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Owesny 2023 MiP2023

From Bioblast
Owesny Patricia
Impairment of cardiac function and mitochondrial energy metabolism through diet induced obesity in aging.

Link: MiP2023 Obergurgl AT

Owesny Patricia (2023)

Event: MiP2023 Obergurgl AT

Authors: Owesny Patricia, Hegemann N, Kuebler WM, Ost Mario, Grune T, Ott C

Cardiac aging is a multifactorial process, which is associated with increased oxidative stress, cell death and mitochondrial abnormalities. These factors can lead to an overall impairment of cardiac function and substrate utilization [1,2]. With the increased prevalence of obesity and related comorbidities, especially coronary heart disease, it was proposed that obesity could present a condition of premature heart aging [3]. Therefore, our aim is to compare the impact of obesity and aging on heart function, as well as the cardiac energy metabolism, focusing on mitochondria.
Our experimental design of diet-induced obesity contains three different age groups (22, 76 and 106 weeks), where male C57BL/6J mice receive either a High fat/High-carb or a Standard diet for 8 weeks. After dietary intervention, mice underwent echocardiographic or metabolic treadmill analysis. Heart tissue was used for the Oroboros O2k measurement of mitochondrial bioenergetics. In further studies of cardiac energy metabolism Western blot and qPCR in heart tissue and isolated cardiomyocytes were performed.
Echocardiography revealed a decline in cardiac output in mice 76 and 106 weeks of age with a further decrease by High fat/High-carb diet. Interestingly, these effects were more pronounced in 76 weeks group. In the same group we investigated indications of an impaired mitochondrial energy metabolism, specifically associated with cardiomyocytes. Although, loss of cardiac function with age has been previously described, we demonstrate here a key role for mitochondrial energy metabolism in this loss of function.

  1. Houtkooper R H, Argmann C, Houten S M, Cantó C, Jeninga E H, Andreux P A, Thomas C, Doenlen R, Schoonjans K, Auwerx J (2011), The metabolic footprint of aging in mice.
  2. Lazzeroni D, Villatore A, Souryal G, Pili G, Peretto G (2022), The Aging Heart: A Molecular and Clinical Challenge.
  3. Ren J, Dong F, Cai G-J, Zhao P, Nunn J M, Wold L E, Pei J (2010), Interaction between age and obesity on cardiomyocyte contractile function: role of leptin and stress signaling.


Figure 1: Interplay between aging, obesity and energy metabolism and the impact of heart.


Owesny Patricia1,3, Hegemann N2,3, Kuebler WM2, Ost M4, Grune T1,3,5, Ott C1,3
  1. Dept of Molecular Toxicology, German Inst of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany
  2. Dept of Physiology, Charité Univ medicine Berlin, Berlin, Germany
  3. ZHK (German Center for Cardiovascular Research), partner site Berlin, Berlin, Germany
  4. Paul Flechsig Inst of Neuropathology, Univ hospital Leipzig, Leipzig, Germany
  5. German Center for Diabetes Research (DZD), München-Neuherberg, Germany
Corresponding author:

Labels: Pathology: Obesity 

Organism: Mouse  Tissue;cell: Heart 

HRR: Oxygraph-2k  Event: E2