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)

An intravenous injection of 40 or 65 mg/kg streptozotocin induced not only diabetes but also severe hypertension in rats. Whereas the hyperglycemia developed fully within a few days after the injection of streptozotocin, the hypertension progessively advanced and reached maximum level several weeks after the treatment and lasted more than 20 weeks. Twenty mg/kg streptozotocin did not induce hyperglycemia but significantly increased blood pressure several weeks after the treatment. Arrest of growth, polyuria, glycosuria, hyperlipemia and lenticular cataracts developed in the animals treated with 40 or 65 mg/kg streptozotocin, but in none of the animals treated with 20 mg/kg. In histological examinations in the 24th week after the treatment, degranulation and necrosis in the pancreatic beta-cells, and vacuolization and deposition of PAS-positive materials in the renal proximal tubules were found in the animals treated with 40 or 65 mg/kg streptozotocin.
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PMID:Chronic hypertension induced by streptozotocin in rats. 15 77

The influence of experimentally induced hyperlipidemia and aging on the development of pulmonary foam cells (PFCs) was examined in Fischer 344 rats. The male and female rats were administered orally with cholesterol at a dosage level of 1000 mg/kg/day for 30 days from 6 to 10 weeks or from 33 to 37 weeks of age. The control rats received the vehicle only in the same manner. Plasma levels of total cholesterol, phospholipid, triglyceride (TG), beta-lipoprotein (beta-LP) and calcium in both control and cholesterol-administered groups were higher at 37 weeks than at 10 weeks of age. Plasma beta-LP and TG levels in the treated groups were significantly higher or tended to be higher than those of the controls at 10 and 37 weeks of age. Males of the treated group showed the highest level of beta-LP at 37 weeks of age, positively correlated with the highest incidence of PFCs. PFCs developed singly or in a small cluster in peribronchial and subpleural regions. PFCs had an abundant cytoplasm filled with many fine vacuoles containing neutral lipid and cholesterol. PFCs stained with PAS and reacted immunohistochemically with both anti-rat monocytes/macrophages monoclonal antibody and anti-lysozyme antibody. Moderately swollen macrophages with a foamy appearance were detected in perivascular connective tissues of the lungs and they were considered to represent an initial stage of the development of PFCs. These observations suggest that hyperlipidemic conditions, particularly hyper beta-lipoproteinemia, resulting from cholesterol administration or aging may be involved in the development of PFCs in rats.
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PMID:Influence of cholesterol administration and aging on the development of pulmonary foam cells in F344 rats. 260 22

A 35-years old female with Jordans' anomaly was reported. She had been treated for diabetes mellitus and hypertension at another hospital. She was admitted to our hospital for operation for diabetic retinopathy on July 9, 1992. Wright-Giemsa stained peripheral blood smear revealed multiple vacuoles in the cytoplasm of the granulocytes and monocytes. Histochemical studies of these vacuoles showed positive for Sudan III but negative for peroxidase, alkaline phosphatase and PAS staining. Electron microscopic examination revealed that lipid containing vacuoles had no clear membrane and were not associated with cell organelles. Laboratory findings of the serum showed hyperglycemia (FBS 188mg/dl), high HbA1c level (9.4%) and mild type IIa hyperlipidemia. Abdominal sonogram and abdominal CT showed no remarkable abnormalities except for mild fatty liver. Her elder sister and daughter had similar morphological findings in granulocytes, monocytes and lymphocytes.
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PMID:[A case of Jordans' anomaly]. 786 17

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

To clarify how Syrian hamsters of the APA strain (APA hamsters) keep a diabetic condition for a long period, the functional and histochemical changes in the pancreatic islets of diabetic APA hamsters were examined. By glucose tolerance test, no glucose-induced insulin secretion was seen in the diabetic APA hamsters. By immunohistochemistry, it was revealed that at 24 hr after SZ-injection, the number of islets had decreased and that remnant islets had become markedly smaller. The islets had hardly any insulin-immunoreactive cells and consisted of cells stained by anti-glucagon and somatostatin antibodies. One, three and six months after SZ-injection, a small number of cells with vacuolative changes, which were positive for PAS staining, were observed in most islets and the vacuolated cells were stained mainly by anti-insulin antibody. In addition, a number of PCNA-positive cells were observed, especially in the periphery of the vacuolated cells, while TUNEL-positive cells were not detected. This data suggests that beta-cells proliferating as a result of the replication of the resident beta-cells in islets had fallen into degeneration and necrosis by a stress, such as the glycogen deposition in hyperglycemia and hyperlipidemia. Consequently, secretion of insulin was maintained at low levels, which allowed the hamsters to live without insulin therapy in the diabetic condition for over 6 months.
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PMID:Functional and histochemical analysis on pancreatic islets of APA hamsters with SZ-induced hyperglycemia and hyperlipidemia. 1187 Nov 58

The involvement of hyperlipidemia in aggravation of nephrosis has remained controversial. In this study, to examine the influence of cholesterol on the kidney, normal SD rats were loaded with a normal diet(4.4% fat, 0.09% cholesterol) plus 0.25% cholesterol for 10 months, and the urinary excretion of protein, blood cholesterol level and histological renal changes were compared with those in the control group given the normal diet alone. The urinary protein excretion was increased after 4 months of cholesterol loading and was about 6 times the control value at the end of the study(10 months). At 10 months, the blood levels of total, HDL- and LDL + VLDL-cholesterols were also increased, and the arteriosclerosis index(HDL/LDL + VLDL ratio) was about 1.3 times the control value. Histologically, segmental lesions of glomeruli containing sclerosis/PAS positive material were stronger than in the control animals. Thus, this study revealed increased blood cholesterol and urinary protein excretion and aggravated histological changes of the kidney in rats given a long-term cholesterol load, suggesting that cholesterol may be a risk factor affecting the kidney.
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PMID:[Influence of a long-term load of dietary cholesterol on the rat kidney]. 1280 72