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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A peroxidized model of atherosclerosis devised by the authors and the results of using antioxidants in these conditions as well as of literature sources on the deficiency of the antioxidant action substances in the current ration, on the peroxidation syndrome in this illness in man and animals, all this allowed the following concept to be formulated. Overeating, continued deficiency of antioxidants in natural products and hypodynamia contribute to the derangement of the physiological antioxidant system. An intensified free-radical oxidation calls forth decomposition of the beta-lipoproteids, lipoid infiltration of the intima, destruction of the elasticity, fibrosis and calcinosis. An alimentary prophylaxis of atherosclerosis should repose on the utilization of food mixtures representing complexes of the antioxidants of the direct and indirect action and trace elements entering the composition of the antiperoxidized enzymes.
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PMID:[Alimentary factors in the genesis of atherosclerosis]. 36 37

A 39-year-old woman with long-standing anorexia nervosa was admitted to our hospital because of extreme weakness and cachexia. During a hyperalimentation therapy, she developed chest pain, revealing the electrocardiogram and cardiac enzymes a myocardial infarction of the inferior wall. We suggest that anorexia nervosa does not 'protect' against coronary atherosclerosis, and that some of the cases of sudden death could be related to myocardial ischemia.
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PMID:Anorexia nervosa and myocardial infarction. 796 Feb 53

We and others have demonstrated that T lymphocytes are prominent components of atherosclerotic lesions. We hypothesized that if T cells were necessary for the development of atherosclerosis it would be possible to demonstrate its prevention or retardation in T-cell-suppressed mice. To test this hypothesis, CyA, a potent suppressor of T-cell activation, was used to treat C57BL/6 mice undergoing lipid hyperalimentation. Mice receiving normal mouse chow were completely free of atherosclerotic lesions. In mice receiving the atherogenic diet plus control oil injections, lesions of the aorta and coronary arteries were observed at 135 days and increased progressively in area until 310 days. Somewhat surprisingly, mice given the atherogenic diet plus CyA injections displayed even larger lesions at all three observed time intervals. Although CyA did suppress T-cell reactivity sufficiently to obtain the expected prolongation of skin allografts, it did not suppress the development or progression of atherosclerotic lesions.
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PMID:Accelerated atherosclerosis in hyperlipidemic C57BL/6 mice treated with cyclosporin A. 850 58

The JCR:LA-cp rat is obese, insulin resistant, and hyperlipidemic, and the males develop atherosclerosis and ischemic myocardial disease. Benfluorex at 35-40 mg.kg-1 body weight was administered in the food from 10 to 14 weeks of age and resulted in an initial 50% decrease in food consumption. Body weights of male and female rats initially decreased by about 7% and thereafter remained relatively constant, whereas control animals gained about 28% in weight over the treatment period. Pair-fed rats showed body weights virtually identical with those of benfluorex-treated animals. Benfluorex treatment and pair feeding decreased serum triacylglycerol concentrations by about 50%; there was a preferential loss of triacylglycerols containing longer chain fatty acids in the males, whereas this selectivity was not seen in the females. Hyperinsulinemic euglycemic insulin clamp studies were performed using [1-3H]glucose, a tracer that allows for the measurement of total glucose turnover, including hepatic uptake and release. In male cp/cp rats, hyperinsulinemia does not stimulate total glucose turnover, reflecting the very severe insulin resistance, and neither benfluorex treatment nor pair feeding increased total glucose turnover. Hyperinsulinemia in male cp/cp rats decreases hepatic glucose output, and benfluorex treatment or pair feeding reduced this insulin-mediated diversion of glucose to hepatic lipid synthesis. Hyperinsulinemia increases total glucose turnover in female cp/cp rats, and this was not increased further by benfluorex treatment or pair feeding. These effects emphasize the sex-specific differences in metabolic response of the rats to hyperinsulinemia and benfluorex treatment. Benfluorex ameliorates the obesity-insulin resistance-hyperlipidemia syndrome in this experimental model mainly by decreasing hyperphagia, with an accompanying improvement in hepatic glucose metabolism and a related reduction in hypertriglyceridemia.
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PMID:Effects of benfluorex on serum triacylglycerols and insulin sensitivity in the corpulent rat. 896 Mar 76

