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Copyright of Zeitschrift für Gerontologie und Geriatrie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aims: Inverse relationships have been described between the largely genetically determined levels of serum/plasma lipoprotein(a) [Lp(a)], type 2 diabetes (T2D) and fasting insulin. Here, we aimed to evaluate the nature of these relationships with respect to causality. Methods: We tested whether we could replicate the recent negative findings on causality between Lp(a) and T2D by employing the Mendelian randomization (MR) approach using cross-sectional data from three independent cohorts, Berlin Aging Study II (BASE-II; n = 2012), LIFE-Adult ( n = 3281) and LIFE-Heart ( n = 2816). Next, we explored another frequently discussed hypothesis in this context: Increasing insulin levels during the course of T2D disease development inhibits hepatic Lp(a) synthesis and thereby might explain the inverse Lp(a)-T2D association. We used two fasting insulin-associated variants, rs780094 and rs10195252, as instrumental variables in MR analysis of n = 4937 individuals from BASE-II and LIFE-Adult. We further investigated causality of the association between fasting insulin and Lp(a) by combined MR analysis of 12 additional SNPs in LIFE-Adult. Results: While an Lp(a)-T2D association was observed in the combined analysis (meta-effect of OR [95% CI] = 0.91 [0.87-0.96] per quintile, p = 1.3x10), we found no evidence of causality in the Lp(a)-T2D association ( p = 0.29, fixed effect model) when using the variant rs10455872 as the instrumental variable in the MR analyses. Likewise, no evidence of a causal effect of insulin on Lp(a) levels was found. Conclusions: While these results await confirmation in larger cohorts, the nature of the inverse Lp(a)-T2D association remains to be elucidated. [ABSTRACT FROM AUTHOR]

Background: Pharmacological options for the treatment of sarcopenia currently do not exist. However, off-label treatment options of some established drugs have been suggested. Objectives: The aim of this study was to assess differences in various muscle and physical performance parameters in relation to the intake of angiotensin-converting enzyme (ACE) inhibitors in a cohort of community-dwelling older people. Methods: Eight hundred and thirty-eight participants from the Berlin Aging Study-II (BASE-II) were included. Appendicular lean mass was assessed with dual-energy X-ray absorptiometry and related to height and body mass index. Muscle strength was measured by grip strength and related to muscle mass (arm muscle quality) and functional status was assessed via the timed 'Up and Go' test. Results: Users of ACE inhibitors had higher lean mass related to height but significantly lower lean mass related to body mass index ( p = 0.001 for women and p < 0.0001 for men). Moreover, they exhibited lower arm muscle quality ( p = 0.032 for women and p = 0.031 for men) and reported difficulties in climbing stairs more often than non-users ( p = 0.014 for women and p = 0.004 for men). After adjustment for confounders, there were no significant differences regarding lean mass, arm muscle quality and the timed 'Up and Go' test according to the use of ACE inhibitors. Conclusions: In BASE-II, no positive relationship was found between the intake of ACE inhibitors and lean mass, strength, muscle quality or function. Moreover, remarkable differences between parameters of absolute and relative lean mass in relation to the use of ACE inhibitors became evident. Fat mass proved to be an important confounder and therefore muscle mass cannot be viewed irrespectively of whole body composition. [ABSTRACT FROM AUTHOR]

Copyright of Zeitschrift für Gerontologie und Geriatrie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)