The Fed and Fasting State

Which of the following hormones increase blood glucose by inhibiting insulin? Check all that apply.

Which hormone increases blood glucose by inhibiting insulin over a long period of time?

Which hormone counteracts insulin by stimulating glucose and lipid metabolism but shares insulin's anabolic properties with respect to protein?

Which hormone stimulates insulin secretion after food intake before blood glucose increases?

Which type of glucose transporters are present on the B cells of the islets of Langerhans?

Which glucose kinase is present in the B cells of the islets of Langerhans?

Fill in the blanks to describe the stimulation of insulin secretion from the pancreatic B cells. 1. The B cells have [blank_start]GLUT2[blank_end] glucose transporters - these have [blank_start]low[blank_end] affinity so glucose only enters these cells at [blank_start]high[blank_end] concentration. 2. [blank_start]Gluco[blank_end]kinase is present in the B cells which has [blank_start]high[blank_end] Km so [blank_start]phosphorylates[blank_end] glucose with [blank_start]low[blank_end] affinity. This initiates [blank_start]glycolysis[blank_end]. 3. [blank_start]ATP[blank_end] from [blank_start]glycolysis[blank_end] inhibits [blank_start]ATP[blank_end]-sensitive [blank_start]K+[blank_end] channels on the membrane. 4. The prevention of [blank_start]K+[blank_end] leakage causes the membrane to become [blank_start]depolarised[blank_end]. 5. [blank_start]Voltage[blank_end]-gated [blank_start]Ca2+[blank_end] channel proteins open. 6. [blank_start]Ca2+[blank_end] enters the cell stimulating [blank_start]vesicular fusion[blank_end] and release of insulin.

What is proinsulin?

How do we activate proinsulin?

What type of receptor is the insulin receptor?

Which domain are the 2 a-subunits of the insulin receptor found?

Which domain are the 2 b-subunits of the insulin receptor found?

The insulin receptor is described as being catalytic.

What happens when insulin binds to the insulin receptor?

Fill in the blanks below to describe the activation of protein kinase B by insulin. 1. Insulin binds to its [blank_start]tyrosine[blank_end] receptor. 2. This binding stimulates [blank_start]autophosphorylation[blank_end] of [blank_start]tyrosine[blank_end] residues. 3. This [blank_start]phosphorylation[blank_end] allows [blank_start]phosphorylation[blank_end] of [blank_start]Insulin Receptor Substrate[blank_end] (IRS 1/2). 4. [blank_start]Insulin Receptor Substrate[blank_end] activates [blank_start]P13 kinase[blank_end]. 5. [blank_start]P13 kinase[blank_end] phosphorylates [blank_start]PiP2[blank_end] to [blank_start]PiP3[blank_end] in the cell membrane. 6. [blank_start]PiP3[blank_end] activated [blank_start]PDK1[blank_end]. 7. [blank_start]PDK1[blank_end] activates [blank_start]protein kinase B[blank_end].

Fill in the blanks below to describe how insulin activates glycogen synthesis. 1. When insulin binds to its tyrosine kinase receptor, [blank_start]protein kinase B[blank_end] is activated by a series of [blank_start]phosphorylations[blank_end]. 2. [blank_start]Protein kinase B[blank_end] causes [blank_start]GLUT4[blank_end] channels to be translocated to the membrane via [blank_start]vesicular fusion[blank_end] to encourage glucose uptake. 3. [blank_start]Protein kinase B[blank_end] phosphorylates [blank_start]glycogen synthase kinase[blank_end]. This [blank_start]inactivates[blank_end] glycogen synthase kinase. 4. [blank_start]Glycogen synthase[blank_end] remains unphosphorylated so remains in its [blank_start]active[blank_end] form. 5. Glycogen syntheiss can take place.

The active form of glycogen synthase kinase is...

The active form of glycogen synthase is...

Fill in the blanks below to describe how insulin inhibits lipolysis. 1. When insulin binds to its [blank_start]tyrosine kinase[blank_end] receptor, [blank_start]protein kinase B[blank_end] is activated by a series of [blank_start]phosphorylations[blank_end]. 2. [blank_start]Protein kinase B[blank_end] phosphorylates [blank_start]phosphodiesterase[blank_end] to activate it. 3. [blank_start]Phosphodiesterase[blank_end] converts [blank_start]cAMP[blank_end] to AMP. 4. [blank_start]Protein kinase A[blank_end] is therefore inhibited and thus [blank_start]hormone sensitive lipase[blank_end] is not activated. 5. Triacylglycerols are not hydrolyses and the triacylglycerol store in adipose tissue is preserved.

What hormone activates hormone sensitive lipase to cause TAG hydrolysis?

