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

In fed rats the effects of catechloamines and adrenergic antagonists on blood glucose, free fatty acids (FFA), and liver glycogen levels were investigated in order to determine the role of alpha- and beta-adrenergic receptors in metabolic responses to catechloamines. Hyperglycemic responses to dopamine (DA), noradrenaline (NA), adrenaline (A) and isoprenaline (ISP) were dose-related and accompained by a depletion of liver glycogen. The relative potencies in producing hyperglycemia and in causing liver glycogenolysis were in descending order of potency, A, NA, DA and ISP. Hyperlipemic response was most potent to NA and DA, weaker to ISP, and least potent to A. Phentolamine antagonized completely both hyperglycemia and hepatic glycogen depletion induced by all catecholamines. Propranolol impaired only hyperglycemic responses to A and ISP. Phentolamine antagonized hyperlipemia induced by DA and NA but only partially impaired hyperlipemia after A. Propranolol only partially antagonized hyperlipemic responses to NA and ISP without influencing DA--and A-induced hyperlipemia. The results indicate that in fed rats hyperglycemic responses to catecholamines are mediated mainly by an alpha-adrenergic receptor, and hyperlipemic responses do not fit inton the alpha-receptor or beta-receptor classification.
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PMID:Effect of catecholamines and adrenergic antagonists on blood glucose, free fatty acids and liver glycogen levels in fed rats. 75 44

The metabolic effects of celiprolol, a new beta-adrenoceptor blocking agent with intrinsic sympathomimetic activity and alpha 2-blocking properties, were evaluated in a series of patients with hypertension, both with and without hyperlipidemia. Propranolol was tested as the reference drug in a randomized double-blind trial. Of the 35 patients of both sexes who completed the study, 17 were hyperlipidemic (low-density lipoprotein cholesterol greater than or equal to 170 mg/dl) and 18 were normolipidemic. Both drugs exerted a similar hypotensive effect after gradual dose adjustment; however, propranolol reduced heart rate to a higher extent (-20.5%) than celiprolol (-7.7%). Propranolol determined a significant rise of total and very low-density lipoprotein (VLDL) associated triglyceridemia, whereas high-density lipoprotein cholesterol (HDL cholesterol) levels and the total cholesterol/HDL cholesterol ratios were significantly depressed, particularly in hyperlipidemic patients. Celiprolol, in contrast, slightly decreased triglyceridemia (significantly in the hyperlipidemic group at week 12) and caused a 5% increase of the HDL cholesterol levels. The total cholesterol/HDL cholesterol ratio was reduced by celiprolol at week 16 in both hyperlipidemic and normolipidemic patients. The effects of the two beta-adrenoceptor blockers on HDL cholesterol and triglyceride levels differed significantly after 12 and 16 weeks of treatment, which confirm the divergent metabolic effects of the two agents.
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PMID:Lipid effects of celiprolol, a new cardioselective beta-blocker, versus propranolol. 256 18

The effect of body weight excess and hyperlipidemia on stimulated growth hormone (GH) secretion and serum somatomedin activity (SSA) has been investigated. Among 40 obese men gradually impairment of GH secretory response during the insulin hypoglycemia test was shown. Propranolol-L-DOPA administration elicited satisfactory GH secretory response only in the subgroup of patients with the mild weight excess. SSA was found to be in the normal range among the whole group of obese patients, however, it was significantly depressed in subjects with average weight excess higher than 100%. Obese men with hypertriglyceridemia and hypercholesterolemia presented low SSA even when their weight excess was relatively moderate, i.e., 52% and 57%, respectively.
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PMID:Serum somatomedin activity and growth hormone level in obese men: dependence on degree of obesity and hyperlipidemia. 355 17

The metabolic effects of acebutolol, a cardioselective beta-adrenergic blocker, and of propranolol, a nonselective beta blocker, were evaluated. Our subjects were 20 men with chronic stable angina; none had diabetes. An initial 4-wk, single-blind control phase was followed by two drug treatment periods, each a 3-wk double-blind titration phase (using increasing doses of acebutolol or propranolol), followed by a 5-wk double-blind maintenance phase. Metabolic studies were performed at the end of the control and maintenance phases. Propranolol induced elevation in basal serum glucose concentrations and both propranolol and acebutolol decreased glucose tolerance at 2.5 and 3 hr. There was no noticeable effect on insulin secretion by either drug. Neither propranolol nor acebutolol induced hyperlipidemia. There was a small decrease in total serum cholesterol after propranolol. Both drugs decreased low-density lipoprotein cholesterol. No effects were noted on the levels of serum triglycerides, high-density lipoprotein cholesterol, or free fatty acids.
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PMID:Glucose and lipid metabolism during acebutolol and propranolol therapy of angina in nondiabetic patients. 633 62

