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Saturday, January 6, 2018

Introduction to Biochemistry - End of session 3.7, 3.8 assessment

The change indicates an activation, therefore, the answer is

Addition of the allosteric ATCase activator, ATP
Performing the same experiment with the purified catalytic subunit of ATCase.

Heterotropic -> Different molecule
Allosteric -> Different site
Inhibition -> T state

Thefore the answer is:

A small molecule binds the enzyme at a site other than the active site, stabilizing the T state of the enzyme.

D - there is no reason for the substrate for D to accumulate when the free energy change is so large.

A high ratio of [ATP] over [AMP] in muscle cell means the energy state is high, so slow glycolysis.

Abundant citrate in muscle cell means we don't need pyruvate for the citric acid cycle, so slow glycolysis.

A high concentration of glucose in liver cells means we have a lot of substrate, so rapid glycolysis.

Glucagon signaling in the liver means the blood glucose is low, so slow glycolysis.

Liver pyruvate kinase and PFK-2.

This reaction is almost energy neutral (so that the equilibrium does not go one-way to either side)

The answer is shown in above.

An excess of acetyl CoA will inhibit the pyruvate dehydrogenase complex, and acetyl CoA will activate pyruvate caboxylase. The net result is an increase in gluconeogenesis.

3 and 6 are the concentration of the substrate, so they are
Fructose 6-Phosphate and Fructose 1,6-Bisphosphate respectively.

Fructose 2,6-Bisphosphate is an allosteric activator for PFK-1 and an allosteric inhibitor for FBPase-1, so the answer for 1, 2, 4, 5 are


High blood glucose stimulates the release of insulin.
The liver is more responsive than the muscle to glucagon.
Glycogenolysis is simulated by glucagon.

Glucose binds allosterically to glycogen phosphorylase

Individual with type I diabetes have reduced insulin production which lead to hyperglycemia

Hyperglycemia is too much sugar in the bloodstream.


Type II Diabetes
Gestational Diabetes

Type I Diabetes
Type II Diabetes
Gestational Diabetes

Individual has type I diabetes, the 0 actually represents birth so this is young onset.

Individual has type II diabetes.

Patient 1 has diabete
Patient 2 is prediabetic

Ketone body production is the direct cause of metabolic acidosis.


False, the viral infection is environmental.

False, mutation in TYK2 is genetic.

Cytoplasmic receptors

Pro-apoptotic factors - beta cells handles infection by killing itself. That's why we have diabetes.

Mutation in PTPN2 results in reduced activity and increased risk for type I diabetes.

Pancreatic beta-cells undergo epitope spreading upon viral infection.

Insulin promotes glucose uptake and glycogen synthesis in muscle.
Insulin promotes glucose uptake and fat synthesis in adipose tissue.

When insulin level drops, plasma membrane glucose transporters are internalized and recycled.

It stimulates glycogen synthesis in response to insulin
It phospho-inhibits glycogen synthase kinase

It phospho-inhibits HSL, and
It promotes the synthesis of glycerol 3-P

Increased osmotic pressure of blood due to hyperglycemia

Inactive adipose tissue LPL due to lack of insulin correct
Increased liver VLDL release due to lack of insulin correct

It leads to vascular stiffening and retinopathy.

Fat layer under skin

Hypoglycemia is defined as too little sugar in the bloodstream.

IRS-1 activates phosphatidylinositol 3-kinase (PI3K) 

IRS-1 phosphorylation on serine residue
Conversion of PIP3 to PIP2 by a phosphatase

100:1 ratio of insulin to C-peptide and low glucose.

In type II diabetes, blood glucose is increased and blood fatty acids are increased.

Patient 1.

Increased intracellular calcium triggers the release of insulin vesicles

Potassium channels are closed by increased intracellular ATP

Sulfonylurea drugs close potassium channels leading to insulin release both in the presence and absence of glucose.

In Type II diabetes, insulin resistance develops in childhood, hyperglycemia develops in late adulthood, and decrease insulin production occurs in late adulthood.

Insulin secretion is normal in the first stage of the disease but tissues don’t respond to it as well.

Ectopic fat deposition interferes with GLUT-4 translocation
MCP-1 secreted from enlarged adipocytes recruits macrophages
TNFalpha stimulates fatty acid release from adipocytes that leads to ectopic fat deposition

Obesity is a major risk factor for Type II diabetes
Lipotoxicity and inflammation promote insulin resistance

Introduction to Biochemistry - Quiz 3.8.6

The onset of Type II diabetes is gradual and typically occurs in adulthood.

Both Type I and Type II

Normal - in the first stage, the problem is not about secretion, it is about resistance.

Target organs respond less to the insulin message in the first stage of Type II diabetes.

Lipotoxicity and inflammation promote insulin resistance.

Intestinal cells primarily absorb carbohydrates in the form of Monosaccharides.

Insulin promotes fusion of intracellular GLUT-4 vesicles to the plasma membrane.

Glucagon causes muscle to decrease glucost uptake by altering GLUT-4 levels present on the plasma membrane.

Auto-phosphorylates and Activates IRS-1

Activate PI3K

Insulin receptor dephosphorylation
Proteolytic degradation of insulin receptor and IRS-1
IRS-1 phosphorylation on Threonine residue

Accumulation of misfolded insulin in the Golgi system.

In Type II diabetes both glucose and fatty acid levels increase in the blood.

Reduced glucose uptake due to insulin resistance.
Increased liver glucose production through glycogenolysis and gluconeogenesis.

Lifestyle modifications such as exercise, reduced caloric intake, and better diet.
Drugs that increase insulin production and sensitivity.