Abstract
Linking peak energy metabolism to lifespan and aging remains a major question especially when focusing on lactation in females. We studied, if and how lactation affects in vitro mitochondrial oxygen consumption and mitochondrial fatty acid composition. In addition, we assessed DNA damage, lipid peroxidation and protein carbonyls to extrapolate on oxidative stress in mothers. As model system we used C57BL/6NCrl mice and exposed lactating females to two ambient temperatures (15 °C and 22 °C) while they nursed their offspring until weaning. We found that state II and state IV respiration rates of liver mitochondria were significantly higher in the lactating animals than in non-lactating mice. Fatty acid composition of isolated liver and heart mitochondria differed between lactating and non-lactating mice with higher n-6, and lower n-3 polyunsaturated fatty acids in the lactating females. Surprisingly, lactation did not affect protein carbonyls, lipid peroxidation and DNA damage, nor did moderate cold exposure of 15 °C. We conclude that lactation increases rates of mitochondrial uncoupling and alters mitochondrial fatty acid composition thus supporting the “uncoupling to survive” hypothesis. Regarding oxidative stress, we found no impact of lactation and lower ambient temperature and contribute to growing evidence that there is no linear relationship between oxidative damage and lactation.
Highlights
Linking peak energy metabolism to lifespan and aging remains a major task that has intrigued scientists for a long time
We propose that the adjustments occurring in isolated mitochondria from lactating females might further contribute to the processes occurring around peak lactation, i.e., sustained energy intake [4,5,6]
We conclude that lactation significantly increased in vitro mitochondrial oxygen consumption and rates of mitochondrial uncoupling
Summary
Linking peak energy metabolism to lifespan and aging remains a major task that has intrigued scientists for a long time. A decrease in ROS production should affect metabolism at most during peak phases of energy expenditure such as lactation in mammals but surprisingly few studies are available on this topic. In this contribution we aimed to test if mitochondrial metabolism and respiration would be altered during lactation by affecting oxidative stress in the females. Non-shivering thermogenesis is largely shut down [5] to limit hyperthermia during lactation [6] Do these fundamental changes in metabolism affect mitochondrial respiration, and, if so, to what extent? Do these fundamental changes in metabolism affect mitochondrial respiration, and, if so, to what extent? At this end, we were interested in effects of these changes on known side effects of chronic and intense production of ROS on macromolecules such as DNA, proteins and lipids
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