Energy metabolism in trauma and sepsis: the role of fat.

摘要: There seems little doubt that there are signals for the increased mobilization of fat in shock, trauma, and sepsis. Whether those reflected by an actual increase is dependent on many variables including cardiovascular status. A hypothetical scheme based our own experiments hyperdynamics phases response to burn injury sepsis presented Figure 8. According this scheme, catecholamines stimulate lipolysis adipose tissue, resulting release glycerol FFA into plasma at rates. The cleared liver converted glucose--a process stimulated by, among other things, glucagon. Some flux also liver, whereupon fatty acids incorporated VLDL released again plasma. levels exert a dampening effect factors stimulating hepatic glucose production. At periphery, as well taken up rate. tissues attuned oxidation fat, consequence most energy production derived from oxidation. inhibitory complete glucose, so although may be accelerated rate, relative contribution total fall. Rather than being completely oxidized, pyruvate reduced lactate then contributes completing cyclical called Cori Cycle. Although all aspects supported data highlighted paper, it certainly must oversimplification overall substrate metabolism trauma It purpose highlighting potential role controller metabolic response, suggest enhanced one fundamental responses stress.