Help fill in the blanks Extended fasting will activate the processes of [glycolysis/gluconeogenesis] and [fatty acid synthesis/b-oxidation]. These processes will work to deplete [oxaloacetate/acetyl-CoA] and increase [oxaloacetate/acetyl-CoA]. As a result, flux through the citric acid cycle will [increase/decrease]. Ketone bodies will be produced in this state allowing for [NAD+/CoA/glucose] to be recycled. Ketosis also occurs in people on a [carb-rich/carb-poor] diet for similar reasons. Bafflingly at first, hyperglycemia in diabetics may also cause ketosis. The problem is not in the bloodstream in these patients, but in the hormones. Without insulin, [GLUT1/ GLUT2/GLUT4] will not appear on muscle cell membranes to clear glucose, and liver cells continue to receive signals from glucagon. Glucagon will [activate/inhibit] pathways that catabolize carbohydrate and [activate/inhibit] pathways that catabolize fatty acids to preserve the carbohydrate fuel of choice for the [liver/brain] and again causing ketosis. Lack of insulin thus results in an apparent feast in the bloodstream which cells do not realize is present.
Help fill in the blanks
Extended fasting will activate the processes of [glycolysis/gluconeogenesis] and [fatty acid synthesis/b-oxidation]. These processes will work to deplete [oxaloacetate/acetyl-CoA] and increase [oxaloacetate/acetyl-CoA]. As a result, flux through the citric acid cycle will [increase/decrease].
Step by step
Solved in 2 steps
