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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is not known if vitamin E in hyperlipidemia and hypercholesterolemia of longer duration has any beneficial or adverse effects on electrolytes, and liver and kidney function. The objectives of this study are to determine (i) if long duration of mild hypercholesterolemia has any adverse effects on serum electrolytes, glucose and enzymes related to liver and kidney functions; (ii) if vitamin E has any effects on serum electrolytes, glucose and enzymes related to liver and kidney function in hypercholesterolemia. Blood samples were collected from the rabbits before and at various intervals during administration of a high cholesterol diet (0.25%) for 2 and 4 months, and while on a high cholesterol diet with vitamin E following a high cholesterol diet. Measurements of serum total cholesterol (TC), glucose, aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), gamma-glutamyltransferase (GGT), albumin, creatinine, electrolytes [sodium (Na), potassium (K), chloride (Cl), and carbon dioxide (CO2)] were made. High cholesterol diet for 2 months produced hypercholesterolemia which was associated with reductions in serum glucose, unaltered serum electrolytes, ALT, ALP, GGT, albumin and creatinine, and increased levels of AST. Hypercholesterolemia for 4 months had effects similar to hypercholesterolemia for 2 months except it lowered serum ALP. Vitamin E did not affect any of the parameters except serum glucose and Cl, which decreased compared to the values at month 2. Hypercholesterolemia for short and long term does not have adverse effects on liver or kidney function, and serum electrolytes. Vitamin E during hypercholesterolemia does not affect serum electrolytes or liver and kidney function.
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PMID:Effects of vitamin E on serum enzymes and electrolytes in hypercholesterolemia. 1973 Sep 89

In reviewing the literature, no description of a lipemia occurring in relation to simple hemorrhage was found, so that the observation of the phenomenon here recorded would seem to be new. Very high percentages of fat have been found in the blood of diabetics. Fischer's case showed 18.1 per cent total ether extract. Of this very little was free fat (0.0018 gm. potassium hydroxide per gram of fat); iodine absorption was 60.6 per cent.; cholesterin, 2.6 per cent. Chatin's case, cited by Fischer, showed 1.2 per cent. cholesterin, 66.5 per cent. olein, 32.2 per cent. margarin in the fat. Neisser and Derlin in the ether extract of blood from a patient with diabetic coma found 19.7 per cent. fat, with melting point of from 39 degrees to 41 degrees C.; iodine absorption was 53.6 per cent. Javal in a similar case found 25.4 per cent. of fat in ether extract of dry serum (perhaps by Soxhlet method); 21 per cent. of the fat was lecithin. Bleibtreu produced alimentary lipemia in geese by feeding barley and butter. Ether extract of serum showed 6 per cent. of fat. The serum was milky with invisible droplets. Iodine absorption was 57 to 58 per cent. The fat was quite different, chemically, from the fat in the food. Lipemia disappeared a few days after discontinuing the forced feeding. Our experiments suggest, by analogy, the possible occurrence of lipemia in human anemias. In this connection it is of interest to note that we have recently demonstrated a moderate lipemia in a case of marked secondary anemia from hemorrhoids. The emaciation in such cases, as contrasted with the well-recognized conservation of the fat in pernicious anemia, suggests in human pathology a still further analogy which we now have under investigation. The fat in our lipemic rabbits differs from fats described above in its insolubility, as well as in its "constants." The change after precipitation of calcium from the serum suggests that the fat may be present in the serum as a protein-calcium-lecithin combination which is decomposed by decalcifying. While we are not prepared to offer an explanation of the mechanism of this lipemia, it is possible that the great loss of tissue proteins may have some influence on the abnormal fat metabolism. That the fat is derived from the tissues is a fair inference when its occurrence in connection with the loss of weight and the previous disappearance of the body fat are taken into consideration. A more careful study of the lipase in the blood and tissues is desirable. It may be that lowered oxidation following great loss of red cells plays a part.
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PMID:EXPERIMENTAL LIPEMIA IN RABBITS. 1986 66

