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)

Estradiol implants in chicks resulted in marked elevation of all major plasma lipids with greatest increase in triglyceride (TG) followed by phospholipid (PL) and cholesterol (C). During the two-wk period, plasma TG level in estrogen (E)-treated chicks increased to about 45 times that of controls (139.6 vs 6,368.3 mg/dl). The level of cholesterol also increased steadily during the same period, attaining nearly a six-fold increase in comparison with the control (150.7 vs 871.8 mg/dl), and the level of PL was markedly elevated from 209 to 2,861 mg/dl. Besides the induction of hyperlipidemia, E treatment also resulted in a notable alteration in the fatty acid composition of plasma lipids; there was an increase in oleic acid concomitant with a decrease in polyunsaturated fatty acids, particularly, linoleic acid. One day after implantation, the percentage of oleic acid in TG fraction increased from 39.2 to 43.7%, reaching 55.4% of the total fatty acids at day 14. In contrast, the levels of linoleic and arachidonic acid decreased significantly from 16.1 to 8.3% and 4.3 to 0.6%, respectively, during the same period. In cholesteryl ester (CE) and PL, the oleic acid level also increased from 25.2 to 47.3% in the former and from 11.9 to 29.6% in the latter, reflecting enhanced hepatic lipogenesis. Analysis of plasma lipoproteins in E-treated chicks revealed dramatic alterations in the concentrations of lipids and protein in individual lipoprotein fractions, especially very low density lipoprotein (VLDL) fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in plasma lipids, lipoproteins, triglyceride secretion and removal in chicks with estrogen implants. 339 19

The hormone levels in the anterior pituitary gland and serum in Nagase analbuminemia rats (NAR), a mutant strain established from Sprague-Dawley rats with hyperlipidemia, were examined. For the anterior pituitary gland, the prolactin, TSH, GH, LH and FSH contents in male NAR were significantly lower than those of normal rats. In female NAR, prolactin, TSH and LH levels were also lower than those in normal rats, whereas FSH and GH were normal. For the serum, the concentrations of TSH, total T3, total and free T4, estradiol-17 beta and testosterone were examined. The serum testosterone concentration in NAR was lower than that of normal rats. Histochemical examination of the hydroxysteroid dehydrogenase (HSD) activity of testes was made in relation to the serum testosterone level. NAR testes, which are rather small compared with those of normal rats, have lower HSD activity. A higher level of serum TSH was seen in NAR. Total and free T4 concentrations were low in the male NAR only. Estradiol-17 beta and T3 concentrations in NAR were unchanged. Changes in serum LH and FSH levels during the estrous cycle in NAR were also studied. Their patterns of change are normal.
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PMID:Hormone levels of anterior pituitary gland and serum in Nagase analbuminemia rats. 643 Jun 88

The present investigation was designed to examine the influence of genetic Type IV hyperlipoproteinemia on the metabolism of lipids in response to estrogen exposure. The influence of 17-Beta-estradiol * was examined in a dose-response study over a range of hormone concentration from 10 to 100 pg/ml in genetic hyperlipidemic Zucker rats. In oophorectomized female rats, replacement levels of plasma estradiol of 40 pg/ml resulted in maximal hypertriglyceridemia of approximately 500 mg/dl representing a 5-fold exaggeration of that observed in control genetically norm-lipemic animals. This hypertriglyceridemia was associated with an increased production of triglyceride (TG) in excess of clearance, with a resulting production: clearance ratio of approximately 1.5. Exposure to maximum blood levels of estradiol, approximately 100 pg/ml, resulted in sub-normal levels of plasma TG (-145 mg/dl) in association with a reduced production: clearance ratio of approximately 0.36. In contrast to the marked hypocholesterolemic response to maximum estrogen exposure seen in normolipemic animals, the genetic Type IV hyperlipemic animal failed to demonstrate reduced plasma cholesterol concentration. This phenomenon was related to a rise in plasma LDL concentration in conjunction with parallel reduction in plasma HDL2 levels.Thus, an abnormal ratio of excessive LDL: HDl emerged in response to estrogen exposure in this model of human Type IV lipemia. This observation suggests that the genetic predisposition of the host may be critical to both the quantitative as well as the qualitative response to estrogen.
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PMID:Influence of genetic hyperlipemia in the Zucker rat upon the lipemic response to graded estradiol exposure. 707 97

We hypothesized that estradiol treatment would improve vascular dysfunction commonly associated with obesity, hyperlipidemia, and insulin resistance. A sham operation or 17beta-estradiol pellet implantation was performed in male lean and obese Zucker rats. Maximal vasoconstriction (VC) to phenylephrine (PE) and potassium chloride was exaggerated in control obese rats compared with lean rats, but estradiol significantly attenuated VC in the obese rats. Estradiol reduced the PE EC50 in all groups. This effect was cyclooxygenase independent, because preincubation with indomethacin reduced VC response to PE similarly in a subset of control and estrogen-treated lean rats. Endothelium-independent vasodilation (VD) to sodium nitroprusside was similar among groups, but endothelium-dependent VD to ACh was significantly impaired in obese compared with lean rats. Estradiol improved VD in lean and obese rats by decreasing EC50 but impaired function by decreasing maximal VD. The shift in EC50 corresponded to an upregulation in nitric oxide synthase III protein expression in the aorta of the estrogen-treated obese rats. In summary, estrogen treatment improves vascular function in male insulin-resistant, obese rats, partially via an upregulation of nitric oxide synthase III protein expression. These effects are counteracted by adverse factors, such as hyperlipidemia and, potentially, a release of an endothelium-derived contractile agent.
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PMID:Estrogen has opposing effects on vascular reactivity in obese, insulin-resistant male Zucker rats. 1196 Sep 55