It is generally thought that typical atherosclerotic lesions do not develop in the rodent. The Goto-Kakizaki (GK) rat is a nonobese strain in which a spontaneous type of non-insulin-dependent diabetes mellitus develops without apparent macroangiopathy. In our previous study, making ventromedial hypothalamic (VMH) lesions in GK rats induced hyperphagia and a further deterioration in glucose metabolism. In the current study, male GK rats in which VMH lesions were made were examined for vascular changes, with special reference to atherosclerotic lesions. Marked hyperglycemia in GK rats with VMH lesions (hereafter referred to as VMH lesion rats) was revealed over an observation period (plasma glucose levels 16 weeks after the operation: VMH lesion GK rats, 19.3 +/- 2.0 mmol/L, vs sham-operated GK rats, 10.1 +/- 1.3 mmol/L; p < 0.0001). Light microscopic observation of the descending aorta in VMH lesion GK rats 16 weeks after the surgery revealed that the intimal thickening and the number of infiltrating cells into the intima were significantly increased as compared with sham-operated GK rats (17531 +/- 3747 microm2 vs 3072 +/- 1192 microm2, p < 0.0001; 15.6 +/- 3.1 per one transverse section vs 6.8 +/- 2.5 per one transverse section, p < 0.0005). Electron microscopic observations demonstrated an increased number of microvilli and lysosomes in endothelial cells, infiltration of macrophages and lymphocytes into the intima, and migration of medial smooth muscle cells into the intima that are considered to be early events in atherosclerosis. These morphologic changes could be induced by a deterioration in glucose metabolism. This rat may thus be useful for studying the process of the initiation of atherosclerosis in diabetes mellitus.
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PMID:Early morphologic changes of atherosclerosis induced by ventromedial hypothalamic lesion in the spontaneously diabetic Goto-Kakizaki rat. 901 56

Some genes are expressed differently in earlier and later generations of most cell lines. Many diseases become clinically expressed only later in life, and show clustering of the age at onset in the affected siblings, which may be related to the changing expression with age of the genes involved. Because insulin and its receptor are extremely ancient and well preserved structures with almost universal mitogenic effects, insulin may serve a paradigm of this process. It is suggested that by stimulating cell proliferation, hyperinsulinemia speeds up the appearance of later generations of cells with different expression of the genes. Insulin resistance, accompanying any hyperinsulinemia and considered to be a pathogenetic factor of some common later-age diseases, involves only some biochemical, but not mitogenic effects of the hormone. In humans, high levels of insulin in blood are encountered both physiologically after meals and in many pathological conditions: insulin therapy inevitably causes peripheral hyperinsulinemia; in type 2 diabetes hyperinsulinemia precedes hyperglycemia by many years; hyperinsulinemia is an independent risk factor of atherosclerosis, of type 2 diabetes itself, of some forms of dementia and other diseases; obesity is an obligatory hyperinsulinemic condition. The opposite of hyperalimentation, i.e. calorie restriction (at least, in rodents) may exert its life-prolonging effects through decreasing insulinemia and therefore the rate of cell proliferation. Insulin is only one example, and different mitogens regulate proliferation of different cells. It is likely that growth factors in general accelerating the replication of cells, play a role in speeding up the appearance of later-age diseases involving these cells.
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PMID:Mitogenic factors accelerate later-age diseases: insulin as a paradigm. 966 95

