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.

Biochemistry
9th Edition
ISBN:9781319114671
Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Chapter1: Biochemistry: An Evolving Science
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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.  

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