Abstract
Oxytocin (Oxt) is a nine amino acid peptide important in energy regulation and is essential to stress-related disorders. Specifically, low Oxt levels are associated with obesity in human subjects and diet-induced or genetically modified animal models. The striking evidence that Oxt is linked to energy regulation is that Oxt- and oxytocin receptor (Oxtr)-deficient mice show a phenotype characterized by late onset obesity. Oxt−/− or Oxtr−/− develop weight gain without increasing food intake, suggesting that a lack of Oxt reduce metabolic rate. Oxt is differentially expressed in skeletal muscle exerting a protective effect toward the slow-twitch muscle after cold stress challenge in mice. We hypothesized that Oxt potentiates the slow-twitch muscle as it does with the uterus, triggering “the oxytonic contractions”. Physiologically, this is important to augment muscle strength in fight/flight response and is consistent with the augmented energetic need at time of labor and for the protection of the offspring when Oxt secretion spikes. The normophagic obesity of Oxt−/− or Oxtr−/− mice could have been caused by decreased skeletal muscle tonicity which drove the metabolic phenotype. In this review, we summarized our findings together with the recent literature on this fascinating subjects in a “new oxytonic perspective” over the physicology of Oxt.
Highlights
According to the principle of “maximum parsimony” enunciated by Galileo Galilei as “Nature does not work with many things what it can operate with few,” means that every natural phenomenon is always realized with the minimum expenditure of both matter and energy [1,2,3]
A special emphasis will be given to the effects of Oxt on skeletal muscle and to our recent paradigm shifting hypothesis that Oxt may increase the tone of the slow-twitch muscle upregulating its receptor and triggering the “oxytonic contraction” after cold stress challenge in mice [10,11]
oxytocin receptor (Oxtr) regulates the coordinated gene response to cold stress (CS) through a feed-forward loop in brain [5]. This is supported by the fact that in a regression study upon elimination of Oxtr expression gene data in brain, we report a loss of correlation in gene expression of mice at thermoneutrality versus gene expression of cold-stressed mice [6]
Summary
According to the principle of “maximum parsimony” enunciated by Galileo Galilei as “Nature does not work with many things what it can operate with few,” (dialogue concerning the two chief world systems, Galileo Galilei, 1632) means that every natural phenomenon is always realized with the minimum expenditure of both matter and energy [1,2,3]. From an evolutionary point of view, the biological advantage of this pleiotropic mechanism is that the lack of effects of a specific gene following challenging situations as pathophysiological conditions or gene downregulation after cold stress challenge for example [5] can be counterbalanced by the action of other genes [5,6]. This brief explanation is to introduce that in this review, we will present data that Oxt has several effects different from the well-known effects on uterocontractility and lactation [7,8]. A special emphasis will be given to the effects of Oxt on skeletal muscle and to our recent paradigm shifting hypothesis that Oxt may increase the tone of the slow-twitch muscle upregulating its receptor and triggering the “oxytonic contraction” after cold stress challenge in mice [10,11]
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