Table of contents

1. Introduction to Biochemistry4h 34m
2. Water3h 23m
3. Amino Acids8h 10m
4. Protein Structure10h 4m
5. Protein Techniques14h 5m
6. Enzymes and Enzyme Kinetics13h 38m
7. Enzyme Inhibition and Regulation 8h 42m
8. Protein Function 9h 41m
9. Carbohydrates7h 49m
10. Lipids5h 49m
11. Biological Membranes and Transport 6h 37m
12. Biosignaling9h 45m
Review 1: Nucleic Acids, Lipids, & Membranes2h 47m
Review 2: Biosignaling, Glycolysis, Gluconeogenesis, & PP-Pathway3h 12m
Review 3: Pyruvate & Fatty Acid Oxidation, Citric Acid Cycle, & Glycogen Metabolism2h 26m
Review 4: Amino Acid Oxidation, Oxidative Phosphorylation, & Photophosphorylation1h 48m

12. Biosignaling

Recap Of Insulin Signaling in Glucose Metabolism

Biochemistry

12. Biosignaling

Recap Of Insulin Signaling in Glucose Metabolism

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Multiple Choice

IRS-1 is an essential adaptor protein in the insulin signaling pathway. If IRS-1 was overexpressed in muscle cells, what effect would you expect to see on glycogen synthesis?

Protein kinase B would remain inactive, resulting in increased glycogen synthesis.

Protein kinase B would be overstimulated, resulting in increased glycogen synthesis.

Protein kinase B would remain inactive, resulting in decreased glycogen synthesis.

Protein kinase B would be overstimulated, resulting in decreased glycogen synthesis.

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Verified step by step guidance

Understand the role of IRS-1: IRS-1 (Insulin Receptor Substrate 1) is a key adaptor protein in the insulin signaling pathway. It facilitates the transmission of signals from the insulin receptor to downstream signaling molecules.

Consider the effect of IRS-1 overexpression: Overexpression of IRS-1 in muscle cells would likely enhance the insulin signaling pathway, as more IRS-1 would be available to propagate the signal.

Analyze the downstream effects: Enhanced insulin signaling typically leads to the activation of Protein Kinase B (PKB, also known as Akt). PKB plays a crucial role in promoting glycogen synthesis by phosphorylating and inactivating glycogen synthase kinase 3 (GSK-3), which otherwise inhibits glycogen synthase.

Predict the outcome on glycogen synthesis: With IRS-1 overexpressed, PKB would be overstimulated, leading to increased glycogen synthesis due to the inactivation of GSK-3 and subsequent activation of glycogen synthase.

Evaluate the options: The correct answer aligns with the understanding that overstimulation of PKB results in increased glycogen synthesis, as opposed to decreased synthesis or PKB remaining inactive.