Effect of nutrition on combined hyperlipidemia

Academic education for nursing has made a major impact on the development of nursing science, on the quality of nursing practice, and on the image of nursing. This was possible because of the close cooperation between education and nurses working in the various health services. Examples from several countries illustrate the process and outcomes of such mutual collaboration.     

Insulin resistance in patients with familial combined hyperlipidemia and coronary artery disease

The minimum model modified by the administration of insulin provides an objective and relatively easily measured index of peripheral sensitivity to insulin which was significantly lower (p <0.02) in familial combined hyperlipidemia (FCH) with ischemic heart disease (IHD) than in FCH without IHD and in control subjects (1.2 +/- 0.6, 1.9 +/- 1.0, 2.9 +/- 1.2 x 10(-4) mU/L/ min, respectively). In patients with FCH, insulin resistance explains, at least in part, their metabolic alterations (hypertension, abnormal glucose tolerance, hyperinsulinemia) and elevated IHD.     

Effect of smoking on vascular resistance in the upper extremities

311 first-degree relatives of 78 consecutive patients with gastric carcinoma and 386 first-degree relative of control probands computer matched from a large Finnish population were studied by means of biopsies from antrum and the fundus and by functional and immunological methods. Both the A and B type of Strickland the McKay as well as the AB types of Pitchumoni and Glass were discernable in the present series and often accumulated in the same families. Particularly the A type associated with high serum gastrin values and parietal cell antibodies revealed a family accumulation. In general members of the same family tended to behave similarly with regard to morhology, function and immunology of the antro-fundal mucosa. The 386 computer matched controls from the general population were treated by means of mathematical methods derived from stochastic theory. It appeared that on a family level there was clearly discernable a line representin families with predominance of fundal gastritis (A type?) which significantly deviated from the main population. However, no such behavior was found as to the families with predominantly antral gastritis (B type?) which behaved like the population at large.     

Effect of night smoking, sleep disturbance, and their co-occurrence on smoking outcomes.

Recent evidence suggests that smoking during the night is an indicator of nicotine dependence and predicts smoking cessation failure. Night smokers are likely to experience disturbance to their sleep cycle when they wake to smoke, but we are not aware of the prevalence of night smokers' self-reported sleep disturbance. Because sleep disturbance also predicts smoking cessation failure, we examined how the pre-cessation risk factors of night smoking and sleep disturbance, and their co-occurrence, predict smoking cessation failure in a 6-week double-blind randomized controlled trial examining whether naltrexone augments the efficacy of the nicotine patch (O'Malley et al., 2006). Smokers (N = 385) completed the Pittsburgh Sleep Quality Index (Buysse, Reynolds, Monk, Berman, & Kupfer, 1989) and a single item of waking at night to smoke pre-cessation. Smoking status was determined at weeks 1, 6, 24, and 48 weeks after quitting. The two main findings were: (a) night smokers reported significantly greater sleep disturbance than nonnight smokers; and (b) smokers with co-occurring night smoking and sleep disturbance experienced significantly greater risk for smoking than smokers with neither risk factor. Results suggest that individuals who both wake during the night to smoke and report clinically-significant sleep disturbance represent a high-risk group of smokers. Future smoking cessation treatment might incorporate strategies related to managing these smokers' sleep habits and physiological dependence on nicotine in order to bolster their cessation outcomes. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.     

Hypertension and insulin resistance

Non insulin dependent diabetes mellitus (NIDDM) and obesity are defined as classical insulin resistant states. Essential hypertension is now also considered to be an insulin resistant state, even in absence of NIDDM or obesity, as shown in epidemiological, clinical and experimental studies. Neither the underlying mechanism nor a direct causality between the two phenomena has been detected as yet, but different hypotheses have been postulated where, on the one hand, insulin resistance and hypertension are considered to be causally related and, on the other hand, they are considered to be parallel phenomena due to genetic and acquired factors. The clarification of the connection between hypertension and insulin resistance seems to be of great clinical importance, since they are both independent risk factors for cardiovascular disease and mortality from cardiovascular complications. This paper gives an overview of the results of recent research on the possible underlying pathogenetic mechanisms linking hypertension and insulin resistance.     

