@article{HaringWylervonBallmoosAppeletal.2014,
  author    = {Haring, Bernhard and Wyler von Ballmoos, Moritz C. and Appel, Lawrence J. and Sacks, Frank M.},
  title     = {Healthy Dietary Interventions and Lipoprotein (a) Plasma Levels: Results from the Omni Heart Trial},
  doi       = {10.1371/journal.pone.0114859},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-111005},
  year      = {2014},
  abstract  = {Background: Increased lipoprotein(a) [Lp(a)] levels are associated with atherosclerotic cardiovascular disease. Studies of dietary interventions on changes in Lp(a) are sparse. We aimed to compare the effects of three healthy dietary interventions differing in macronutrient content on Lp(a) concentration. Methods: Secondary analysis of a randomized, 3-period crossover feeding study including 155 (89 blacks; 66 whites) individuals. Participants were given DASHtype healthy diets rich in carbohydrates [Carb], in protein [Prot] or in unsaturated fat [Unsat Fat] for 6 weeks each. Plasma Lp(a) concentration was assessed at baseline and after each diet. Results: Compared to baseline, all interventional diets increased mean Lp(a) by 2 to 5 mg/dl. Unsat Fat increased Lp(a) less than Prot with a difference of 1.0 mg/dl (95\% CI, -0.5, 2.5; p=0.196) in whites and 3.7 mg/dl (95\% CI, 2.4, 5.0; p<0.001) in blacks (p-value between races=0.008); Unsat Fat increased Lp(a) less than Carb with a difference of 20.6 mg/dl, 95\% CI, -2.1, 0.9; p=0.441) in whites and 21.5 mg/dl (95\% CI, -0.2, -2.8; p=0.021) in blacks (p-value between races=0.354). Prot increased Lp(a) more than Carb with a difference of 0.4 mg/dl (95\% CI, -1.1, 1.9; p=0.597) in whites and 2.2 mg/dl (95\%CI, 0.9, 3.5; p=0.001) in blacks (p-value between races=0.082). Conclusion: Diets high in unsaturated fat increased Lp(a) levels less than diets rich in carbohydrate or protein with greater changes in blacks than whites. Our results suggest that substitutions with dietary mono- and polyunsaturated fatty acids in healthy diets may be preferable over protein or carbohydrates with regards to Lp(a).},
  language  = {en}
}
@article{MayerLoefflerLozaValdesetal.2019,
  author    = {Mayer, Alexander E. and L{\"o}ffler, Mona C. and Loza Vald{\´e}s, Angel E. and Schmitz, Werner and El-Merahbi, Rabih and Trujillo-Viera, Jonathan and Erk, Manuela and Zhang, Thianzhou and Braun, Ursula and Heikenwalder, Mathias and Leitges, Michael and Schulze, Almut and Sumara, Grzegorz},
  title     = {The kinase PKD3 provides negative feedback on cholesterol and triglyceride synthesis by suppressing insulin signaling},
  series = {Science Signaling},
  journal   = {Science Signaling},
  edition   = {accepted manuscript},
  doi       = {10.1126/scisignal.aav9150},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-250025},
  year      = {2019},
  abstract  = {Hepatic activation of protein kinase C (PKC) isoforms by diacylglycerol (DAG) promotes insulin resistance and contributes to the development of type 2 diabetes (T2D). The closely related protein kinase D (PKD) isoforms act as effectors for DAG and PKC. Here, we showed that PKD3 was the predominant PKD isoform expressed in hepatocytes and was activated by lipid overload. PKD3 suppressed the activity of downstream insulin effectors including the kinase AKT and mechanistic target of rapamycin complex 1 and 2 (mTORC1 and mTORC2). Hepatic deletion of PKD3 in mice improved insulin-induced glucose tolerance. However, increased insulin signaling in the absence of PKD3 promoted lipogenesis mediated by SREBP (sterol regulatory element-binding protein) and consequently increased triglyceride and cholesterol content in the livers of PKD3-deficient mice fed a high-fat diet. Conversely, hepatic-specific overexpression of a constitutively active PKD3 mutant suppressed insulin-induced signaling and caused insulin resistance. Our results indicate that PKD3 provides feedback on hepatic lipid production and suppresses insulin signaling. Therefore, manipulation of PKD3 activity could be used to decrease hepatic lipid content or improve hepatic insulin sensitivity.},
  language  = {en}
}