Alteration of egg yolk cholesterol content and plasma lipoprotein profiles following administration of a totally synthetic HMG-CoA reductase inhibitor to laying hens

1993 ◽  
Vol 41 (7) ◽  
pp. 1094-1101 ◽  
Author(s):  
Robert G. Elkin ◽  
Marisue B. Freed ◽  
Karen A. Kieft ◽  
Roger S. Newton
Keyword(s):  
Reductase Inhibitor ◽  
Laying Hens ◽  
Egg Yolk ◽  
Cholesterol Content ◽  
Plasma Lipoprotein ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Yolk Cholesterol ◽  
Coa Reductase ◽  
Lipoprotein Profiles

The effect of an HMG CoA reductase inhibitor on plasma VLDL cholesterol and egg cholesterol in the laying hen

1994 ◽  
Vol 1994 ◽  
pp. 173-173
Author(s):  
C.D. Huggett ◽  
P.J. Buttery ◽  
A.M. Salter
Keyword(s):  
Cholesterol Synthesis ◽  
Genetic Selection ◽  
Egg Yolk ◽  
Cholesterol Content ◽  
Synthesis Inhibitor ◽  
Very Low Density Lipoproteins ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Yolk Cholesterol ◽  
Coa Reductase

In recent years there has been a concerted effort to reduce the cholesterol content of the human diet. The hens egg is a major source of cholesterol in the diet, and many attempts have been made to reduce its cholesterol content. Genetic selection [1,2], changes to the diet [1] and the use of hypocholesterolaemic drugs [1,3,4,5,6] have all been investigated. While some relatively modest changes have been reported, the majority of these studies suggest that egg yolk cholesterol is relatively resistant to change. However, little explanation has been given to account for these findings.Egg cholesterol is derived from the liver and transported to the developing oocyte within very low density lipoproteins (VLDL). These particles are also responsible for the transport of triacylglycerol to me egg. If egg cholesterol is to be reduced, men VLDL must be specifically depleted of cholesterol. In me present study we investigated the effects of a cholesterol synthesis inhibitor on plasma VLDL concentrations and egg cholesterol. The compound used was simvastatin, known to be a potent inhibitor of mammalian hepatic hydroxymethylglutaryl CoA (HMG CoA) reductase, an important enzyme in regulating cholesterol synthesis.

Effects of an HMG-CoA reductase inhibitor, simvastatin, on human myeloma cells

2004 ◽  
Author(s):  
Takemi Otsuki ◽  
Haruko Sakaguchi ◽  
Tamayo Hatayama ◽  
Tomohiro Fujii ◽  
Takayuki Tsujioka ◽  
...  
Keyword(s):  
Reductase Inhibitor ◽  
Hmg Coa Reductase ◽  
Myeloma Cells ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase ◽  
Human Myeloma Cells

Treatment of hypercholesterolemia with the HMG CoA reductase inhibitor, simvastatin

1989 ◽  
Vol 3 (2) ◽  
pp. 219-227 ◽  
Author(s):  
GMB Berger ◽  
AD Marais ◽  
HC Seftel ◽  
SG Baker ◽  
D Mendelsohn ◽  
...  
Keyword(s):  
Reductase Inhibitor ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

Serum lipoprotein Lp(a) concentrations are not influenced by an HMG CoA reductase inhibitor

1988 ◽  
Vol 66 (10) ◽  
pp. 462-463 ◽  
Author(s):  
J. Thiery ◽  
V. W. Armstrong ◽  
J. Schleef ◽  
C. Creutzfeldt ◽  
W. Creutzfeldt ◽  
...  
Keyword(s):  
Reductase Inhibitor ◽  
Serum Lipoprotein ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

Abstract 180: Synergistic Salutary Effects of HMG-CoA Reductase Inhibitor and Angiotensin II Receptor Blocker on Load-induced Heart Failure

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yasuhiro Maejima ◽  
Mitsuaki Isobe
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Reductase Inhibitor ◽  
Neonatal Rat ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

We have shown previously that combined HMG-CoA reductase inhibitor (statin) and angiotensin II receptor blocker (ARB) therapy significantly improves both symptoms and left ventricular (LV) function over time in patients with heart failure (HF) by a clinical study [ HF-COSTAR Trial]. We elucidated the mechanisms of combination therapy with the ARB (losartan, LOS) and long-acting and statin (simvastatin, SIM) for the treatment of load-induced heart failure. Salt-loaded Dahl salt-sensitive (DS) rats were treated with vehicle, LOS (5mg/kg/day), SIM (2mg/kg/day) and LOS + SIM for 16 weeks. LOS and SIM in combination improved LV dysfunction (ΔLV fractional shortening; LOS = 60%, SIM = 42%, LOS + SIM = 24%, p <0.05), limited LV hypertrophy (ΔLV septal thickness; LOS = −21%, SIM = −18%, LOS + SIM = −13%, p <0.05) and reduced cardiac fibrosis (ΔLV collagen density; LOS = −26%, SIM = −16%, LOS + SIM = −28%, p <0.05) more than LOS or SIM alone. Both Rho and matrix metalloprotease-9 (MMP-9) activity in LV tissue were increased in untreated DS rats, and LOS and SIM in combination decreased these changes more than did LOS and SIM monotherapies. We confirmed that the plasma level of Exp-3174 (E3174), a LOS metabolite and a potent inverse agonist of angiotensin II receptor type 1, was higher in rats treated with LOS and SIM in combination than in those treated with LOS alone (E3174/LOS ratio; LOS = 2.6 ± 0.3 vs. LOS + SIM = 3.2 ± 0.2, p <0.05). Next, to mimic the response of volume-overload heart failure in vitro , cultured neonatal rat cardiomyocytes (CMs) were cyclically stretched. Stretch-induced increased CM hypertrophy was suppressed by pretreatment with both SIM and E3174 more than by pretreatment with LOS, E3174, SIM, or LOS and SIM in combination. Mechanical stretch also induced activation of extracellular signal regulated kinase (ERK) and the stretch-induced ERK activation of CMs was also significantly suppressed by SIM + E3174. In conclusion, LOS and SIM had beneficial myocardial effects in rats with salt-sensitive hypertension, partly through promoting the accumulation of plasma E3174. SIM enhanced the myocardial protective effects of LOS through suppression of Rho and MMP-9 activity. Thus, a combination of ARB with statin has a promising potential as a therapeutic strategy for HF.

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