Alcohol Withdrawal–Induced Change in Lipoprotein(a)

Paassilta, Marita; Kervinen, Kari; Linnaluoto, Markku K.; Kesäniemi, Y. Antero

doi:10.1161/01.atv.18.4.650

Cited by 22 publications

(8 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…36 Serum GH levels were also measured in the present study and these levels were similar in teetotalers and heavy drinkers (1.53Ϯ5.50 versus 1.76Ϯ3.37 pmol/L, NS). These present data, however, do not rule out a role for GH or insulin-like growth factor-binding protein-1 22 in mediating the inverse relation between alcohol intake and Lp(a) levels, as, in our study, blood was drawn during daytime and insulin-like growth factor-binding protein-1 was not measured.…”

Section: Discussioncontrasting

confidence: 89%

“…21 The mechanism by which alcohol withdrawal is associated with an increase in Lp(a) levels is poorly understood and may implicate changes in insulin-like growth factor-binding protein-1. 22 However, whether the inverse association between alcohol intake and serum Lp(a) levels holds true for the entire size spectrum of apo(a) isoforms and whether it is because of altered synthetic function of the liver or changes in sex hormone status has not been investigated. Finally, the association between alcohol intake and Lp(a) levels in individuals of African descent has only been documented incompletely.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Dose-Dependent Inverse Relationship Between Alcohol Consumption and Serum Lp(a) Levels in Black African Males

Fontana

Mooser

Bovet

et al. 1999

ATVB

View full text Add to dashboard Cite

Abstract-Serum or plasma levels of Lp(a) vary widely between individuals and are higher in Africans and their descendants compared with white persons. In whites, high serum levels of Lp(a) are associated with the premature development of atherosclerosis. In both ethnic groups, serum Lp(a) levels are highly genetically determined and only a few environmental or physiological factors, like testosterone or estrogen, have been shown to lower serum Lp(a) levels. In whites, alcohol consumption is associated with lower serum Lp(a) levels. However, the mechanism underlying this association and whether it holds true for blacks is not known. To address these questions, we analyzed serum Lp(a) levels in 333 middle-aged males of African descent from the Seychelles Islands (Indian Ocean). In addition, we analyzed the size of the apo(a) isoforms and the serum levels of albumin and sex hormones in a subset of 279 subjects. Serum Lp(a) levels were similar in teetotalers (median, 32.5 mg/dL; nϭ42) and occasional drinkers (median, 34.1 mg/dL; nϭ112). In contrast, individuals consuming 10 to 80 g of ethanol/d (nϭ83) and heavy drinkers (Ͼ80 g of ethanol/d, nϭ96) had a 9% and 32% lower median Lp(a) level than teetotalers, respectively (Pϭ0.01). The size distribution of the apo(a) isoforms and the mean serum levels of albumin, estradiol, and luteinizing hormone were similar in teetotalers and occasional drinkers compared with moderate and heavy drinkers. These latter 2 groups had lower serum levels of testosterone and sex hormone-binding globulin. These data indicate that alcohol intake is associated in a dosedependent manner with lower serum Lp(a) levels in males of African descent and that this association is not related to the size of the apo(a) isoforms, to the synthetic function of the liver, or to sex hormone biochemical status.

show abstract

Section: Discussioncontrasting

confidence: 89%

mentioning

confidence: 99%

Dose-Dependent Inverse Relationship Between Alcohol Consumption and Serum Lp(a) Levels in Black African Males

Fontana

Mooser

Bovet

et al. 1999

ATVB

View full text Add to dashboard Cite

show abstract

“…Also sensitivity analyses, which were conducted to reduce the risk of information bias by replacing self-reported alcohol consumption by objective markers of alcohol misuse, did not affect the major findings. Intervention studies demonstrated that both alcohol withdrawal (36) and an optimized diet with low content of total fat and refined carbohydrates (37) increases serum IGF1 levels in treated subjects. Thus, with respect to serum IGF1 levels and probably also with respect to the risk of metabolic syndrome, the cause of hepatic steatosis might be less important than hepatic steatosis itself.…”

Section: Ultrasoundkaltk Ultrasoundkaltc Ultrasoundcaltk Ultrasoundcaltcmentioning

confidence: 99%

Association between hepatic steatosis and serum IGF1 and IGFBP-3 levels in a population-based sample

