Young et al described the role

Young et al. [40] described the role of adenine monophosphate-activated protein kinase (AMPK) in the translocation of GLUT4 in the heart. The AMPK is activated during muscle contraction [74] by converting AMP to ATP. The adenosine analog, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), is a cardioprotective agent. It increases the glucose uptake and GLUT4 translocation in left ventricular papillary muscles of the rat [75]. Researchers have found that intracoronary infusion of AICAR also stimulates GLUT1 translocation to the sarcolemma. It was found that AMPK acts independently from the insulin-signaling pathway [75].
Cardiac glucose transporters in diseases
Conclusion
Funding
Stress physiology: the sympathetic nervous system and hypothalamic-pituitary-adrenal axis The central nervous system coordinates the physiological stress response through activation of two distinct systems, the sympathetic division of the autonomic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis. The sympathetic nervous system is responsible for the adaptive fight-or-flight response that enables a rapid and strategic deployment of resources to confront immediate real or perceived threats. Postganglionic sympathetic fibers predominantly signal via the release of catecholamines (norepinephrine and epinephrine) at synapses in target organs. In addition, preganglionic acetylcholinergic fibers innervating chromaffin cells in the adrenal medulla act at neuronal-type nicotinic Triptolide receptors (nAChRs) receptors (Sala et al., 2008) to induce the release of predominantly epinephrine, which enters systemic circulation and acts in a hormonal fashion to influence target tissues throughout the body. The latter system is referred to as the sympatho-adrenomedullary-axis (SAM) (Turner et al., 2012). Thus, the sympathetic nervous system response includes a very rapid release of catecholamines at specific target tissues via postganglionic fibers, and a slightly delayed hormonal action of catecholamines, predominantly epinephrine, acting through hormonal mechanisms. Alongside these relatively rapid physiologic responses to real or perceived threats is an activation of the HPA axis. The HPA axis hormonal cascade involves activation of corticotropin-releasing hormone- (CRH)-producing neurons in the parvocellular region of the paraventricular nucleus of the hypothalamus (PVN), which themselves are under control of a hierarchical system coordinating physiologic and behavioral responses to stressors (Herman and Cullinan, 1997; Herman et al., 2002a, Herman et al., 2002b; Herman et al., 2005; Herman et al., 1996). Upon activation of CRH-synthesizing neurons, CRH is released into the median eminence and subsequently transported via the hypothalamic-hypophyseal portal circulation to the anterior pituitary. Corticotropin-releasing hormone acts on corticotropin-releasing hormone type 1 receptors (CRHR1) on corticotrope cells to release adrenocorticotropic hormone (ACTH) into the systemic circulation (Aguilera, 1998; Aguilera et al., 2004). Adrenocorticotropic hormone acts on melanocortin 2 receptors (MC2R) on cells within the zona fasciculata of the adrenal cortex to stimulate synthesis and release of glucocorticoid hormones (cortisol in humans and fish, corticosterone in other vertebrates) into the systemic circulation (Gallo-Payet, 2016). Glucocorticoids act on intracellular receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) expressed in diverse target tissues including brain, various peripheral organs, and also the immune system, through genomic mechanisms that regulate gene transcription via GR (De Kloet et al., 1998; Hollenberg et al., 1985) and MR (Arriza et al., 1987; De Kloet et al., 1998).
Historical perspectives for interactions between glucocorticoids and monoaminergic uptake/clearance Although the sympathetic nervous system and HPA axis responses to stressors are often considered to act independently, it has been clear that they interact in a synergistic way to amplify adaptive, stress-related physiological responses. For example, early studies demonstrated that while infusion of cortisol had no effect, by itself, on plasma glucose concentrations, when cortisol was infused concurrently with epinephrine, the two compounds had a synergistic effect on plasma glucose concentrations, such that, after 5 h, the rise in plasma glucose concentrations was two-fold greater than the sum of the individual responses (Eigler et al., 1979). This effect was attributed to the ability of cortisol to sustain increases in glucose production induced by epinephrine (i.e., rather than epinephrine-induced changes in glucose clearance or plasma insulin levels) (Eigler et al., 1979). This effect of cortisol was an early example of a class of “permissive” effects or context-dependent effects of glucocorticoid hormones, effects that are now well established in the literature (Sapolsky et al., 2000). A frequently cited example involves the permissive role that glucocorticoids play to allow catecholamines to exert their full actions (Sapolsky et al., 2000), effects that have been documented in vascular and cardiac tissue (Fowler and Cleghorn, 1942; Fritz and Levine, 1951; Grunfeld and Eloy, 1987; Kalsner, 1969; Ramey et al., 1951; Sapolsky and Share, 1994; Schomig et al., 1976; Tanz, 1960). Among the potential mechanisms cited was the ability of glucocorticoids to inhibit catecholamine reuptake (Gibson, 2008; Sapolsky et al., 2000). As will be discussed in detail below, context-dependent effects of glucocorticoids in both the periphery and brain (for review, see Orchinik et al., 2009) may involve inhibition of uptake2, subsequently defined at the molecular level as organic cation transporter 3 (OCT3) (Kekuda et al., 1998; Wu et al., 1998) or extraneuronal monoamine transporter (EMT) (Grundemann et al., 1998b).