Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the regulation of obese (ob) gene expression in obesity and diabetes, we examined ob gene expression in KK mice and congenic lethal yellow obese KKAy mice. Northern blot analysis revealed that the ob mRNA levels are roughly equivalent in each of the epididymal, mesenteric, and subcutaneous white adipose tissue (WAT) from KK and KKAy mice at 4 wk of age, when the obese phenotype of KKAy mice was not apparent. Expression of the ob gene was augmented in the mesenteric and subcutaneous WAT but was unchanged in the epididymal WAT in KKAy mice at 12 wk of age, when KKAy mice developed marked obesity with hyperglycemia, hyperlipidemia, and hyperinsulinemia. The ob gene expression was also examined during fasting in 12-wk-old KK and KKAy mice. After 24 or 72 h of fasting in both mouse strains, ob gene expression was downregulated in the epididymal and mesenteric WAT but was unchanged in the subcutaneous WAT. The present study demonstrates that adipose tissue expression of the ob gene is regulated depending on the nutritional status in KK and KKAy mice.
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PMID:Regulation of obese gene expression in KK mice and congenic lethal yellow obese KKAy mice. 877 28

To clarify the relationship between lipid and glucose metabolism abnormalities in fructose-fed rats, we examined whether an improvement of insulin sensitivity by troglitazone (CS-045) or a decrease in plasma lipids by bezafibrate affects the relationship between serum levels of lipid and glucose. In addition, we also examined changes in liver glycogen metabolism and beta-oxidation in fructose-fed rats. Troglitazone ameliorated fasting hyperlipidemia, hyperglycemia, and hyperinsulinemia. In addition, it augmented glycogen synthase activity by 53%, and decreased the mitochondrial palmitic acid beta-oxidation rate and ketone body production rate by 27% and 55%, respectively. However, hyperglycemia and liver glycogen synthase activity were not improved by bezafibrate treatment despite a marked reduction of serum triglyceride (TG) levels resulting from a 1.76-fold increase in mitochondrial oxidation and a 2.04-fold increase in hepatic ketone body production. These results suggest that abnormalities in glucose and lipid metabolism in fructose-fed rats, which are ameliorated by troglitazone, may be closely linked to reduced glycogen synthase activity in the liver.
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PMID:Effect of troglitazone (CS-045) and bezafibrate on glucose tolerance, liver glycogen synthase activity, and beta-oxidation in fructose-fed rats. 878 34

There is strong evidence that genetic factors contribute to the development of obesity in humans as well as laboratory animals. Another important factor leading to obesity is an increase in energy intake. However, it is difficult to make normal rats obese by controlling daily food intake. There is no report of normal adult male Wistar rats becoming obese and diabetic on a high-fat diet. The aim of the present study was, therefore, to make normal adult Wistar rats obese by infusing high fat and hypercaloric diet through the cannula without disturbing the free movement and to investigate the influence of an increase in the caloric intake on body weight and glucose metabolism. High-fat hypercaloric diet (360 kcal/kg body wt./day; H group) or control diet (180 kcal/kg body wt./day; C group) was continuously infused into the stomach of normal adult male Wistar rats weighing approximately 300 g through gastric cannulas for 27 days. On day 28 after a 24-h fasting, serum concentrations of aspartate aminotransferase, alanine aminotransferase, total cholesterol, triglyceride, phospholipid, and free fatty acids (FFA) were determined, and intragastric glucose loading test (2 g/kg body wt.) was performed. The average weekly body weight gain in the H group was twice as much as that of the C group (40.0 +/- 2.4 vs. 19.4 +/- 1.9 g/week, P < 0.001). Serum levels of triglyceride, phospholipid, total cholesterol, and FFA were significantly elevated in the H group compared to those in the C group. Liver weight in the H group was significantly higher than that in the C group and showed steatosis. Pancreas weight (-13%) as well as protein (-12%), amylase (-53%) and trypsin content (-26%) were all reduced, whereas pancreatic DNA content was significantly increased in the H group compared to those in the C group. Serum glucose and insulin concentrations before and after glucose loading in the H group were significantly higher than those in the C group. Moreover, the insulin response relative to glucose response in the H group was significantly high compared to that in the C group, indicating the presence of insulin resistance. These results indicate that feeding of high-fat hypercaloric diet makes normal Wistar male adult rat obese associated with hyperlipidemia, hyperinsulinemia, and glucose intolerance.
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PMID:High-fat hypercaloric diet induces obesity, glucose intolerance and hyperlipidemia in normal adult male Wistar rat. 879 99