The proponents of fat-restricted diets for children argue that low-fat diets given in childhood will prevent the development of atherosclerosis in adulthood, low-fat diets given a childhood will condition children to prefer low-fat diets in adulthood, and low-fat diets for children are safe. There is no evidence that low-fat diets in childhood will prevent atherosclerosis in adulthood. In fact, studies of migrating populations indicate that immigrants to the United States from Third World countries who consumed low-fat diets in childhood take on the character of their new environments, including higher serum cholesterol levels and more coronary disease. The prevalence of fatty streaks in childhood bears little relationship to the prevalence of atheromatous plaques in adulthood. In fact, girls have more aortic fatty streaks and higher serum cholesterol values in childhood than boys, but fewer plaques in adulthood and less coronary disease. From the PDAY study, it has also been learned that hypercholesterolemia in childhood enhances fatty streak formation, but not that of plaques. It now seems established from autopsy studies that the progression of atherosclerosis from fatty streaks to plaque is arrested in childhood and does not begin to a significant extent until after puberty in males and after menopause in females. So the oft-repeated statement that atherosclerosis begins in childhood is semantically true but very misleading. The particularly harmful form of atherosclerosis (the plaque) does not become significant until much beyond puberty. The effects of low-fat, low-cholesterol diets on serum lipids and lipoproteins are of a lesser magnitude in children than in adults. The 0.78 mmol/L decrease in LDL cholesterol in the intervention group from controls (change 1.5%) in the DISC study was biologically insignificant and reflects the tighter control of lipoprotein and cholesterol synthesis in children compared with adults. It must be remembered that the human body synthesizes all of the cholesterol it needs from acetyl CoA. In general, the larger the amount of dietary cholesterol absorbed, the smaller the rate of biosynthesis of cholesterol. In some adults and most children this homeostatic control is nearly perfect, but in many adults the correction in biosynthesis of cholesterol with increased dietary input is imperfect and LDL cholesterol values increase. The second argument of the proponents of low-fat diets for children is that they are conditioned to continue low-fat diets in adulthood. From the studies of Birch and Fisher (51) this prediction seems unlikely. These investigators found that restricting access to palatable foods enhanced the interest of 3- to 5-year-old children in those foods and increased their desire to obtain and consume those foods. They concluded that "stringent parental controls can potentiate preference for high-fat energy-dense foods, limit children's acceptance of a variety of foods and disrupt children's regulation of energy intake." Brosin (52) has also observed that food restriction in childhood may lead to gluttony in adulthood. Finally, the claim that low-fat diets are safe in childhood is based on observations over too short a time to establish safety. It is true that growth and development of children studied in the DISC study was not changed from the expected increments, but that is not proof of long-term safety. In addition, the lower content of essential nutrients in low-fat, low-cholesterol diets (calcium, zinc, magnesium, phosphorus, vitamin E, vitamin B-12, thiamin, niacin, and riboflavin) must be considered along-term risk (53,54). Furthermore, the published studies of the safety of low-fat diets have been conducted under intensive surveillance in medical centers, conditions very different from those in the homes of free-living families.
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PMID:Is it wise to restrict fat in the diets of children? 1064 98

Acylethanolamides are endogenous compounds with lipid structure including anandamide (AEA), palmitoilethanolamide, oleylamide and oleylethanolamide (OEA). AEA binds to the cannabinoid receptor CB1, located at the central nervous system, while OEA is an endogenous ligand for the alpha subtype of peroxisome-proliferator activating receptor (PPARalpha). Since AEA acts on the same receptor which binds marihuana active derivatives, this group of compounds were called endocannabinoids. Besides typical central effects of cannabinoids, CB1 receptor activation leads to hyperphagia, whereas its pharmacological blockade is followed by changes in energy metabolism favouring substrate oxidation. OEA has inhibitory effects on food intake by acting on PPARalpha receptors which modulate the autonomous nervous system. Both acylethanolamides, AEA and OEA, have opposite effects suggesting that they form part of a satiety sensor system. Whereas fasting triggers AEA release and inhibits OEA synthesis, eating has the reverse effect. Additionally OEA is also produced by adipocytes ad has some effects on lipid metabolism. All these data suggest a role for acylethanolamides and the endocannabinoid system in the pathophysiology of obesity, diabetes and atherosclerosis.
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PMID:[The endocannabinoid system and food intake control]. 1538 9

