According to Squire (2009), the altered respiratory pattern in AMPK KO neonatal mice has attracted a lot of scientific approaches to reach out to traditional answers. Knockout mice and transgenic models have however come up with relativity pyramids, which have been efficient enough in explaining why AMPK KO neonatal exhibit altered respiratory patterns(Bertoldo, et al., 2009). This paper bases its assertions on relevant literature to depict the how AMPK, out of its function as a fuel gauge, plays a critical role in the control of respiratory patterns in neonatal mice.
AMPK protein kinase is a proposed energy regulator. Progressively, AMPK takes on monitoring of the cellular activities in response to environmental and nutritional variations. Once activated by catabolic pathways relevant for ATP production, switches off the entire pathways of lipogenesis in the mice(Bertoldo, et al., 2009). The consequences of AMPK functions in various energy production can be long term or short term, depending on the host.In the near future; AMPK alters phosphorylation of the regulatory proteins. Alteration of ATP anabolic pathways, in the long run, may have an effect on gene expression, as evident with AMPK KO neonatal whose altered respiratory patterns could be as a result of long-term AMPK effects (Bertoldo, et al., 2009).
Pharmacological activators have endeavored at giving specifics in explaining how ATP deactivation may eventually lead to respiratory system alterations. Notably, intracellular ATP concentration has to be maintained within a narrow range to sustain metabolism for the neonatal mice. ATP concentration levels necessary for sustained metabolism has to occur both at the system and cellular levels (Ahima, 2011). Substrate release or storage accompanied with the regulation of catabolic and anabolic pathways trigger the energy efficiency in the entire host. Respiration, being core to both cellular and system activities thus exhibits the primary effects of the ATP regulations.
Nurse (2012) asserts that numerous activities related to respiratory regulations in AMPK KO neonatal mice are triggered by varying ATP levels, further unearthing the relationship between AMPK activities and the respiratory systems. Central to the activities is the balancing of ATP/ AMP ratios. In response to activation of the AMPK, interrelated downstream activities ensue. Thus, stimulation of catabolic pathways, shutting down of anabolic pathways leading to soaring energy limitations or acquiring new sources of energy is eminent. Such activities are consequential to systematic operations of the AMPK KO neonatal mice. Synthesis of micro molecules relevant for respiratory activities such as the production of fatty acids, proteins lipids, glycogen, and cholesterol are highly inhibited. Pathophysiological role of AMPK is, therefore, critical to the explanation of how AMPK KO neonatal mice exhibit altered respiratory patterns (Ahima, 2011).
The second relevant commentary about the altered respiratory patterns could be that specific beta-activated kinase in the AMPK KO neonatal mice models. Before, it was believed that promotion of phosphorylation is primary activation of AMP and a subsequent binding to the AMPK (Nurse, 2012). Recent studies indicate that activation of β-kinase occurs through entire inhabitation of DE phosphorylation in Thr172 typically catalyzed by protein 2Cα(Bryne, Hiedelberger, &Waxham, 2014). The homologs have been evident in the whole mammal subunits. More specifically, Drosophila melanogaster well as the primitive Giardia lamblia, have shown the affinity to alterations (Nurse, 2012). All these studies exhibit high degree observations that signaling circuits have an ancient involvement in the regulation of broad-spectrum respiratory and metabolic homeostasis in AMPK KO neonatal mice models. From the discussion herein, altered respiratory patterns in AMPK KO neonatal mice models are as a result of the inhibiting characteristics of the AMPK or the normally in β-kinase activities either of which have to influence on cellular and system events.
References
Ahima, R. S. (2011). Metabolic Basis of Obesity. New York: Springer
Bertoldo, J. M. et al. (2009). AMPK: A Master Energy Regulator for Gonadal Function. Retrieved from: http://www.ncbi.blm.nih.gov/pmc/articles/PMC4500899
Bryne, J. H., Hiedelberger, R., &Waxham, M. N. (2014).From Molecules to Networks: An Introduction to Cellular and Molecular. Academic Press
Nurse, C. A. (2012). Arterial Chemoreception: From Molecules to Systems. Dordrecht: Springer
Squire, L. R. (2009). Encyclopedia of Neuroscience. Amsterdam: Elsevier