We developed an animal model for non-insulin-dependent diabetes mellitus, a genetically obese rat strain, Wistar fatty. These rats show obesity-related features such as hyperinsulinemia and hyperlipemia, and only males develop diabetic features including hyperglycemia, glucoseuria and polyuria as they age. Histopathological study demonstrated a deposition of PAS-positive granules in the epithelial cells and a diffuse thickening of the mesangial area and moderate changes of the renal tubules. We found that ICAM-1 is expressed on the glomeruli of male Wistar fatty rats and the expression is associated with the development of nephropathy; it is weak at 5 weeks, becomes markedly strong at 15 weeks and progresses further at 29 weeks of age. We tried in vivo administration of monoclonal antibody, anti-ICAM-1 alone or together with anti-LFA-1 into male Wistar fatty rats during the period from 5 weeks to 17 weeks of age. The treatment, however, could not prevent the development of nephropathy. ICAM-1 expressed on the glomeruli of Wistar fatty rats seems not to play a key role in development of the nephropathy by mediating leukocyte infiltration. It will be a useful marker of the development of the disease.
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PMID:Expression of ICAM-1 on glomeruli is associated with progression of diabetic nephropathy in a genetically obese diabetic rat, Wistar fatty. 880 76

Atherosclerotic cardiovascular disease is the major cause of morbidity and mortality in NIDDM patients. But the exact pathophysiology of accelerated atherosclerosis seen in NIDDM is not completely understood. Hyperinsulinemia and hyperlipidemia frequently coexist in these subjects. Present study was undertaken to demonstrate relationship of serum insulin with atherogenic lipids in 92 (male = 62, female = 30) newly diagnosed, middle-aged, nonsmoking, uncomplicated and untreated NIDDM patients with normal body mass index (BMI). Fourty (male = 20, female = 20) non-diabetic healthy subjects with a negative family history of diabetes served as control. After an overnight fasting, venous blood was collected for plasma glucose, serum insulin and lipid profile. ECG and oral glucose tolerance test (OGTT) were done in all subjects. Diabetes mellitus was diagnosed by WHO criteria. Total cholesterol, LDL-c, LDL/HDL ratio, TG (p always < 0.001) and fasting serum insulin (p = 0.033) were significantly higher and HDL-c was significantly lower (p = 0.001) in NIDDM than control subjects. Fasting serum insulin was inversely related to the degree of hyperglycemia in NIDDM subjects (r = -0.1867; p = 0.037). NIDDM with hyperinsulinemia (n = 18) had a strong negative correlation (r = -0.449, p = 0.031) with HDL-c. Neither total cholesterol nor LDL-c had any significant correlation with insulin. The results indicate that diabetic state itself is associated with atherogenic lipid disorder.
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PMID:Lipid profile and its relation to fasting insulin level in non-insulin dependent diabetes mellitus (NIDDM). 881 64