The various mechanisms that may explain the association between brain dysfunction and the pathogenesis of metabolic syndrome (MS) leading to cardiovascular disease and type 2 diabetes have been reviewed. A Medline search was conducted until September 2003, and articles published in various national and international journals were reviewed. Experts working in the field were also consulted. Compelling evidence was found that saturated and total fat and low dietary n-3 fatty acids and other long-chain polyunsaturated fatty acids (PUFAs) in conjunction with sedentary behavior and mental stress combined with various personality traits can enhance sympathetic activity and increase the secretion of catecholamine, cortisol and serotonin, all of which appear to be underlying mechanisms involved in MS. Excess secretion of these neurotransmitters in conjunction with underlying long-chain PUFA deficiency may damage the neurons in the ventromedial hypothalamus and insulin receptors in the brain, in particular during fetal life, infancy and childhood, and lead to their dysfunction. Since 30-50% of the fatty acids in the brain are long-chain PUFAs, especially omega-3 fatty acids which are incorporated in the cell membrane phospholipids, it is possible that their supplementation may have a protective effect. Omega-3 fatty acids are also known to enhance parasympathetic activity and to increase the secretion of anti-inflammatory cytokines as well as acetylecholine in the hippocampus. It is possible that a marginal deficiency of long-chain PUFAs, especially n-3 fatty acids, due to poor dietary intake during the critical period of brain growth and development in the fetus, and later in the infant and also possibly in the child, adolescent and adult may enhance the release of tumor necrosis factor-alpha (TNF-alpha) interleukin (IL)-1, 2 and 6 and cause neuronal dysfunction. Experimental studies indicate that ventromedial hypothalamic lesions in rats induce hyperphagia, resulting in glucose intolerance and insulin resistance. Treatment with neuropeptide Y abolished hyperphagia and ob mRNA (leptin mRNA) in this animal model. Long-term infusion of norepinephrine and serotonin into the ventromedial hypothalamus impaired pancreatic islet function inasmuch as ventromedial hypothalamic norepinephrine and serotonin levels were elevated in hyperinsulinemic and insulin-resistant animals. Treatment with insulin was associated with restoration of hypothalamic neurotransmitter abnormalities, indicating that ventromedial hypothalamus dysfunction can impair pancreatic beta cells resulting in metabolic abnormalities consistent with MS. Treatment with omega-3 fatty acids, beta blockers, ACE inhibitors, estrogen, and meditation may have a beneficial effect on insulin receptors and ventromedial hypothalamic dysfunction. However, no definite or precise insight into the pathophysiological link between MS, brain function and nutrition is available. Despite this, epidemiological studies and intervention trials indicate that treatment with n-3 fatty acids may be adopted in clinical practice and used to direct therapy for prevention of type 2 diabetes, hypertension, coronary artery disease (CAD), and atherosclerosis, thereby indicating that MS may also respond to this treatment.
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PMID:Can brain dysfunction be a predisposing factor for metabolic syndrome? 1575 41

Coronary heart disease remains a major cause of morbidity and mortality in the United States, and its incidence is rising worldwide. Because atherosclerosis is a chronic process, and it is often associated with certain lifestyle and risk factors such as hypertension, dyslipidemia, and insulin resistance, much emphasis is being placed on lifestyle modification and control of risk factors. It is being recognized that some lifestyle patterns such as overeating result in metabolic syndrome, which may play a role in the development of chronic kidney disease and coronary heart disease. Here, we focus on an important relationship between these 3 conditions, and we provide evidence that microalbuminuria develops in many patients with metabolic syndrome, may be an important correlate of chronic kidney disease and coronary heart disease, and may represent an important prognostic marker. Although the pathogenesis of microalbuminuria in metabolic syndrome is not clear, we suggest that microalbuminuria, chronic kidney disease, and coronary heart disease share common pathways involving inflammation and oxidative stress. We also discuss that a healthy lifestyle is essential for preventing and treating chronic kidney disease and coronary heart disease seen in patients with metabolic syndrome.
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PMID:Triad of metabolic syndrome, chronic kidney disease, and coronary heart disease with a focus on microalbuminuria death by overeating. 2163 30


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