Explain why adipocytes need glucose as well as fatty acids in order to synthesize triacylglycerols.

In the indicated tissues, how will each process or the activity of each enzyme below be affected by the signal sent upon Glucagon secretion? Use an up (t) or down (1) arrow or NC (no change). (Hint: Decide what pathways will be up-regulated first, then look at the enzymes below!) + Triacylglygerol Lipase (Adipocytes) Phosphofructokinase-2 (Liver) Insulin secretion (Pancreas) Pyruvate Kinase (Muscle) Glycogen Phosphorylase (Liver) Phosphofructokinase-1 (Liver) Fructose-1,6-bisphosphatase 1 (Liver) Fatty Acid Biosynthesis (Liver) PEP Carboxxkinase (Liver) Phosphorylation of Perilipins (Adipocytes) Adenylate Cyclase (Liver) Glycogen Synthase (Liver) Acetyl CoA Carboxylase Hexokinase II (Muscle)

In the fasted state, FADH2 and NADH for oxidative phosphorylation are mainly provided by fatty acid oxidation. Explain how fatty acids are mobilised from adipose tissue by the action of glucagon.

During hyp[erglycemia or diabetes - what two regulatory enzymes are active? Why are they active?

For an individual whose liver is regulated by glucagon binding, when energy is needed - what is the major carbon source used to produce acetyl CoA? Fatty acids Glucose Glyoxylate Amino acids

The removal of fatty acids from triacylglycerols leaves glycerol. Show how the actions of glycerol kinase and glycerol-3-phosphatedehydrogenase on glycerol produce an intermediate of glycolysis.

Arrange the step in the dropdown menu in the image.

Suggest an explanation for the fact that the amount of glycogen in type I glycogen-storage disease (von Gierke disease) is increased.

Give some characteristics of adipocytes.

Eventually when glucose consumed is so low gluconeogenesis is also inhibited. Explain how this happens.