To explain why some of us are svelte and others accumulate more reserves,we often refer to our metabolism and its intensity. This internal pace of life when we are at rest is also called basal metabolic rate. However, why and how the intensity of our basal metabolism varies between individuals or even species is not easy to explain. A recent theory suggests that the chemical composition and physical properties of cellular membranes function as a`metabolic pacemaker'. The activity of proteins floating in a phospholipid membrane will depend on the membrane's composition and will thus have a generalized effect on cellular activity and metabolism. So far, the theory seems to stand up as observations of many species and groups of animals have shown a relationship between cellular membrane phospholipid composition and basal metabolic rate. Pawel Brzęk, Katarzyna Bielawska, Aneta Ksiązek an d Marek Konarzewski from the University of Bialystok in Poland have investigated the mechanism that could explain variations in basal metabolism within a species and the role of membranes as metabolic pacemakers.
By selectively breading mice with higher or lower than average metabolic rate for more than 20 generations, the team has ended up with mice that have the same body mass but a 20% difference in metabolic rate at rest. Next, the team used their selected mouse lines to test the hypothesis that higher metabolic rate would be associated with an increase in the size of metabolically active organs (such as the heart, liver and kidneys) in combination with changes in the cell membrane phospholipid composition of these organs. Following the metabolic rate measurements, Brzęk's group weighed internal organs and analyzed the composition of membrane phospholipids of the liver and kidneys. It turned out that mice selected for higher metabolic rate had larger livers, kidneys and hearts, as predicted. The differences suggest a genetic correlation between the size of these organs and basal metabolic rate. In other words, evolutionary changes in basal metabolic rate are correlated with changes in size of these metabolically active organs. Still, the magnitude of the difference in metabolic rate could not be accounted for solely by variation in organ mass.
Next, the team investigated cellular membrane composition. The membrane pacemaker theory predicts that increased cellular metabolism is associated with a change in the membrane's composition (an increase in the occurrence of double bonds – unsaturation – in lipid chains). Of the two organs studied, both the liver and kidneys showed some differences in membrane composition between the high and low metabolic rate mice, but not according to the theory. Liver membranes from mice selected for a high metabolic rate had fewer double bonds in their lipid chains. The authors' observations clearly do not support the membrane pacemaker theory to explain small changes in basal metabolic rate within a species, at least not with the selection regime imposed. Still, the observed differences for many unsaturated lipids is puzzling and the team suspects that other aspects of cellular metabolism may also contribute to basal metabolic rate variation, such as altered mitochondrial enzyme activity.
Evolution of metabolic rate is hard to track but studies such as that of Brzęk and colleagues are helping to bridge the gap between the large variations found across species, and more subtle differences between individuals.