'True' fasting serum insulin level, insulin resistance syndrome and coronary artery disease

BACKGROUND: Increased fasting serum insulin level not associated with hypoglycemia is considered to be a practical indicator of the insulin resistance syndrome, a frequent risk factor for atherosclerosis in industrialized countries. However, in most studies, insulin was measured by using antibodies which cross-react with proinsulin and 31/32, 32/33 split products of insulin. We re-examined the correlations between the insulin resistance syndrome and 'true' fasting serum insulin level. METHODS: We studied 242 post-menopausal women (age 63 +/- 8 years), a population in whom insulin resistance syndrome is particularly frequent. Serum insulin was measured by a recent specific microparticle immunoassay. RESULTS: There was a significant correlation between elevated 'true' fasting serum insulin level and various constituents of the insulin resistance syndrome, such as obesity, dyslipidemia (hypertriglyceridemia, increased apolipoprotein B and decreased high-density lipoprotein cholesterol and apolipoprotein A1 concentrations), increased serum glucose, uric acid levels, and plasminogen activator inhibitor type I concentration, as well as increased frequency of diabetes. There was also a correlation between insulin level and various manifestations of coronary artery disease: patients in the highest quartile of 'true' insulin level had significantly more entirely occluded coronary arteries than in the lowest one. Similarly, in the highest insulin quartile more patients had occluded arteries with lumen diameter stenoses greater than 50% (P < 0.05) and more of them had history of previous myocardial infarction approaching the level of significance (P = 0.0587) than in the lowest one. Most of these correlations were also noted in nondiabetic people. CONCLUSIONS: An increase of 'true' fasting serum insulin level is a useful practical index to identify patients with the insulin resistance syndrome exposed to increased risk of coronary artery disease.     

The insertion allele of the ACE gene I/D polymorphism. A candidate gene for insulin resistance?

BACKGROUND: The insertion/deletion (ID) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with increased coronary heart disease (CHD), although the mechanism of this association is not apparent. We tested the hypothesis that the deletion allele of the ACE gene is associated with insulin resistance. METHODS AND RESULTS: We related ACE genotype to components of the insulin-resistance syndrome in 103 non-insulin-dependent diabetic (NIDDM) and 533 nondiabetic white subjects. NIDDM subjects with the DD genotype had significantly lower levels of specific insulin (DD 38.6, ID 57.1, and II 87.4 pmol.L-1 by ANOVA, P = .011). Non-insulin-treated subjects with the DD genotype had increased insulin sensitivity by HOMA % (DD 56.4%, II 29.4%, P = .027) and lower levels of des 31,32 proinsulin (DD 3.3, II 7.6 pmol.L-1, P = .012) compared with II subjects. There were no differences in prevalence of CHD or levels of blood pressure, serum lipids, or plasminogen activator inhibitor-1 (PAI-1) activity between the three ACE genotypes. In nondiabetic subjects there were no differences in insulin sensitivity, levels of insulin-like molecules, blood pressure, PAI-1, serum lipids, or CHD prevalence between the three ACE genotypes. CONCLUSIONS: We conclude that increased cardiovascular risk of the DD genotype is not mediated through insulin resistance or abnormalities in fibrinolysis. Conversely, we report an increased sensitivity in NIDDM subjects with the ACE DD genotype.     

Obesity and insulin resistance syndrome

Obesity is commonly associated with insulin resistance. The etiology of insulin resistance syndrome such as syndrome X or deadly quartet is not clear. We have proposed visceral fat syndrome, in which fat accumulation is predominant in the intra-abdominal cavity, frequently accompanied by disorders of glucose and lipid metabolism, and also hypertension. Excess free fatty acid of the portal circulation may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. Enhanced production of PAI-1 by increased visceral fat may be partly responsible for the development of cardiovascular disease in patient with visceral fat assmulation.     

