A scientist has developed an adipocyte cell line that, at 42degC, cannot degrade triglycerides to glycerol and free fatty acids. At 25degC, the triglyceride degradation is normal. Which one of the following best reflects enzymes in which a temperature-sensitive mutation may lead to this phenotype?

Insulin levels decrease, and glucagon levels rise, stimulating lipolysis. (Epinephrine and other hormones promote lipolysis by the same mechanism.)a. cAMP levels rise, and PKA is activated.b. PKA phosphorylates perilipin-1, which then dissociates from the enzyme ATGL.c. When free of perilipin-1, ATGL is active and converts triacylglycerol to a free fatty acid and DAG.d. PKA directly phosphorylates and activates hormone sensitive lipase, which converts DAG to a free fatty acid and monoacylglycerol.e. Monoglyceride lipase then converts the monoacylglycerol to a free fatty acid and glycerol.The hormone-sensitive lipase of adipose tissue is responsible for degrading diacylglycerol to a free fatty acid and monoacylglycerol. The enzyme is activated by glucagon via a cAMP-mediated process (the activation of protein kinase A). Thus, mutations in PKA or the glucagon receptor may interfere with the eventual phosphorylation and activation of the hormone-sensitive lipase. Adenylate kinase is not involved in this cascade (although a mutation in adenylate cyclase would be involved, as that is the enzyme that produces cAMP). The insulin receptor promotes triglyceride synthesis and storage in the adipocyte, so a mutation in the insulin receptor would not promote triglyceride degradation. Glycerol kinase is only expressed in the liver and is not present in adipose cells.