Question

Q1)Protein kinase A (cAMP-dependent protein kinase) is responsible for

1. activating glycogen synthase

2. activating phosphorylase kinase

3. activating glycogen synthase and activating phosphorylase kinase

4. inactivating glycogen synthase and activating phosphorylase kinase

Q2) Which of the following statements regarding the phosphoinositide signaling pathway is FALSE?

1. Diffusion of inositol trisphosphate in the cytoplasm results in the opening of Ca²⁺ channels.

2. The influx of Ca²⁺ intiates a kinase cascade.

3. Diacylgycerol interacts directly with protein kinase A and sequesters it at the membrane.

4. Diacylgycerol interacts with a cellular protein that requires Ca²⁺ for full activation.

5. The downstream effects of Ca²⁺ influx is most often mediated by the calcium-binding protein calmodulin.

Q3) Which of the following hormones acts as an appetite suppressor?

1. insulin 2. leptin 3. adiponectin

Answer 1

ANSWER 1

Protein kinase A (PKA) is activated by elevated cAMP levels. It is a kinase enzyme which phosphorylates glycogen synthase on at least three different sites. Phosphorylation lead to deactivation of glycogen synthase. Dephosphorylation of glycogen synthase is carried by protein phosphatase 1 (PP1) and thus activates glycogen synthase.

Phosphorylase kinase (PhK) is a kinase enzyme. Without modification, enzyme is inhibited. Phosphorylation of alpha and beta subunits of phosphorylase kinase by protein kinase A (PKA) decrease the inhibitory activities. Thus, PKA activates the Phosphorylase kinase (PhK). But PhK is fully activated only when delta subunit of PhK is bound by calcium ions.

Correct Option:

2. activating phosphorylase kinase (PKA activates the Phosphorylase kinase)

Incorrect Options:

1. activating glycogen synthase (PKA inactivates glycogen synthase)

3. activating glycogen synthase and activating phosphorylase kinase (PKA inactivates glycogen synthase)

4. inactivating glycogen synthase and activating phosphorylase kinase (PKA inactivates glycogen synthase, but phosphorylase kinase is fully activated only after calcium binding to delta subunits)

Option 4 is also correct. But among 2 and 4, option 2 is more appropriate.

ANSWER 2

Phosphoinositide signalling pathway

Phospholipase C is activated by G protein coupled receptors (GPCRs) and receptor tyrosine kinases (activate different isoforms of PLC). This enzyme breaks down membrane bounded PIP2 into IP3 (inositol triphosphate) and DAG (diacylglycerol). Both are intracellular mediator. IP3 binds to IP3 sensitive calcium channel on Endoplasmic reticulum and release calcium ions. These calcium ions activates various calcium regulated intracellular signals including kinases. Diacylgycerol (DAG) remain bound to cytosolic face of membrane and interacts directly with protein kinase A and sequesters it at the membrane. DAG together with phosphatidyl serine and calcium ion activates Protein kinase C (PKC). PKC phosphorylates specific serine or threonine on specific target proteins. Many calcium mediated downstream signalling or events occur after binding of calcium to calmodulin regulatory protein and activates calcium-calmodulin dependent kinase and other effector proteins.

So, following options are true for phosphoinositide signaling pathway:

1. Diffusion of inositol triphosphate in the cytoplasm results in the opening of Ca2+ channels.

2. The influx of Ca2+ initiates a kinase cascade.

4. Diacylgycerol interacts with a cellular protein that requires Ca2+ for full activation.

5. The downstream effects of Ca2+ influx is most often mediated by the calcium-binding protein calmodulin.

Following option is false for phosphoinositide signalling pathway:

3. Diacylgycerol interacts directly with protein kinase A and sequesters it at the membrane.

DAG does not interact directly with protein kinase A. It interacts directly with protein kinase C (PKC)

Correct Option: 3

ANSWER 3

2. Leptin is a hormone released by adipocytes (fat cells) of fat tissues.

Leptin stimulates Leptin Receptor on pro-opiomelanocortin (POMC) neurons located in third ventricle in brain.

Activation lead to release of α–melanocyte-stimulating hormone (α-MSH).

This α-MSH released by POMC neurons stimulates melanocortin receptors (MCR-3 and MCR-4) in the paraventricular nuclei (PVN).

This stimulation further activate neuronal pathways that project to the nucleus tractus solitarius and increase sympathetic activity and energy expenditure.

So, leptin suppress appetite until extra fat is burned.

1. Insulin is an anorexigenic hormone that inhibit AGRP-NPY neurons and stimulate adjacent POMC-CART neurons in brain, thus reduce food intake.

3. Adiponectin is a hormone involve in glucose regulation. Its function is similar to leptin.

So, all of these hormones are appetite suppressor.