Glucose metabolism and catecholamines

Abstract

Until now, catecholamines were the drugs of choice to treat hypotension during shock states. Catecholamines, however, also have marked metabolic effects, particularly on glucose metabolism, and the degree of this metabolic response is directly related to the beta2-adrenoceptor activity of the individual compound used. Under physiologic conditions, infusing catecholamine is associated with enhanced rates of aerobic glycolysis (resulting in adenosine triphosphate production), glucose release (both from glycogenolysis and gluconeogenesis), and inhibition of insulin-mediated glycogenesis. Consequently, hyperglycemia and hyperlactatemia are the hallmarks of this metabolic response. Under pathophysiologic conditions, the metabolic effects of catecholamines are less predictable because of changes in receptor affinity and density and in drug kinetics and the metabolic capacity of the major gluconeogenic organs, both resulting from the disease per se and the ongoing treatment. It is also well-established that shock states are characterized by a hypermetabolic condition with insulin resistance and increased oxygen demands, which coincide with both compromised tissue microcirculatory perfusion and mitochondrial dysfunction. This, in turn, causes impaired glucose utilization and may lead to inadequate glucose supply and, ultimately, metabolic failure. Based on the landmark studies on intensive insulin use, a crucial role is currently attributed to glucose homeostasis. This article reviews the effects of the various catecholamines on glucose utilization, both under physiologic conditions, as well as during shock states. Because, to date (to our knowledge), no patient data are available, results from relevant animal experiments are discussed. In addition, potential strategies are outlined to influence the catecholamine-induced effects on glucose homeostasis.

Ractopamine effect on lipid metabolism and GLUT4 amount of finishing pigs

“…As with catecholamines, the use of synthetic β-agonists may cause increased concentrations of glucose and nonesterified fatty acids in the plasma of supplemented animals; these changes have already been reported (14,22).…”

Impaired Fasting Glucose Is the Major Determinant of the 20‐Year Mortality Risk Associated With Metabolic Syndrome in Nondiabetic Patients With Stable Coronary Artery Disease

“…Acute event‐related glucose elevation is driven by a highly complex interplay of counterregulatory hormones, such as catecholamines, growth hormone, cortisol, and cytokines 45, 46, 47. Although the mechanism seems to be well known, the impact on DM development remains scarce 44, 48, 49.…”

Hyperglycemia in Aneurysmal Subarachnoid Hemorrhage: A Potentially Modifiable Risk Factor for Poor Outcome

“…This activation results in an increase in the levels of stress hormones such as cortisol and catecholamines up to day 10 after the aSAH (Naredi et al, 2000;Vergouwen et al, 2010). These hormones enhance glycogenolysis, gluconeogenesis, proteolysis, and lipolysis, all resulting in excessive glucose production (Barth et al, 2007;Seematter et al, 2004). Moreover, catecholamines inhibit glucose transport by inhibition of insulin binding, resulting in insulin resistance with hyperinsulinemia (Gearhart and Parbhoo, 2006;Hunt and Ivy, 2002).…”