Pancreatic beta cells are specialised endocrine cells that continuously sense the levels of blood sugar and other fuels and, in response, secrete insulin to maintain normal fuel homeostasis. During postprandial periods an elevated level of plasma glucose rapidly stimulates insulin secretion to decrease hepatic glucose output and promote glucose uptake into other tissues, principally muscle and adipose tissues. Beta cell mitochondria play a key role in this process, not only by providing energy in the form of ATP to support insulin secretion, but also by synthesising metabolites (anaplerosis) that can act, both intra- and extramitochondrially, as factors that couple glucose sensing to insulin granule exocytosis. ATP on its own, and possibly modulated by these coupling factors, triggers closure of the ATP-sensitive potassium channel, resulting in membrane depolarisation that increases intracellular calcium to cause insulin secretion. The metabolic imbalance caused by chronic hyperglycaemia and hyperlipidaemia severely affects mitochondrial metabolism, leading to the development of impaired glucose-induced insulin secretion in type 2 diabetes. It appears that the anaplerotic enzyme pyruvate carboxylase participates directly or indirectly in several metabolic pathways which are important for glucose-induced insulin secretion, including: the pyruvate/malate cycle, the pyruvate/citrate cycle, the pyruvate/isocitrate cycle and glutamate-dehydrogenase-catalysed alpha-ketoglutarate production. These four pathways enable 'shuttling' or 'recycling' of these intermediate(s) into and out of mitochondrion, allowing continuous production of intracellular messenger(s). The purpose of this review is to present an account of recent progress in this area of central importance in the realm of diabetes and obesity research.
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PMID:Regulation of insulin secretion: role of mitochondrial signalling. 2022 32

Glucose and lipids are essential to the body, but excess glucose or lipids lead to metabolic syndrome. ATP-binding cassette (ABC) proteins are involved in the homeostasis of glucose and lipid in that they regulate insulin secretion and remove excess cholesterol from the body. Sulfonylurea receptor (SUR) is a subunit of the ATP-sensitive potassium channels, which regulate insulin secretion from pancreatic beta-cells by sensing cellular metabolic levels. ABCG1 removes excess cholesterol from peripheral tissues and functions in reverse cholesterol transport to the liver. ABCG5 and ABCG8 suppress the absorption of cholesterol in the intestine and exclude cholesterol from the liver to the bile duct. ABCG1 and ABCG4, expressed in the central nervous system, play roles in lipid metabolism in the brain. These ABC proteins are targets of drugs and functional foods to cure and prevent diabetes, hyperlipidemia, and neurodegenerative diseases. In this review, recent knowledge of the physiological function and regulation of ABC proteins in the homeostasis of glucose and lipids is discussed.
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PMID:ATP-binding cassette proteins involved in glucose and lipid homeostasis. 2046 Jul 28

Calcific aortic valve disease is associated with increased morbidity and mortality, especially in the elderly. To date, pharmacological therapies have not proven as effective as surgical intervention. Here, we used a hyperlipidemic rabbit model to investigate the potential effects of selective aldosterone inhibition on the early stages of aortic valve calcification, a pharmacological strategy that has not yet been tested. Forty New Zealand male rabbits fed a standard diet for 4 weeks were separated into three groups: (1) control (n=10), fed a standard diet; (2) vehicle (n=15), fed a hyperlipidemic diet (cholesterol 1%) plus vehicle; and (3) eplerenone (n=15), fed a hyperlipidemic diet plus 100 mg/kg/d eplerenone (last 4 weeks). After 8 weeks, animals were sacrificed and prepared aortic valve sections were examined with Von Kossa silver stain and by immunostaining for mineralocorticoid receptor, macrophages and angiotensin-converting enzyme. The presence of calcium deposits was confirmed by scanning electron microscopy. Eplerenone increased aldosterone levels but did not affect blood pressure, cholesterol or potassium levels. Hyperlipidemia induced macrophage accumulation and angiotensin-converting enzyme expression, as well as calcium deposition in the leaflets. All markers were decreased by eplerenone treatment. Immunohistochemistry for mineralocorticoid (aldosterone) receptors revealed similar expression in the leaflets of both control and hyperlipidemic groups. Collectively, these results indicate that aldosterone receptors are present in rabbit aortic valve leaflets and their selective blockade with eplerenone inhibits formation of the sclerotic lesions induced by a high fat diet.
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PMID:Aldosterone receptor blockade inhibits degenerative processes in the early stage of calcific aortic stenosis. 2055 22