Fill in the blanks below to describe how insulin affects gene expression. 1. Insulin binds to its [blank_start]tyrosine kinase[blank_end] receptor stimulating [blank_start]autophosphorylation[blank_end] of [blank_start]tyrosine[blank_end] residues. 2. This phosphorylation leads to activation of [blank_start]RasGTP[blank_end]. 3. [blank_start]RasGTP[blank_end] activates the protein kinase cascade to phosphorylate first [blank_start]RAF[blank_end], then [blank_start]MEK[blank_end], then [blank_start]ERK[blank_end]. 4. [blank_start]ERK[blank_end] or MAPK activates or inhibits [blank_start]transcription factors[blank_end] leading to gene activation or suppression.

The brain and erythrocytes will always take up glucose and metabolise it. Why?

In excess, how will pyruvate from glycolysis leave the liver?

Why does muscle and adipose tissue only uptake glucose at very high concentrations?

Which biomolecules deposit fatty acids into adipose tissue in the fed state? Select all that apply.

What are the actions of cortisol?

The liver is engaged in gluconeogenesis at all times except during...

Why is the glucose kinase in the liver glucokinase, which has low affinity?

During the fed state, acetyl CoA carboxylase is activated to form malonyl CoA. What does malonyl CoA do?

Why does the brain rely on glucose as fuel?

Glucose transport into the brain and erythrocytes is independent of insulin.

The erythrocytes have no mitochondria.

When do blood glucose concentrations peak?

Following a meal, when have blood glucose levels normally returned to normal by?

Why can't fatty acids be used in gluconeogenesis?

Which of the following molecules are gluconeogenic substrates?

Ketone bodies consist of two molecules of what bonded together?

What is the purpose of the ketone bodies?

In the fasting state, glucagon activates [blank_start]glycogen phosphorylase kinase[blank_end]. Thus, [blank_start]glycogen phosphorylase[blank_end] is phosphorylated and put into its [blank_start]active[blank_end] state. This means [blank_start]glycogen[blank_end] is phosphorylated and [blank_start]glucose[blank_end] can enter the blood.

Where is lactate sourced from for gluconeogenesis?

Why do the erythrocytes produce lactate?

When does acetyl CoA form ketone bodies?

Why do ketone bodies stimulate insulin secretion?

The brain can use ketone bodies in metabolism.

When does urea excretion and thus protein breakdown peak during starvation?

Why does urea excretion and thus protein breakdown decrease over time?

Why do the muscle begin to utilise fatty acids for energy as starvation progresses?

For how long can a human survive without food?

Fill in the blanks below to describe type 1 diabetes. Type 1 diabetes is caused by the [blank_start]autoimmune[blank_end] destruction of [blank_start]B[blank_end] cells in the [blank_start]pancreas[blank_end]. It often has an [blank_start]early[blank_end] onset. Symptoms include polyuria, polydipsea, [blank_start]polyphagia[blank_end] (excessive appetite), fatigue and weakness as well as weight loss and muscle wasting. It requires treatment with exogenous [blank_start]insulin[blank_end] whereby the dosage is matched with [blank_start]carbohydrate intake[blank_end].

Which of these indicate type 1 diabetes?

Fill in the blanks below to describe Type 2 diabetes. Type 2 diabetes is caused by insulin [blank_start]resistance[blank_end]. Is is usually [blank_start]later[blank_end] onset than type 1. Type 2 diabetes can be treated with dietary changes and oral [blank_start]hypoglycaemic[blank_end] agents.

What do biguanides do in the treatment of Type II diabetes?

What do sulphonylureas do in the treatment of Type 2 diabetes?

Which hormone acts unopposed in diabetes mellitus?

In a healthy individual, [blank_start]ketone bodies[blank_end] stimulate [blank_start]insulin[blank_end] release to limit muscle protein breakdown. In diabetics, this cannot occur. Thus, protein is broken down in an uncontrolled matter, [blank_start]gluconeogenesis[blank_end] is not controlled, fat breakdown is not controlled and [blank_start]ketone body[blank_end] production is not controlled. Glucose and [blank_start]ketone bodies[blank_end] may be present in the urine.

Drag and drop the correct pathologies to name some of the complications of diabetes mellitus. [blank_start]Microangiopathy[blank_end] - disease of the capillaries causing thickening of the wlals [blank_start]Retinopathy[blank_end] - damage to the retina affecting vision [blank_start]Nephropathy[blank_end] - damage to the kidneys [blank_start]Neuropathy[blank_end] - results in impotence, foot ulcers etc

To be diagnosed with metabolic syndrome, patients must have any 1 of: [blank_start]high[blank_end] fasting glucose, [blank_start]insulin[blank_end] resistance or [blank_start]type 2[blank_end] diabetes. Patients must also have any 2 of [blank_start]hyper[blank_end]tension, [blank_start]dyslipidemia[blank_end] (abnormal lipid content in blood), [blank_start]central[blank_end] obesity (fat buildup around the abdomen) or microalbuminuria