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Explain the reason why liver glycogen phosphorylase enzyme would not be prone to allosteric regulation by glucose 6-phosphate as opposed to muscle glycogen phosphorylase.
Typically glucose 6-phosphate acts allosterically on glycogen phosphorylase causing it to be stuck in the stuck in the “T” state (more tense and less active). The reason why liver glycogen phosphotylase would not be prone to allosteric regulation by G6P is because the liver contains an enzyme called Glucose 6-phosphatase. This enzyme will convert all of the free Glucose 6-phosphate to Glucose leaving no G6P to bind to Glycogen Phosphorylase.
Can you explain/reason why glycogen phosphorylase is phosphorylated by only one kinase to be activated, whereas the glycogen synthase is inactivated progressively by many kinases?
Glycogen synthase is a tetrameric enzyme consisting of four identical subunits. Kinase activity acts on four different serine residues on the four different subunits (one serine per subunit). Every time one of these serine residues gets phosphorylated it results in an increased state of inactivation. On the other hand, glycogen phosphorylase is activated by phosphorylation of one residue.
Can Von Gierke’s patients carry out gluconeogenesis normally? If not, explain why?
Von Gierke’s patients cannot carry out gluconeogenesis because Von Gierke’s disease acts to mutate the translocase that moves the G6P into the ER and the phosphatase that will convert G6P to Glucose once into the ER.
Which of the tissues (liver or muscle) would contain more total glycogen per gram of tissue?
Skeletal Muscle- 400g compared to 100g in Liver.
What is/are the physiological advangtage(s) of having branched glycogen as opposed to linear glycogen in mammals?
The body is able to start the breakdown of glycogen at many terminal ends and thus get the benefits of energy release at a much quicker pace than if the glycogen molecule was linear and had only one point of glycogen breakdown.
Can we conceive how much liver glycogen is used for its own metabolism ( not including glucose pumped into blood)
No actual statements of usage turned up in brief searches. However if we look at Venks packet it states that the brain consumes around 75% of the glucose the liver produces ergo most of the glycogen it stores. Since the liver is also supplying glucose to numerous other tissues one could postulate that the majority of glycogen is not used by the liver for its own metabolism.
Describe the relationship between glycogen/glucose metabolism in type 1 and 2 diabetes.
-Type 1: Since there is not enough insulin produced there will be a high concentration of blood glucose due to depressed ability to store as glycogen.
-Type 2: There will also be high blood glucose as in type 1 however this is because insulin insensitivity decreases the ability to react to insulin levels and glucose concentration is increased, primarily from the liver.
Type 1 diabetes can be better controlled by insulin administration t/f
True, since there is a lack of insulin production the administration of more will lead to positive affect versus the insensitivity that would be seen in type II
Can we come up with a hypothesis as to why type 2 diabetics are obese?
Obesity is a risk factor for Type 2 diabetes (IE the copout answer if B then A), however if we are looking at mechanical effects I can think of it this way. If blood glucose concentration is high, that means its availability for energy production is also high. This availability could reduce the amount of free fatty acids going into energetic cycles and thus they could be converted back to stored trigylcerides (fat).
Describe the biochemical basis of diabetic retinopathy.
Because glucose is a reactive molecule it can have deleterious effects. In simple terms high blood glucose can cause a reactive signal cascade that initiates apoptosis. The blood vessels in the eye are affected by this mechanism.
Describe the production of Gluticol/Sorbitol
The excess Glucose in the blood is reduced via non-specific dehydrogenase from an aldehyde to an alcohol Gluticol (aka Sorbitol). This is important especially in patients with Diabetes. Sorbitol accumulates and disturbs the nerves of the eye and can lead to Diabetic Retinopathy.
What is glycation?
This process takes place when simple sugar molecules such as fructose of glucose become attached to proteins or lipid fats without the moderation of an enzyme. This results in the formation of rogue molecules and can promote certain health risks. Apparently this can take place outside of the body as well and it something people are concerned about because it causes aging.