PAI-1, obesity, insulin resistance and risk of cardiovascular events

Circulating (PAI-1) levels are elevated in patients with coronary heart disease and may play an important role in the development of atherothrombosis. Many clinical studies have indicated that the insulin resistance syndrome, which is a situation predisposing to diabetes and ischemic heart disease, may be a major regulator of PAI-1 expression, especially in determining plasma PAI-1 levels. Central obesity is a characteristic of insulin resistance and is a well recognized risk factor for coronary heart disease. Recently the production of PAI-1 by adipose tissue, in particular by tissue from omentum, has been demonstrated and could be an important contributor to the elevated plasma PAI-1 levels observed in insulin resistant patients. Besides the effect of the metabolic status on plasma PAI-1 levels, the role of a genetic control has been emphasized, but according to recent results obtained in a family segregation study, its participation seems limited. Prospective cohort studies of patients with previous myocardial infarction or angina pectoris have underlined the association between increased plasma PAI-1 levels and the risk of coronary events, but the predictive capacity of PAI-1 disappears after insulin resistance marker adjustments. Taken together these results support the notion that PAI-1 can be a link between obesity, insulin resistance and cardiovascular disease.     

2型糖尿病合并高脂血症患者中医体质类型及与血脂指标的相关性研究

目的 探讨2型糖尿病合并高脂血症患者的中医体质分布规律,研究中医体质与血脂指标的相关性.方法 选择100例2型糖尿病合并高脂血症患者,根据"中医体质分类与判定表"判定体质类型并观察分布情况;通过检测总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)、糖化血红蛋白(HbAlc)、体重指数(BMI)、腰臀比(WHR),比较不同体质患者的血脂指标、BMI及WHR,观察BMI,HbAlc与血脂指标的相关性.结果 100例患者中平和质占14.0%,气虚质占22.0%,阳虚质占16.0%,阴虚质占24.0%,瘀血质占7.0%,痰湿质占10.0%,湿热质占5.0%,气郁质占2.0%,特禀质占0.0%.湿热质患者TC,LDL-C均值最高,且与平和质比较差异有统计学意义(P＜0.05).痰湿质患者WHR较平和质患者升高(P＜0.05).超重组、肥胖组与正常组比较HDL-C,ApoAl均降低(P＜0.05).HbAlc良好组、差组与理想组比较TG升高(P＜0.05).结论 2型糖尿病合并高脂血症患者以阴虚质、气虚质为主,湿热质患者TC,LDL-C在各体质类型中最高.     

Mutant insulin receptors in syndromes of insulin resistance

To date, mutations of the insulin receptor remain the only well-established causes of severe insulin resistance. There is a broad correlation between the extent of impairment of signal transduction seen when the mutant receptors are expressed in vitro with the severity of the clinical phenotype. Thus leprechaunism, Rabson-Mendenhall syndrome and Type A insulin resistance appear to represent points on a continuum of severity of receptor dysfunction, rather than completely distinct syndromes. In other syndromes of insulin resistance, insulin receptor abnormalities remain the exception. However, functional studies of expressed naturally occurring insulin receptor mutations have acted as experiments of nature and greatly aided attempts to dissect the structure-function relationships of the receptor. The next few years will no doubt begin to reveal the contributions made by defects in the post-receptor signalling cascade to the syndromes of insulin resistance in man.     

Hyperinsulinemia, hyperproinsulinemia and insulin resistance in the metabolic syndrome

For better comprehension of the metabolic syndrome, it is necessary to differentiate the effect of insulin on glucose metabolism on the one hand, and on other metabolic activities on the other hand. Whereas glucose utilization is affected by insulin resistance, the effect of insulin on lipid metabolism, ion and aminoacid transport does not seem to be diminished. Lipid metabolism, however, seems to play a crucial role in the induction of the vicious cycle. Increased energy and fat ingestion may be due to an increased number of galanin secreting cells in the hypothalamus. The excessive fat intake results in an increased rate of release of insulin and increased influx of triglycerides into the blood. From these triglycerides an excess of free fatty acids is released by the action of lipoprotein lipase. The increased plasma free fatty acid level then results in insulin resistance affecting glucose metabolism. Also, these free fatty acids may impair the secretion of insulin. Induction of insulin resistance results in higher glucose levels, which may cause hyperinsulinemia. Hyperinsulinemia maintains the elevation of triglycerides. When diabetes becomes overt and elevated glucose levels prevail, the hyperinsulinism acts on the metabolic pathways which are still sensitive to insulin, namely lipid metabolism, aminoacid transport and ion transport.     