Hyperinsulinemia, insulin resistance, or both have been described in a proportion of patients with essential hypertension, and also are considered a risk for atherosclerotic cardiovascular disease. In this study, we have examined whether salt sensitivity and hyperinsulinemia are associated in patients with essential hypertension. We have measured blood insulin and glucose response to an acute oral glucose load in a group of hypertensive patients, classified according to their salt sensitivity. To determine salt sensitivity, patients received a diet containing a low (20 mEq/day) Na+ intake for 1 week followed by a high (250 mEq/day) Na+ intake for 1 week more. Twenty-nine patients were classified as salt sensitive, and 23 as salt resistant. Baseline plasma glucose and insulin were not different between salt-sensitive and salt-resistant patients. Following an oral glucose load, the area-under-the curve of glucose was greater (P < .05) in salt-sensitive than in salt-resistant hypertensive patients (900 +/- 26.4 and 810 +/- 29.1 mmol/L x 2 h, respectively). The area-under-the curve of insulin was greater (P < .01) in salt-sensitive (52,664 +/- 3,666 pmol/L x 2 h) than in salt-resistant patients (37,977 +/- 3,300 pmol/L x 2 h). A direct correlation was present between insulin area-under-the curve and salt sensitivity (r = 0.26), but did not reach statistical significance (P < .06). Salt-sensitive patients manifested increased serum levels of total cholesterol, LDL-cholesterol and increased urinary albumin excretion when compared with salt-resistant patients. In conclusion, these studies have demonstrated that in response to an oral glucose load, salt-sensitive patients with essential hypertension manifest increased insulin secretion. The studies have confirmed the presence of increased urinary albumin excretion and serum levels of atherogenic lipoproteins in salt-sensitive compared with salt-resistant patients. In salt-sensitive hypertensive patients, hyperinsulinemia, hyperlipidemia and microalbuminuria form a cluster with possible atherogenic potential. Salt sensitivity can be a marker for increased cardiovascular risk in patients with essential hypertension.
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PMID:Clustering of cardiovascular risk factors in salt-sensitive patients with essential hypertension: role of insulin. 883 3

Vascular access dysfunction is an important cause of morbidity for dialysis patients and a major contributor to hemodialysis cost. Thrombosis is a leading cause of vascular access failure, and usually results from stenotic lesions in the venous outflow system. This study was designed to explore the impact of serum levels of various risk factors for thrombosis and accelerated fibrointimal hyperplasia on progressive stenosis, and the subsequent thrombosis of hemodialysis fistula. A cross-sectional and 2-yr prospective pilot study was performed in 30 nondiabetic hemodialysis patients with primary arteriovenous fistula. Venous dialysis pressure, urea recirculation, color Doppler sonography, and angiography were used to monitor vascular access patency. Eleven patients (37%) developed a progressive stenosis in the venous circuit, which was complicated by thrombosis in three patients. Compared with the patients without fistula dysfunction, these patients had higher serum levels of monocyte chemoattractant protein-1 and interleukin-6, two cytokines that regulate the proliferation of vascular smooth muscle cells, which is the key mechanism in the pathogenesis of fistula stenosis. In addition, they had hyperinsulinemia, hyperlipidemia, and increased plasma levels of two hemostasis-derived risk factors for thrombosis: plasminogen activator inhibitor type 1 and factor VII. Monocyte chemoattractant protein-1, interleukin-6, plasminogen activator inhibitor type 1, factor VII, triglycerides, and the ratios for cholesterol/HDL-cholesterol, apolipoprotein (apo) A-I/ apo C-III, apo A-I/apo B, and glucose/insulin were independent predictors of fistula dysfunction. This study demonstrates the influece of cytokines, hemostasis-derived vascular risk factor, hyperinsullnemia, and abnormallties of lipids and apolipoproteins on primary fistula survival. The assessment of these factors might be useful for the identification of the patients at risk of fistula stenosis and thrombosis.
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PMID:Risk factors for vascular disease and arteriovenous fistula dysfunction in hemodialysis patients. 886 9

An association of obesity and hypertension is well recognised and there is a direct positive relationship between body weight or body mass index (BMI) and blood pressure (BP), although the mechanisms responsible for weight-related increases of BP are still unknown. Obesity does appear to be an independent risk factor for premature mortality, especially when it is associated with other risk factors such as hyperinsulinemia and glucose intolerance (or diabetes), hyperlipidemia, and hypertension. However, there are differences among racial and ethnic subgroups. The aim of our study was the investigation of the prevalence of obesity and its severity among Greek hypertensive patients in comparison to normotensive controls. We have studied a large enough sample of Greek hypertensives consisting of 1101 patients (504 male/597 female, 23-85 years of age) and 242 normotensive controls (136 male/106 female, 23-75 years of age). In all patients and normotensive controls BMI (ie weight/height in 2mm) was measured, as well as the waist-to-hip (W/H) ratio. A BMI of less than 27 was accepted as normal, a BMI of 27-32 as indicating mild to moderate obesity, a BMI of 32-37 as an index of severe obesity, and a BMI > 37 as a measure of very severe obesity. Obesity in hypertensive patients was more frequent than in normotensive controls (62.5% vs 54.2%, P = 0.024), and hypertensive women were more commonly obese than hypertensive men (67.16% vs 56.8%, P = 0.002). Severe and very severe obesity was more common in hypertensive women than in men (20.7% vs 9.68%, P < 0.001, and 8.1% vs 0.52%, P < 0.0001, respectively), although obesity of severe and very severe degree was equally found in hypertensives and normotensives of both sexes. BMI of all hypertensives was significantly greater in comparison to that of normotensives (30.13 +/- 0.44 vs 26.74 +/- 0.76, mean +/- s.e., P < 0.0001); W/H ratio of hypertensives was significantly greater than that of normotensives, indicating more frequent central obesity in hypertensives. We conclude that obesity in Greek hypertensive patients is more frequent than in normotensive controls, while hypertensive women have more severe obesity than hypertensive men, and are more frequently obese than men.
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PMID:Prevalence of obesity in Greek hypertensives. 887 30