Völzke

Nauck²,

Rettig³

et al. 2009

European Journal of Endocrinology

View full text Add to dashboard Cite

Context: It is assumed that hepatic steatosis plays a role in the development and progression of the metabolic syndrome and its cardiovascular sequelae. Low serum IGF1 levels might mediate these associations. Objectives: The aims of this study were i) to investigate the associations of hepatic steatosis with serum IGF1 and IGF binding protein-3 (IGFBP-3) levels using ultrasound and serum alanine aminotransaminase (ALT) data to define hepatic steatosis, and ii) to analyze the specific role of alcohol consumption in this context. Design: We analyzed data from the population-based Study of Health in Pomerania. Methods: We used data from 3863 subjects (1971 women) aged 20-79 years who had no history of viral hepatitis, liver cirrhosis, or malignant diseases. Liver hyperechogenicity was diagnosed using ultrasound. Serum IGF1 and IGFBP-3 levels were determined by automated two-site chemiluminescence immunoassays. Results: Hyperechogenic liver pattern was associated with low serum IGF1 levels and low serum IGF1/IGFBP-3 ratios. The lowest serum IGF1 and IGF1/IGFBP-3 values and highest IGFBP-3 levels were present in subjects who had a hyperechogenic liver pattern and increased serum ALT levels. All of these associations were independent of alcohol consumption. Conclusions: Our data show that hepatic steatosis is associated with low serum IGF1 levels. This association is independent of alcohol consumption.

show abstract

“…The chronic consumption of ethanol results in a marked decrease of the Lp(a) concentration which is dose-dependent and has no relationship with the size polymorphism of apo(a) [2,156,157]. Vice versa the Lp(a) concentration rises again after termination or reduction of alcohol consumption [158][159][160]. The mechanism of action is not completely known.…”

Section: Influence Of Nutrition and Life-style On Lp(a) Plasma Concenmentioning

confidence: 99%

“…The mechanism of action is not completely known. It is discussed that it involves insulin-like growth factor (IGF)-binding protein [2,159].…”

Section: Influence Of Nutrition and Life-style On Lp(a) Plasma Concenmentioning

confidence: 99%

Lipoprotein(a) - Structure, Epidemiology, Function and Diagnostics of a Cardiovascular Risk Marker

Siekmeier¹,

Scharnagl²,

Kostner³

et al. 2008

TOCCHEMJ

View full text Add to dashboard Cite

Decades after its first description by Berg 1963 lipoprotein(a) (Lp(a)) is an established risk marker of cardiovascular diseases which is independent from other risk markers. The main difference of Lp(a) compared to LDL is the apo(a) residue which is covalently bound to apoB. Apo(a) is a glycoprotein which underlies a large genetic polymorphism. The latter is caused by a variation of the kringle-IV-type-2 repeats of the protein which is characterized by a large structural homology to plasminogen. The Lp(a) plasma concentration in the population is highly skewed and determined to more than 90 % by genetic factors. In healthy subjects the Lp(a)-concentration is correlated to its synthesis and not to its metabolism. Plasma concentrations of Lp(a) are affected by different diseases (e.g. diseases of liver and kidney), hormonal factors (e.g. sexual steroids, glucocorticoids, thyroid hormones), individual and environmental factors (e.g. age, cigarette smoking) as well as pharmaceuticals (e.g. derivatives of nicotinic acid) and therapeutic procedures (lipid apheresis). However, even though a large number of studies on Lp(a) were performed up to now many details of its physiological function and regulation of plasma concentration are not yet understood. In addition, studies showed contradictory results because there were large differences of the included patients, use of not sufficiently validated tests as well as analysis of frozen samples. Aim of our review was to describe function and physiological regulation of Lp(a) as well as factors influencing its plasma concentration.

show abstract

Alcohol Withdrawal–Induced Change in Lipoprotein(a)

Cited by 22 publications

References 54 publications

Dose-Dependent Inverse Relationship Between Alcohol Consumption and Serum Lp(a) Levels in Black African Males

Dose-Dependent Inverse Relationship Between Alcohol Consumption and Serum Lp(a) Levels in Black African Males

Association between hepatic steatosis and serum IGF1 and IGFBP-3 levels in a population-based sample

Lipoprotein(a) - Structure, Epidemiology, Function and Diagnostics of a Cardiovascular Risk Marker

Contact Info

Product

Resources

About