Oxidative stress energy utilization

The actions of epinephrine and norepinephrine in the liver, the adipocyte, the skeletal muscle cell, and the a and 3 cells of the pancreas direcdy influence fuel metabolism (Fig. 43.6). These catecholamines are counterregulatory hormones that have metabolic effects directed toward mobilization of fuels from their storage sites for oxidation by cells to meet the increased energy requirements of acute and chronic stress. They simultaneously suppress insulin secretion, which ensures that fuel fluxes will continue in the direction of fuel utilization rather than storage as long as the stressful stimulus persists. 

The oxidation of fuels converts approximately 25% of the potential energy present in the foods ingested by humans to ATP. This relative inefficiency of the human engine leads to the production of heat as a consequence of fuel utilization. This inefficiency, in part, allows homeothermic animals to maintain a constant body temperature in spite of rapidly changing environmental conditions. The acute response to cold exposure is shivering, which is probably secondary to increased activity of the sympathetic nervous system in response to this stressful stimulus. 

To generate a specific structure or texture on the adherend surface. Even though mechanical interlocking may not be responsible for primary bonding, the complex structures present on, for example, conversion-coated or anodized surfaces may help increase joint fracture energies by redistributing the stresses away from any interphasial polymer. These structures also create an extended surface area, which may be utilized if the adhesive is able to flow into, for example, the pores on anodic oxides. 

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