Poor nutrition in the first year of a mother's life and undernutrition in utero, infancy, childhood, and adulthood predispose individuals to stroke in later life, but the mechanism of increased stroke risk is unclear. Overnutrition also increases the risk of stroke, probably by accelerating the development of obesity, hypertension, hyperlipidaemia, and diabetes. Reliable evidence suggests that dietary supplementation with antioxidant vitamins, B vitamins, and calcium does not reduce the risk of stroke. Less reliable evidence suggests that stroke can be prevented by diets that are prudent, aligned to the Mediterranean or DASH (Dietary Approaches to Stop Hypertension) diets, low in salt and added sugars, high in potassium, and meet, but do not exceed, energy requirements. Trials in progress are examining the effects of vitamin D and marine omega-3 fatty acid supplementation on incidence of stroke. Future challenges include the need to improve the quality of evidence linking many nutrients, foods, and dietary patterns to the risk of stroke.
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PMID:Nutrition and the risk of stroke. 2217 22

The prevalence of hypertension in the United States has grown dramatically in recent years. Thiazide diuretics have played a major role in the rising rate of blood pressure (BP) control. Accompanying this has been the appearance of adverse drug events, including hospitalizations associated with thiazide-associated hyponatremia (HTAH). Hyponatremia is a common yet often overlooked side effect of this drug class. Identification of HTAH risk factors may aid in creating strategies to prevent hospitalizations. This is a retrospective, case-controlled study of 10,805 patients (1802 cases, 9003 controls) examining HTAH risk factors within a group-model integrated-care organization. Multivariate analysis revealed that age (odds ratio [OR], 1.75; 95% confidence interval [CI], 1.58-1.93), angiotensin-converting enzyme (ACE) inhibitor use (OR, 1.53; 95% CI, 1.16-2.00), and hypokalemia (OR, 40.94; 95% CI, 26.46-66.33) were most associated with HTAH. Urinary tract infection (UTI), type 2 diabetes, hyperlipidemia, and gastroesophageal reflux disease (GERD) were also found to be HTAH risk factors. Potassium supplements (OR, 0.60; 95% CI, 0.44-0.83) and weight (OR, 0.91; 95% CI, 0.88-0.93) had protective effects. A predictive model was developed to determine overall HTAH risk given the presence of individual risk factors. Age, weight, hypokalemia, GERD, type 2 diabetes, UTI, and ACE inhibitor use independently correlated with an increased risk of HTAH. This model may be applied in clinical practice to guide thiazide prescribing.
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PMID:Evaluations of hospitalizations associated with thiazide-associated hyponatremia. 2294 68