Effect of smoking on sudden and premature death

BACKGROUND: Smoking has been related to coronary heart disease, and, in men, to sudden death. The results of a case-control study designed to assess the relationship between smoking and all causes of sudden and premature death are reported. METHODS: A questionnaire on the previous history and causes of death of all people buried in the Municipal Cemetery of Valencia (1986-1987) was administered to the relatives of the deceased. Among 4718 deaths, 284 victims of sudden death were identified, and 495 people who had not died suddenly were randomly sampled as controls. RESULTS: The proportion of smokers among the women studied was extremely low in contrast to 58.9% of men in the sudden death study group and 59.2% of men in the non-sudden death study group who smoked. Smokers died on average 10 years younger than non-smokers in the sudden-death group (63.3 +/- 12.3 and 73.3 +/- 11.0 years respectively; P < 0.001), and 8 years earlier in the non-sudden death group (68.5 +/- 13.3 and 76.8 +/- 13.2 years, respectively; P < 0.001). A logistic regression model showed that smokers had an adjusted relative risk of 0.81 for sudden death compared with non-smokers (95% confidence interval [CI]: 0.45-1.46). Smokers 65 years of age or under had a 2.7 times greater risk (95% CI: 1.49-5.04) of premature death than non-smokers. Similar results were found in patients from the coronary- and cardiac-death subgroups. CONCLUSIONS: Smoking is an independent risk factor for premature death but not for sudden death.     

Clinical significance of insulin resistance

Insulin resistance has emerged in the last 20 years as a concept familiar to clinicians in many specialties. No easily performed laboratory test is available to assess insulin action in routine clinical practice. Several rare syndromes of severe insulin resistance are recognized but most clinicians will encounter insulin resistance as a manifestation of common diseases. Physiological and treatment induced changes in insulin sensitivity influence insulin doses required in insulin-dependent diabetes mellitus. In non-insulin-dependent diabetes mellitus insulin resistance is fundamental to pathogenesis but it is also influenced by standard dietary and pharmacological treatment, and probably mediated by changes in prevailing glycaemia. Antihypertensive agents appear to have diverse effects on the insulin resistance of essential hypertension though the long term significance of these remains unclear. The importance of insulin as a risk factor for coronary heart disease and the concept of an insulin resistance syndrome as a common precursor of conditions with increased vascular risk remains controversial.     

Effects of docosahexaenoic acid on serum lipoproteins in patients with combined hyperlipidemia: a randomized, double-blind, placebo-controlled trial

OBJECTIVE: The objective of this study was to evaluate the effects of daily dietary supplementation with 1.25 g or 2.5 g of docosahexaenoic (DHA), in the absence of eicosapentaenoic acid (EPA), on serum lipids and lipoproteins in persons with combined hyperlipidemia (CHL) [serum low-density lipoprotein cholesterol (LDL-C) 130 to 220 mg/dL and triglycerides 150 to 400 mg/dL]. METHODS: After a 6-week dietary stabilization period, subjects entered a 4-week single-blind placebo (vegetable oil) run-in phase. Those with adequate compliance during the the run-in were randomized into one of three parallel groups (placebo, 1.25, or 2.5 g/day DHA) for 6 weeks of treatment. Supplements were administered in a triglyceride form contained in gelatin capsules. Primary outcome measurements were plasma phospholipid DHA content, serum triglycerides, high-density lipoprotein cholesterol (HDL-C). LDL-C and non-HDL-C. RESULTS: The DHA content of plasma phospholipids increased dramatically (2 to 3 fold) in a dose-dependent manner. Significant (p < 0.05) changes were observed in serum triglycerides (17 to 21% reduction) and HDL-C (6% increase) which were of similar magnitude in both DHA groups. Non-HDL-C [+1.6 (NS) and +5.7% (p < 0.04)] and LDL-C [+9.3% (NS) and +13.6% (p < 0.001)] increased in the DHA treatment groups. All lipid effects reached an apparent steady state within the first 3 weeks of treatment. CONCLUSION: Dietary DHA, in the absence of EPA, can affect lipoprotein cholesterol and triglyceride levels in patients with combined hyperlipidemia. The desirable triglyceride and HDL-C changes were present at a dose which did not significantly increased non-HDL-C or LDL-C. These preliminary findings suggest that dietary supplementation with 1.25 g DHA/day, provided in a triglyceride form, may be an effective tool to aid in the management of hypertriglyceridemia.     

