatty acids, antioxidants and specific starches and nonstarch polysaccharides. The anti-atherogenic effects of specific antioxidants and of n-3 fatty acids in fish probably explain the lower than expected CAD rates in several countries. Although many of the risk factors are common, important regional differences demand national strategies, while providing wider perspectives on the multifactorial nature of the disease and the value of certain traditional diets.
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PMID:Controlling coronary risk through nutrition. 758

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

Many models of diabetes dyslipidemia are available. Animals with chemically-induced diabetes have been used to study insulin-dependent diabetes. Hypercholesterolemia in streptozotocin-induced diabetes in rats results from increased intestinal absorption and synthesis of cholesterol. Lipoproteins from diabetic rats are oxidized and demonstrate cytotoxicity, a feature which can be prevented by insulin or antioxidant treatment. Diabetic rabbits fed a cholesterol-rich diet do not develop atherosclerotic lesions because accumulated VLDL are apo E-depleted, too large and do not enter into the arterial wall. Models for non-insulin-dependent diabetes (NIDDM) are obtained through selective breeding or dietary conditions. The obese Zucker rat (fa/fa) is characterized by hyperphagy, hyperglycaemia, hyperinsulinemia, insulin-resistance, hypertriglyceridemia and hypercholesteolemia. It responds to dietary, hormonal and drug treatments, but does not develop atherosclerosis spontaneously. It is used as a model for obesity, NIDDM and type IV hyperlipidemia. The JCR:LA cp rat bears the corpulent gene and develops similar characteristics to those of the Zucker rat. However, insulin-resistance is more severe in homozygous males (cp/cp), and cardiovascular lesions are observed. Their appearance is reduced by treatments which decrease hyperinsulinemia and insulin resistance but not by lowering lipid levels alone. The sand rats (Psammomys obesus) develop obesity and NIDDM when fed a laboratory diet. When cholesterol and anti-thyroid drug are added to the diet, they develop cardiovascular lesions. This species constitutes a new model for studying atherosclerosis-related diabetes.
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PMID:Dyslipidemia and diabetes: animal models. 762 69

Hypercholesterolemia is the most frequently identified coronary heart disease risk factor in childhood, with 25% or more of children in the United States reported to have borderline high or high levels. This article provides a summary of current recommendations for cholesterol screening, evaluation, treatment, and follow-up in the pediatric office or clinic setting. Detection and treatment of pediatric dyslipidemia, however, is only one component of preventive cardiology and should be addressed in routine well child and adolescent care along with major efforts to prevent cigarette smoking, obesity, inactivity, and hypertension.
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PMID:Guidelines for screening, evaluating, and treating children with hypercholesterolemia. 762 80

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 management of essential hypertension can no longer be directed toward an isolated reduction in arterial pressure. Optimal reduction in the risk factors associated with hypertension and cardiovascular disease hopefully will reduce coronary heart disease, angina, fatal and nonfatal myocardial infarction, left ventricular hypertrophy, congestive heart failure, and sudden death. Hypertension is a genetic and acquired syndrome that consists of dyslipidemia, insulin resistance and carbohydrate intolerance, central obesity, renal abnormalities, structural abnormalities of smooth muscle, and ion transport abnormalities (membranopathy). The selection of pharmacologic agents should improve the components of the hypertensive syndrome by utilizing the "subsets of hypertension approach" to treatment.
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PMID:The management of hypertension and associated risk factors for the prevention of long-term cardiac complications. 769 47

The early lesions of atherosclerosis in youth are strongly related to antemortem levels of total and low-density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and triglyceride to ponderal index and to blood pressure. The major apolipoproteins of LDL and high-density lipoprotein (HDL), apoB and apoA1 respectively, and levels of Lp(a) lipoprotein are often abnormal in children born in a family with premature coronary artery disease (CAD). Other risk factors for CAD include obesity, high blood pressure, cigarette smoking, diabetes mellitus, positive family history of CAD, and physical inactivity. Children from families with premature CAD, dyslipidemia, or hypertension, and/or two other risk factors should have a lipoprotein profile determined. Treatment begins with a diet low in total fat, saturated fat, and cholesterol, combined with treatment of overnutrition and obesity, if necessary, and regular habits of aerobic physical activity. Children with inherited disorders of LDL metabolism may require the addition of lipid-lowering therapy. The early detection and treatment of youth at risk for premature CAD offer the greatest promise to decrease morbidity and mortality.
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PMID:Detection and treatment of elevated blood lipids and other risk factors for coronary artery disease in youth. 769 75


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