Describe the basis of diabetic nephropathy.
The excess Glucose in the blood is reduced via non-specific dehydrogenase from an aldehyde to an alcohol Gluticol (aka Sorbitol). In turn this messes with the osmotic pressures of the kidneys and changes the gradient for nutrients and ions. This leads to kidney damage and causes other problems and leads to hypertension which makes the heart work harder and leads to #38.
Explain the basis of Diabetes being a cardiovascular problem.
The excess Glucose in the blood is reduced via non-specific dehydrogenase from an aldehyde to an alcohol Gluticol (aka Sorbitol). This leads to the blood becoming more viscous (he related it to water vs honey). This eventually leads to hypertension and many cardiovascular problems.
Hemoglobin A1c levels are used as an indicator to assess the severity of diabetes. Explain this in biochemical terms.
The A1C test measures your average blood glucose control for the past 2 to 3 months. It is determined by measuring the percentage of glycated hemoglobin, or HbA1c, in the blood. Glycated hemoglobin (GHb) is formed by a posttranslational, non-enzymatic, substrate-concentration dependent irreversible process of combination of aldehyde group of glucose and other hexoses with the amino-terminal valine of the β-chain of hemoglobin. The A1c levels should be kept below 7% in diabetics.
Explain the biochemical basis of hypoglycemia
This involves a dysregulation in insulin secretion with defects in glucose counter-regulatory hormones. There may also be an increased insulin sensitivity in some cases. The unregulated insulin secretion drives glucose into the insulin sensitive tissues, especially skeletal muscle, adipose tissue and liver, causing profound hypoglycemia. This is compounded by the fact that insulin simultaneously inhibits glycogenolysis, gluconeogenesis, lipolysis and ketogenesis.
What are GLUT’s?
GLUTs are integral membrane proteins that contain 12 membrane-spanning helices with both the amino and carboxyl termini exposed on the cytoplasmic side of the plasma membrane. GLUT proteins transport glucose and related hexoses according to a model of alternate conformation, which predicts that the transporter exposes a single substrate binding site toward either the outside or the inside of the cell.
What is the normal fasting levels of glucose in blood (explain it in percent and mM concentrations).
A normal fasting blood glucose target range for an individual without diabetes is 70-100 mg/dL (3.9-5.6 mmol/L). The American Diabetes Association recommends a fasting plasma glucose level of 70–130 mg/dL (3.9-7.2 mmol/L) and after meals less than 180 mg/dL (10 mmol/L).
Muscle can respond to insulin, however it doesn’t respond to glucagon. Explain and rationalize why evolution made it this way? (What is so special about muscle compared to liver?)
In muscles however glucose 6-phosphate is never converted into glucose, rather glucose 6-phosphate is used in glycolysis. There are 2 reasons for this. The first reason is that muscle cells lack glucose 6-phosphatase, which converts glucose 6-phosphate into glucose. Second, muscle cells need a constant supply of ATP in order for them to contract, so they would want to make ATP by glycolysis.
Describe the major connecting point between glycogen and gluconeogenesis metabolism.
Both pathways involve glucose. Gluconeogenesis creates glucose, whereas glycogen is stored glucose with alpha 1-4 linkages and branched alpha 1-6 linkages. Both pathways have methods that can create glucose.
Why are proteins more prone to non-enzymatic glycation?
Glycoconjugates (protein and glucose) are formed by the reactive aldehyde of glucose that forms linkages with many proteins either with the amino terminal residue or with reactive lysines.
Explain in biochemical/biophysical terms why glucose molecule in excess concentration is a big problem maker?
Glucose can be converted into glucitol (sorbitol) by a non-specific dehydrogenase enzyme. Sorbitol will increase the osmotic pressure of the cells and can disrupt many tissues like kidney, retina, etc.
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