The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension

The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension (EH) was explored. After the measurement of blood pressure in 15 EH patients and 8 control subjects, EH patients were divided into two groups by the elevation of plasma NE (delta NE) 5 min after standing: 7 normoadrenergic EH (delta NE < 140 pg/ml) and 8 hyperadrenergic EH (delta NE > or = 140 pg/ml). On the morning after a 12-h overnight fast, regular insulin (0.1 U/kg) was injected intravenously, and glucose disappearance rate (GDR) was measured and used as an index of insulin sensitivity. On the following day, the test was reinvestigated following the administration of mabuterol, a beta 2 agonist. Plasma growth hormone (GH), cortisol, norepinephrine (NE) and epinephrine (Epi) were measured before and after the mabuterol administration. Although there were no significant differences of basal GDR among these three groups, mabuterol induced a considerable decrease in GDR in EH patients but not in control subjects. There was no significant difference in the decrease of GDR between normo- and hyperadrenergic EH. The decrease in GDR tended to correlate with the mean blood pressure at rest in EH but not in normal subjects. Plasma glucose and serum insulin in EH patients were increased more than in normal subjects. Plasma GH, cortisol and Epi were not elevated by mabuterol, but plasma NE increased in each group, significantly in hyperadrenergic EH. There was no correlationship between the increase in plasma NE and the decrease in GDR after mabuterol.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of captopril, losartan, and bradykinin on early steps of insulin action

Insulin initiates its metabolic and growth-promoting effects by binding to the alpha subunit of its receptor, thereby activating the kinase in the beta subunit. This event leads to tyrosyl phosphorylation of its cytosolic substrate, insulin receptor substrate 1 (IRS-1), which in turn associates with and activates phosphatidylinositol (PI) 3-kinase. The clinical use of ACE inhibitors has been associated with increased insulin sensitivity. However, the exact molecular mechanism is unknown. In the present study, we examined the phosphorylation status of the insulin receptor and IRS-1, as well as the association between IRS-1 and PI 3-kinase in the liver and muscle of 20-month-old rats treated acutely with captopril, using immunoprecipitation with antipeptide antibodies to the insulin receptor and IRS-1, and immunoblotting with antiphosphotyrosine and anti-PI 3-kinase antibodies. Insulin stimulation increased receptor autophosphorylation to 462 +/- 253% (P < 0.05) in the liver and 697 +/- 78% (P < 0.001) in the muscle of ACE inhibitor-treated rats. There were also increases to 250 +/- 17% (P < 0.001) and 280 +/- 50% (P < 0.05) in the insulin-stimulated IRS-1 phosphorylation levels in the liver and muscle, respectively, of animals treated with captopril. The insulin-stimulated IRS-1 association with PI 3-kinase rose to 305 +/- 20% (P < 0.001) in liver and 267 +/- 48% (P < 0.05) in muscle. Losartan, an ANG receptor blocker, had no significant effect on insulin-stimulated IRS-1 phosphorylation in both tissues. The acute administration of bradykinin increased insulin-stimulated tyrosine phosphorylation of the insulin receptor and IRS-1 in the liver and muscle. These data demonstrate that ACE inhibitors modulate the early steps of insulin signaling, and that this effect may be simulated by the administration of bradykinin.