scholarly journals Estrogen Replacement Therapy Increases Plasma Ghrelin Levels

2005 ◽  
Vol 90 (5) ◽  
pp. 2954-2963 ◽  
Author(s):  
Eija Kellokoski ◽  
Seppo M. Pöykkö ◽  
Anna H. Karjalainen ◽  
Olavi Ukkola ◽  
Jorma Heikkinen ◽  
...  

Ghrelin is a novel peptide hormone that has GH releasing activity and also other endocrine and metabolic functions. The purpose of this study was to investigate the effects of estrogen replacement therapy on plasma active ghrelin levels in 64 hysterectomized postmenopausal women receiving peroral estrogen (PE) or transdermal estrogen therapy for 6 months. Active ghrelin was measured using commercial RIA. Estrogen therapy increased plasma active ghrelin from 479 ± 118 to 521 ± 123 pg/ml (P = 0.002) among all the study subjects. PE therapy increased plasma ghrelin levels from 465 ± 99 to 536 ± 104 pg/ml (P = 0.001). Transdermal estrogen therapy did not increase plasma ghrelin levels significantly (from 491 ± 132 to 509 ± 138 pg/ml; P = 0.332). The relative changes in plasma ghrelin levels were associated with the relative changes in serum estradiol concentrations (r = 0.299; P = 0.017). During the estrogen therapy, negative associations were found between plasma active ghrelin levels and several plasma lipids (total cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, total triglycerides, and very low-density lipoprotein triglycerides). As a conclusion, estrogen replacement therapy increased active plasma ghrelin levels, particularly PE therapy. Additional studies are needed to determine the possible underlying mechanisms.

2020 ◽  
pp. 175-178
Author(s):  
L Steyn

Cholesterol plays a pivotal role in the functioning of healthy cells. Being mostly lipophilic, cholesterol is transported in the blood inside lipophilic particles, e.g. high-density lipoprotein (HDL), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL). Hypercholesterolaemia refers to elevated low-density lipoprotein cholesterol (LDL-C) levels, and increases the risk for premature atherosclerotic cardiovascular disease (ASCVD). Low-density lipoprotein receptors (LDL-R) on the surface of hepatocytes, are the primary receptors involved in clearing circulating LDL-C.


2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Aditya D Hendrani ◽  
Renato Quispe ◽  
Seth S Martin ◽  
Krishnaji R Kulkarni ◽  
Peter P Toth ◽  
...  

Background: RLP-C is comprised of atherogenic triglyceride- (TG-) rich lipoproteins, commonly defined as the sum of intermediate-density lipoprotein cholesterol (IDL-C) and very low-density lipoprotein cholesterol remnants (VLDL 3 -C). In clinical practice, the VLDL-C/TG ratio is used to diagnose type III dyslipidemia, a primary lipoprotein disorder characterized by high levels of RLP-C. Methods: Serum lipids of 556,307 U.S. adults with TG ≥130 mg/dL were analyzed by ultracentrifugation (VAP, Atherotech, Birmingham, AL). We estimated TG content in VLDL (VLDL-TG) as the product of VLDL-C and validated variable TG/VLDL-C factors. Non-VLDL-TG was then calculated as total TG minus VLDL-TG, for which negative values represented the presence of RLP-C. We examined the relationship of non-VLDL-TG to 1000 quantiles of VLDL-C/TG ratio. We defined a VLDL-C/TG ratio cutpoint for presence of RLP-C based on the quantile at which median non-VLDL-TG≤0. Results: We found median non-VLDL-TG≤0 at VLDL-C/TG = 0.18 (Figure) . There were 174,907 adults who did not meet diagnostic criteria for type III dyslipidemia (VLDL-C/TG 0.18 to <0.30), whose levels of RLP-C and non-VLDL-TG levels were 37 (31-46) and -20 (-40 to -8) mg/dL, respectively. A total of 1,550 adults met classical diagnostic criteria for type III dyslipidemia (VLDL-C/TG ≥0.3), whose plasma levels of RLP-C and non-VLDL-TG levels were 80 (67-101) and -187 (-290 to -129) mg/dL, respectively. Conclusion: A threshold of VLDL-C/TG ≥0.18 correlates with the accumulation of RLP-C in plasma. If validated in future studies, these findings will improve identification of individuals who are at greater risk for atherosclerotic disease.


1977 ◽  
Vol 23 (7) ◽  
pp. 1238-1244 ◽  
Author(s):  
P N Demacker ◽  
H E Vos-Janssen ◽  
A P Jansen ◽  
A van 't Laar

Abstract We evaluated the dual-precipitation method for quantitative measurement of lipoproteins as described by Wilson and Spiger [J. Lab. Clin. Med. 82, 473 (1973)] for normo- and hyperlipemic sera, by comparison with the results obtained with ultracentrifugation. If serum with an above-normal triglyceride concentration is analyzed, the very-low-density lipoprotein cholesterol value obtained with the precipitation method is usually too low. For measurement of high-density lipoprotein cholesterol the ultracentrifugation and precipitation procedures give comparable results, but the latter method is preferred because sinking pre-beta-lipoproteins present in the high-density lipoprotein fraction isolated by means of the ultracentrifuge may result in falsely high values for cholesterol in that fraction. Therefore, at least for the determination of very-low-density lipoprotein cholesterol in hyperlipemic serum, the use of an ultracentrifuge remains necessary. Because few laboratories have an ultracentrifuge at their disposal, it seemed important to look at the stability of sera in view of the forwarding of samples. Also, a way of increasing the efficiency of the ultracentrifuge was studied. Sera can be stored for a week at 4 degrees C or for 54 h at room temperature without noticeable effect on lipoprotein values. Moreover, reliable values can be obtained with an ultracentrifugation time of 8 h (0.8 X 10(8) g-min).


1990 ◽  
Vol 36 (9) ◽  
pp. 1673-1675 ◽  
Author(s):  
M González Estrada ◽  
C R Rodríguez Ferrer ◽  
I R Astarloa ◽  
E M Lahera

Abstract The values of low-density lipoprotein cholesterol obtained according to the Friedewald formula (Clin Chem 1972; 18:499-502), or by the De Long transformation (J Am Med Assoc 1986;256:2372-7), were compared with the values obtained when the individual cholesterol/triglyceride ratio of very-low-density lipoprotein was used for estimating the contribution of this lipoprotein to the total cholesterol. We found that these formulas gave the greatest errors for individuals with a low serum cholesterol/triglyceride ratio. We propose criteria for deciding when the numerically calculated value of low-density cholesterol is appropriate, and when it is not.


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