06 - Transport of Glucose & Amino Acids

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06 - Transport of Glucose & Amino Acids
2014-08-22 20:15:55
transport glucose amino acid
Transport of Glucose & Amino Acids
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  1. How many different facilitative glucose transporters are there?
    13; GLUT1-GLUT13; they are carrier-mediated but do not involve the expenditure of energy
  2. What does GLUT1 do?
    • It has a high affinity for glucose (Km­= 1-2mM); it is responsible for glucose uptake in erythrocytes and the uptake of glucose into
    • the brain across the blood-brain barrier
  3. Where is GLUT1 most commonly found?
    Ubiquitous, but most commonly found in red blood cells and at the blood-brain barrier
  4. What disease do mutations in GLUT1 cause?
    GLUT1 deficiency syndrome; this results in impairment of glucose delivery into the brain
  5. What are the symptoms of GLUT1 mutations?
    Early onset encephalopathy (syndrome of global brain dysfunction), seizures, developmental delay, hypotonia, a complex movement disorder, hypoglycorrhachia (decreased glucose levels in the cerebrospinal fluid) with normal blood levels of glucose
  6. How are GLUT1 mutations treated?
    Children with the disorder are treated with a ketogenic diet
  7. In what cells is GLUT1 over-expressed?
    Tumor cell; it is over-expressed to support the increased energy demands of tumor cells
  8. How is PET scan being used for tumor detection?
    Regions of a tissue with cancer have a higher capacity to accumulate 2-deoxy-D-glucose, a non-metabolizable glucose analog recognized as a substrate by GLUTs, because of the differential expression GLUT1; this technique is known as 18FDG-PET
  9. GLUT2
    • This transporter has a low affinity for glucose, but has a high capacity for glucose, therefore, it is used to sense when there are high levels of glucose in the small intestines and insulin needs to be released; it
    • increases its transport activity in response to high levels of glucose
  10. Where is GLUT2 most commonly found?
    In the liver, the β-cells of the pancreas, the intestines and in the kidney
  11. How does GLUT2 cause β-cells to secrete insulin?
    • When plasma glucose increases, GLUT2 in the pancreatic β-cells allows more glucose to enter the cell, this increases glucose metabolism and ATP production; when the ATP levels raise, K+ channels are shut down
    • which depolarizes the cell; once the cell is depolarized the voltage-sensitive Ca2+‑ channels are activated, allowing an influx of Ca2+; this influx of Ca2+ triggers the release of insulin
  12. What do mutations leading to the inactivation of sulfonylurea receptor cause?
    These mutations are the cause for the genetic disease Familial Persistent Hyperinsulinemic Hypoglycemia of Infancy (PHHI)
  13. What disease do mutations in GLUT2 or glucokinase cause?
    Mutations which lead to inactivation of GLUT2 or glucokinase cause hypoinsulinemia and diabetes
  14. What drugs are used to treat non-insulin-dependent diabetes mellitus?
    Sulfonylureas; Oral hypoglycemics which inhibit the ATP-sensitive K+ channel in β-cells; this inhibition causes depolarization, which triggers the voltage-sensitive Ca2+ channel to allow an influx of Ca2+ which trigger release of insulin
  15. Where is GLUT4 most commonly found?
    Most commonly found in adipocytes, skeletal muscle and heart muscle
  16. GLUT4
    GLUT4 is an insulin-sensitive glucose transporter regulated by insulin; when the insulin receptor in the cell is activated, GLUT4 rapidly moves from intracellular pools into the plasma membrane
  17. What negative side effect can result from the activation of GLUT4?
    Because of the sudden influx of glucose into muscle or adipose, insulin-induced hypoglycemia can occur; exercise also recruits GLUT4 so it can hypoglycemic episodes can occurring during or soon after exercise as well; this particularly can happen to type 1 diabetics who control their blood glucose levels with insulin injection
  18. How does the sodium coupled glucose transporter 1 work?
    The sodium coupled glucose transporter 1 (SGLT1) transports D-glucose and D-galactose; it utilizes the Na+ gradient generated by the Na+/Kpump for energy; if there is an inhibition of the Na+/Kpump or a decrease in ATP production there will be a decrease in glucose absorption in the intestines
  19. What happens to individuals with genetic defects in SGLT1?
    Leads to the disorder called glucose-galactose malabsorption; children born with this cannot absorb glucose and galactose but can absorb fructose, so they frequently suffer with glucose-galactose malabsorption, osmotic diarrhea; they can be treated with fructose
  20. Where is SGLT1 predominantly found?
    In the intestines
  21. Where is SGLT2 predominantly found?
    In the kidney; it is the major contributing transporter for renal absorption of glucose
  22. What is Hartnup disease?
    Defect in the intestinal and renal absorption of neutral AAs; absorption of free AAs is the major transport mode in the kidney b/c circulating levels of small peptides are very low; there is no significant impairment of proper nutrition
  23. Why is Hartnup disease relatively benign in developed nations?
    • Because developed nations have a relatively nutritious diet; there may be symptoms of niacin deficiency caused by low levels of tryptophan and cerebellar ataxia (lack of voluntary coordination of muscle movement
    • originating from the cerebellum)
  24. What is cystinuria?
    A disease associated with a defect in the intestinal and renal absorption of cationic AAs (lysine and arginine) and cystine; extretion of all other AAs is normal; kidney damage due to cystine-containing stones in the urinary tract is a major complication
  25. How is cystinuria treated?
    Alkalinzation of urine or stimulation of urine production; alternatively, the use of penicillamine to form mixed disulfides with cystine in the nephron would enhance cystines solubility thus decreasing stone formation