Effect of diet-induced weight loss on lipoprotein(a) levels in obese individuals with and without type 2 diabetes

Berk, Kirsten A.; Yahya, R.; Verhoeven, Adrie J.M.; Touw, J. F.; Leijten, Frank; Rossum, Elisabeth FC van; Wester, Vincent L.; Lips, Mirjam A.; Pijl, Hanno; Timman, Reinier; Erhart, Gertraud; Kronenberg, Florian; Lennep, Jeanine E. Roeters van; Sijbrands, Eric J.G.; Mulder, Monique

doi:10.1007/s00125-017-4246-y

Cited by 32 publications

(21 citation statements)

References 47 publications

(40 reference statements)

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“…Further studies have found that weight loss may not independently reduce Lp(a) concentrations. A pooled analysis of cohorts found that as weight loss ensued, Lp(a) concentrations surprisingly increased . Baseline Lp(a) concentrations on average between the four cohorts analyzed were approximately 40 mg/dL, well above the >20 mg/dL threshold reported in the initial study .…”

Section: Discussionmentioning

confidence: 75%

Consumption of a defined, plant‐based diet reduces lipoprotein(a), inflammation, and other atherogenic lipoproteins and particles within 4 weeks

Najjar

Moore

Montgomery

2018

Clinical Cardiology

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A defined, plant-based diet has a favorable impact on Lp(a), inflammatory indicators, and other atherogenic lipoproteins and particles. Lp(a) concentration was previously thought to be only minimally altered by dietary interventions. In this protocol however, a defined plant-based diet was shown to substantially reduce this biomarker. Further investigation is required to elucidate the specific mechanisms that contribute to the reductions in Lp(a) concentrations, which may include alterations in gene expression.

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Section: Discussionmentioning

confidence: 75%

Consumption of a defined, plant‐based diet reduces lipoprotein(a), inflammation, and other atherogenic lipoproteins and particles within 4 weeks

Najjar

Moore

Montgomery

2018

Clinical Cardiology

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“…The detection limit of the assay was 3.0 mg/dL and the mean intraassay variability was 2.8%. Sampling at two different time points in 28 healthy controls with an interval of 2-4 months did not reveal significant changes in Lp(a) level [27]. At baseline, the number of apo(a) KIV repeats was determined by SDS agarose gel electrophoresis and immunoblotting, as previously described [26].…”

Section: Anthropometric and Laboratory Measurementsmentioning

confidence: 99%

Statin Treatment Increases Lipoprotein(A) Levels In Subjects With Low Molecular Weight Apolipoprotein(A) Phenotype

et al. 2019

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High levels of Lp(a) may contribute to the residual cardiovascular risk in statin-treated dyslipidemic patients. • Reported data on modulatory effects of statins on plasma Lp(a) levels are inconsistent. • Statin treatment increases Lp(a) levels in patients with dyslipidemia, exclusively in those with the LMW apo(a) phenotype. • The increase in Lp(a) levels upon statin treatment was not associated with common LPA SNPs or change in LDL cholesterol. A R T I C L E I N F O Keywords: Statin Dyslipidemia lipoprotein(a) KIV2 LPA gene A B S T R A C T Background and aims: We aimed to evaluate the effect of statin treatment initiation on lipoprotein(a) [Lp(a)] levels in patients with dyslipidemia, and the interactions with the apolipoprotein(a) [apo(a)] phenotype, LPA single nucleotide polymorphisms (SNPs) and change in LDL cholesterol.Methods: The study population consisted of patients with dyslipidemia, predominantly familial hypercholesterolemia, who first initiated statin treatment (initiation group; n = 39) or were already on stable statin treatment for at least 4 months (control group; n = 42). Plasma Lp(a) levels were determined with a particle-enhanced immunoturbidimetric assay before and at least 2 months after start of statin treatment in individuals of the initiation group, and at two time points with an interval of at least 2 months in the control group. High and low molecular weight (HMW and LMW, respectively) apo(a) phenotype was determined by immunoblotting, and the common LPA SNPs rs10455872, rs3798220 and rs41272110 by Taqman assay. Results: Plasma Lp(a) levels did not increase significantly in the initiation group (median 20.5 (IQR 10.9-80.7) to 23.3 (10.8-71.8) mg/dL; p = 0.09) nor in the control group (30.9 (IQR 9.2-147.0) to 31.7 (IQR 10.9-164.0) mg/dL; p = 0.61). In patients with the LMW apo(a) phenotype, Lp(a) levels increased significantly from 66.4 (IQR 23.5-148.3) to 97.4 (IQR 24.9-160.4) mg/dL (p = 0.026) in the initiation group, but not in the control group and not in patients characterized by the HMW apo(a) phenotype. Interactions with common LPA SNPs and change in LDL cholesterol were not significant. Conclusions: Statins affect Lp(a) levels differently in patients with dyslipidemia depending on the apo(a) phenotype. Statins increase Lp(a) levels exclusively in patients with the LMW apo(a) phenotype.Abbreviations: Apo(a), apolipoprotein (a); HMW, high molecular weight (apo(a) phenotype); KIV, kringle IV; LMW, low molecular weight (apo(a) phenotype); Lp (a), Lipoprotein (a)