The influence of elevated concentration of lipids in blood on the concentration of drugs in organism was observed in 1976. The following experiments have revealed that pharmacokinetics of lipophilic drugs in hyperlipidemia is altered. The purpose of this paper was to evaluate the effect of hypolipemic treatment on the propranolol pharmacokinetics, to take into account phenotype of hydroxylation and type of primary hyperlipidemia. The study was carried out on 37 patients (34 patients EM and 3 patients PM) with hypercholesterolemia, hypertriglyceridemia and mixed form of hyperlipidemia. Duration of hypolipemic therapy was 30 days. Pharmacokinetic studies were carried out twice i.e. at the onset of the study and following a 30-day period of hypolipemic treatment. Propranolol was given orally as a single dose 80 mg. Blood serum was sampled during administration. HPLC method was used to determine blood serum concentration of propranolol. The one-compartment model was applied for calculation of pharmacokinetic parameters. The obtained results have disclosed that hypolipemic therapy altered pharmacokinetic parameters of propranolol. Intensity and course of these changes depend on the type of hyperlipidemia. The most pronounced changes were observed in patients EM with hypertriglyceridemia. Lowering of propranolol concentration in blood, elevated penetration into tissues and accelerated elimination were revealed (Fig. 3, 4). Similar changes, but lesser intensity were observed in patients with mixed form of hyperlipidemia (Fig 5, 6). Alteration of pharmacokinetic parameters of propranolol in hypercholesterolemic patients were slight and contrasting the patients with hypertriglyceridemia and mixed form of hyperlipidemia. The lowering of cholesterol concentration in blood has slight influence on normalization of propranolol kinetics (Fig 1, 2). In patients with phenotype PM pharmacokinetic parameters of propranolol were changed, under used treatment too. Due to the limited number of patients, conclusions should be carefully drawn. The actual results have disclosed a decrease in lipids concentration, mainly triglycerides, which causes changes in pharmacokinetics of propranolol in patients with phenotype PM as well.
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PMID:[The effect of hypolipemic treatment on the pharmacokinetics of propranolol]. 947 24

The lipophilic beta-adrenoreceptor antagonist propranolol has been studied to define its pharmacokinetic and pharmacodynamic characteristics in hyperlipidemic patients. A total of 48 subjects were allocated to four study groups: (1) healthy volunteers, (2) hypercholesterolemic patients, (3) hypertriglyceridemic subjects, and (4) patients with a mixed form of hyperlipidemia. Propranolol was given orally as a single dose of 80 mg. Heart rate was measured during 12 hours. At each point, the concentrations of propranolol were estimated. Moreover, heart rate and arterial systolic blood pressure were examined at rest and after a submaximal exercise test 3 hours after administration of propranolol (i.e., at the peak of propranolol concentration in the blood serum). A significant increase in the area under the serum concentration-time curve (AUC) by 39% and a reduction of the volume of distribution and total body clearance by 48% and 46%, respectively, without a significant change in the half-life time, were observed in patients with hypertriglyceridemia in comparison with the control group. The acceleration of exercise heart rate and the elevation of systolic blood pressure were comparable in all groups in the study, whereas blood serum concentrations of propranolol in patients with hypertriglyceridemia (group 3) and the mixed form of hyperlipidemia (group 4) were markedly altered from those observed in normolipemic subjects. No relationship between the concentration of propranolol and the heart rate in the group with hypertriglyceridemia was seen. In the light of this study, the authors suggest that lipid metabolism disturbances do not affect the pharmacodynamics of propranolol.
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PMID:Studies on the pharmacokinetics and pharmacodynamics of propranolol in hyperlipidemia. 1043 35

An influence of hydroxylation phenotype on the concentration of propranolol [corrected] was examined in 52 subjects with hyperlipidemia divided into 4 groups: 1--control, normolipemic, 2--hypercholesterolemic, 3--hypertriglyceridemic, and 4--mixed-form hyperlipidemic. Each study group included extensive metabolizers and one subject characterized by a poor hydroxylation phenotype. Propranolol was given intragastrically at a single dose of 80 mg [corrected]. Blood was sampled within 24 hours following the drug administration. HPLC method was used for determining blood serum concentrations of propranolol. In each study group mean blood serum concentrations of propranolol in poor metabolizers were at maximum in subject with hypertriglyceridemia, at minimum in the normolipemic one, and intermediate in hypercholesterolemic (upper) and mixed-form hyperlipidemic ones. Lipid metabolic disturbances also affected blood serum concentrations. They were the highest in hypertriglyceridemic patients, whereas in hypercholesterolemic were, in early stage of observation, even lower then in normolipemic subjects. Blood serum concentrations of propranolol [corrected] attained minimal values in patients with mixed form of hyperlipidemia. In the light of the present study we can state that hyperlipidemia modifies the blood serum concentrations of propranolol [corrected]. Although, the type of hyperlipidemia and lipophilic propranolol are not the only determinants affecting blood serum concentrations of propranolol, but also a genetic factor, i.e. hydroxylation phenotype may play an important role.
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PMID:[Effect of hydroxylation polymorphism on the concentration of propranolol in the blood of humans with hyperlipidemia]. 1071 Sep 48