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What is autophagic intracellular digestion? Why is this type of intracellular digestion intensified in an organism undergoing starvation?
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- How are the protein-digesting enzymes in pancreatic juice activated? What is the logic of this arrangement?Which of the following statements is true about brain metabolism in starvation? a) The brain can use glucogenic amino acids for energy b) The brain can only use glucose as fuel c) Up to a quarter of energy requirement of the brain can come from fatty acids d) Up to a half of energy requirement of the brain can come from ketone bodiesUnder what conditions does the active functioning of pancreatic lipase occur? What is its mechanism of action?
- Why does digestion need regulation and how is it achieved?Why is it necessary for enzymes that digest protein to be secreted in an inactive form?In the intestine, the triacylglycerols must be converted to fatty acids and glycerol by hydrolytic enzymes before transport into enterocytes. Afterward, fatty acids and glycerol are reconverted into triacylglycerols and then packaged into chylomicrons. Suggest why this energy-requiring process is used instead of a direct transport of triacylglycerols into enterocytes.
- Is ketogenesis anabolic or catabolic? Thus, what initiates the ketogenesis in our body?What is the specific role of pepsin and pancreatin in protein digestion? Where can these enzymes be found in the body?Glucose is the only carbohydrate that the brain can use for energy. Which pathway is mobilized to supply the need of the brain during starvation?: a.) glycolysis b.) gluconeogenesis or c.) glycogenesis? Explain.
- During the fed state, which of the following occur(s)? a) insulin stimulation of malonyl CoA formation b) allosteric inhibition of carnitine acyltransferase I c) both a and b d) neither a nor bWhy ALT is considered as more specific than AST regarding liver function? Which one is involved in hepatic urea synthesis? Describe the origin of urea at the molecular level?The following is a typical underlying factor in obesity-induced inflammation a) Increased secretion of the adipokine adiponectin b) Higher lipolysis rate in hypertrophied adipocytes c) Increased insulin sensitivity in adipose tissue d) Conversion of pro-inflammatory M1 macrophages to anti-inflammatory M2 macrophages