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“…Increasing evidence supports elevated Lp(a), which may be defined as >75 nmol/l or 30 mg/dl, for being an independent and important risk factor for CVD (2) . The plasma level of Lp(a) is considered to be determined mostly by the LPA gene locus (3) ; however, lifestyle-induced changes in the plasma level of Lp(a) have been reported (4)(5)(6)(7)(8) .…”

mentioning

confidence: 99%

“…In the reanalysis of the Sydney Diet Heart study, it was shown that the intervention group had higher rates of death than controls (19) ; and in a Mendelian randomisation study, genetically predicted linoleic acid was shown not to be associated with ischemic heart disease but was associated with lower diabetes risk (20) . Recently, Berk et al found increased Lp(a) levels elicited by diet-induced weight loss after a low-fat diet in overweight and obese subjects (4) . However, they found no change in Lp(a) levels after bariatric surgery (4) , suggesting a role of dietary FA in the regulation of Lp(a), rather than weight loss per se.…”

mentioning

confidence: 99%

“…Recently, Berk et al found increased Lp(a) levels elicited by diet-induced weight loss after a low-fat diet in overweight and obese subjects (4) . However, they found no change in Lp(a) levels after bariatric surgery (4) , suggesting a role of dietary FA in the regulation of Lp(a), rather than weight loss per se. Indeed, randomised controlled trials (RCT) have found Lp(a)-increasing effects of low-fat v. low carbohydrate diets (5)(6)(7)(8) .…”

mentioning

confidence: 99%

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Lipoprotein(a) concentration is associated with plasma arachidonic acid in subjects with familial hypercholesterolaemia

et al. 2019

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Elevated lipoprotein(a) (Lp(a)) is associated with CVD and is mainly genetically determined. Studies suggest a role of dietary fatty acids (FA) in the regulation of Lp(a); however, no studies have investigated the association between plasma Lp(a) concentration and n-6 FA. We aimed to investigate whether plasma Lp(a) concentration was associated with dietary n-6 FA intake and plasma levels of arachidonic acid (AA) in subjects with familial hypercholesterolaemia (FH). We included FH subjects with (n 68) and without (n 77) elevated Lp(a) defined as ≥75 nmol/l and healthy subjects (n 14). Total FA profile was analysed by GC–flame ionisation detector analysis, and the daily intake of macronutrients (including the sum of n-6 FA: 18 : 2n-6, 20 : 2n-6, 20 : 3n-6 and 20 : 4n-6) were computed from completed FFQ. FH subjects with elevated Lp(a) had higher plasma levels of AA compared with FH subjects without elevated Lp(a) (P = 0·03). Furthermore, both FH subjects with and without elevated Lp(a) had higher plasma levels of AA compared with controls (P < 0·001). The multivariable analyses showed associations between dietary n-6 FA intake and plasma levels of AA (P = 0·02) and between plasma levels of Lp(a) and AA (P = 0·006). Our data suggest a novel link between plasma Lp(a) concentration, dietary n-6 FA and plasma AA concentration, which may explain the small diet-induced increase in Lp(a) levels associated with lifestyle changes. Although the increase may not be clinically relevant, this association may be mechanistically interesting in understanding more of the role and regulation of Lp(a).

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Effect of diet-induced weight loss on lipoprotein(a) levels in obese individuals with and without type 2 diabetes

Cited by 32 publications

References 47 publications

Consumption of a defined, plant‐based diet reduces lipoprotein(a), inflammation, and other atherogenic lipoproteins and particles within 4 weeks

Consumption of a defined, plant‐based diet reduces lipoprotein(a), inflammation, and other atherogenic lipoproteins and particles within 4 weeks

Statin Treatment Increases Lipoprotein(A) Levels In Subjects With Low Molecular Weight Apolipoprotein(A) Phenotype

Lipoprotein(a) concentration is associated with plasma arachidonic acid in subjects with familial hypercholesterolaemia

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