Based on the hypothesis that consistent hyperglycemia can result in insulin resistance, we explored the induction of non-insulin dependent diabetes mellitus (NIDDM) using diet of high glycemic/low fat index and compared the effects on the physiology and histology of the rats. The rats were divided into 3 groups. DM was induced in the first group by single intraperitoneal injection of 150mg/kg alloxan monohydrate and in the second group by feeding the rats with diet of high glycemic index/low fat for 8 weeks. The pathophysiology and histopathology of DM were studied. Hyperglycemia was recorded in the alloxan and food-induced groups respectively. Both groups were also positive for glycosuria, which confirmed the induction of DM. Concentrations of plasma potassium, calcium, protein and urea were higher (p<0.05) in the alloxan-induced than the food-induced diabetic rats, whereas food-induced rats recorded higher hematological indices than the alloxan-induced group. Coronary risk indices were higher in food-induced diabetic rats than the alloxan-induced, while activities of antioxidant enzymes were significantly higher (p<0.05) in alloxan-induced diabetic rats than the food-induced rats. Marked degenerations of the Islets of Langerhans was observed in pancreas of alloxan-induced diabetic rats, whereas, histological examination of the pancreas of food-induced and control rats revealed no visible lesion. Liver and kidney of all food and alloxan-induced diabetic rats showed marked degeneration of the hepatocytes and the glomeruli respectively. This study presents a rat model of type II diabetes mellitus using food of high glycemic/low fat index with its consequent ionoregulatory disruptions, acute anemia, hyperlipidemia, nephropathy and hepatopathy.
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PMID:Rat model of food-induced non-obese-type 2 diabetes mellitus: comparative pathophysiology and histopathology. 2246 57

We summarize recent advances in the clinical genetics of hypercholesterolemia, hypertrophic cardiomyopathy (HCM), and lethal arrhythmia, all of which are monogenic cardiovascular diseases being essential to understanding the heart and circulatory pathophysiology. Among the issues of hypercholesterolemia which play a pivotal role in development of vascular damages, familial hypercholesterolemia is the common genetic cardiovascular disease; in addition to identifying the gene mutation coding low-density lipoprotein receptor, lipid kinetics in autosomal recessive hypercholesterolemia as well as in proprotein convertase subtilisin/kexin 9 gene mutation were recently demonstrated. As for HCM, some gene mutations were identified to correlate with clinical manifestations. Additionally, a gene polymorphism of the renin-angiotensin system in development of heart failure was identified as a modifier gene. The lethal arrhythmias such as sudden death syndromes, QT prolongation, and Brugada syndrome were found to exhibit gene mutation coding potassium and/or sodium ion channels. Interestingly, functional analysis of these gene mutations helped to identify the role of each gene mutation in developing these cardiovascular disorders. We suggest considering the genetic mechanisms of cardiovascular diseases associated with hyperlipidemia, myocardial hypertrophy, or lethal arrhythmia in terms of not only clinical diagnosis but also understanding pathophysiology of each disease with therapeutic aspects.
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PMID:Current perspectives in genetic cardiovascular disorders: from basic to clinical aspects. 2390 13

Refeeding syndrome (RS) is a serious and potentially fatal disorder. It is caused by a shift of fluids, sodium, potassium, magnesium and phosphorus as well changes in the metabolism of glucose, protein, fat and vitamins following the refeeding of malnourished patients, whether enterally or parenterally. RS has rarely been reported in patients with advanced kidney disease probably due to the pre-existing hyperphosphatemia, hypermagnesemia and hyperkalemia in these patients. In the following report, we present a patient with nephronophthisis type 1 deletion syndrome in whom her main previous nutrition was limited to simply rehydration to avoid renal replacement therapy. On presentation, she was cachectic and dehydrated with advanced kidney failure. She was treated with medical nephrectomy using non-steroidal anti-inflammatory drugs and then placed on maintenance hemodialysis. Percutaneous endoscopic gastrostomy was used for her initial feeding. Care was exercised during her early refeeding with regard to correction of fluids and essential electrolytes, viz. potassium, phosphorus and magnesium, as well as multivitamins to avoid the cardiovascular and neurological complications of RS. However, the changes in the gut, pancreas and liver as well as her hyperlipidemia were a clear obstacle. Fortunately, the ileus and pancreatitis she developed on refeeding improved dramatically with a decrease of the feeding dose to half; however, the liver abnormalities and hyperlipidemia were severe and slow to recover. These improved after addition of ursodeoxycholic acid and permitted successful increase of the dose of feeding subsequently.
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PMID:Refeeding syndrome in a patient with advanced kidney failure due to nephronophthisis. 2423 89


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