In contrast to L-glutamine, lipid emulsions are routinely administered to patients receiving nutritional support. The provision of fat during intravenous feeding is essential, but the potentially toxic byproducts of fatty acid oxidation may have adverse metabolic consequences. In the present study, we have examined the effect of L-glutamine, an inhibitor of fatty acid oxidation, on the development of defective blood glucose regulation caused by a 48-hour infusion of 10% intralipid in rats. Male Sprague-Dawley rats (200-290 g) were anesthetized with sodium pentobarbital, the right femoral vein cannulated, and baseline blood samples were taken. Each rat was placed in a metabolic cage with access to water, in the presence or absence of rodent chow. Two hours after waking, the rats were infused with 10% intralipid with either saline (control), 2% L-glutamine, or 2% L-alanine. After 48 hours, all animals were sacrificed and blood samples were again obtained. The mean +/- SEM plasma glucose levels before and after lipid infusion at the rate of 1 mL/hr in control rats fed ad libitum, were 125 +/- 13 and 170 +/- 5 mg/dL (p < 0.01, n = 7). Similarly, plasma free fatty acids (FFA) in these animals rose from 0.74 +/- 0.11 to 1.34 +/- 0.32 mmol/L (p < 0.05). Plasma insulin levels also increased from 337 +/- 44 to 1278 +/- 88 pg/mL (p < 0.01). Reduction of intralipid dose infusion did not prevent insulin resistance characterized by hyperglycemia and hyperinsulinemia. However, addition of L-glutamine to the high-dose lipid infusion with chow feeding prevented changes in plasma glucose, insulin levels, and FFA but not triglyceride levels. Also, glutamine but not alanine supplementation in intralipid infused rats without chow feeding prevented changes in plasma glucose, insulin, and malondialdehyde levels. In conclusion, these data show that glutamine supplementation during intravenous lipid administration in rats prevents the development of impaired glucose regulation associated with hyperlipidemia.
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PMID:Effect of L-glutamine supplementation on impaired glucose regulation during intravenous lipid administration. 887 24

THE AUTHORS STUDIED THE PREVALENCE AND RISK FACTORS of hypertension in samples of 2053 Japanese ages 40 to 70 in Hiroshima, Hawaii, and Los Angeles. The prevalence of hypertension (systolic blood pressure greater than or equal to 140 mmHg, diastolic blood pressure greater than or equal to 90 mmHg, or receiving antihypertensive drug treatment) was higher in Hawaii and Los Angeles for both sexes and almost all ages than in Hiroshima. The age- and sex-adjusted prevalence of hypertension in Hawaii, Los Angeles, and Hiroshima was 42.6%, 37.2%, and 29.7%. Hypertension was associated with a significant elevation in serum glucose, insulin, triglyceride, and total cholesterol levels in the combined participant population of Hawaii, Los Angeles, and Hiroshima. Age- and sex-adjusted mean values of serum total cholesterol, triglyceride, and insulin were highest in Hawaii and lowest in Hiroshima. The mean body mass index and 2-hour serum glucose levels were greatest in Hawaii and equal in the two other cohorts. These results suggest that hyperinsulinemia and hyperlipidemia may explain the prevalence of hypertension in the research participants.
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PMID:A comparison of the prevalence and risk factors of high blood pressure among Japanese living in Japan, Hawaii, and Los Angeles. 889 78


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