Nutrition- Topic 3

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Nutrition- Topic 3
2012-12-09 13:33:33

CHO metabolism and diabetes
Show Answers:

  1. What is type II diabetes?
    Insulin resistance
  2. What are the functions of glucose?
    • Convert to glycogen to store energy
    • Converted to fat to store energy
    • Oxidized for energy
    • Glycoproteins
    • Precursor of amino acids C-skeleton
    • Prevent Ketosis
  3. How do you get ketosis?
    Oxidization of fatty acids without glucose
  4. What organs use glucose for energy?
    • Brain, RBCs, mammary gland. getus, spermatogenesis
    • NOT the gut (uses AA metabolism for energy)
  5. Can you synthesize glucose from fatty acids?
  6. Where do we get CHO from in our diet?
    • Fibre
    • Starches
    • Sugars
    • Plant-based foods plus milk
  7. What is amylose?
    alpha(1-4) chains of glucose
  8. What is amylopectin?
    alpha(1-4) chains of glucose with alpha(1-6) branches
  9. What are the three types of fibre?
    Soluble, Insoluble, functional
  10. What is soluble fibre?
    Forms a gel in water, pectins (found in fruits)
  11. What is insoluble fibre?
    • Hemicellulose, cellulose
    • Have beta bonds, which we cannot digest
  12. What is functional fibre?
    Psyllium added to foods
  13. What are the freatures of soluble fibre?
    • Viscous gel
    • Delaus gastric emptying
    • Glycemic control
    • Binds Cholesterol and bile acids
    • Fermended by colonic bacteria
    • Low GI
  14. What are the features of insoluble fibre?
    • Bulk (laxitive effect)
    • Delays gastric emptying
    • Some glycemic control
    • Binds cations
    • Minor fermentation by colonic bacteria
  15. How are CHO digested?
    • Mouth- salivary amylase
    • Small intestinal lumen- pancreatic amylase, glucoamylase
    • Small intestinal brush border- sucrase-isomaltase, lactase
  16. What is lactose intolerance?
    • Lactose not digested, reaches colon
    • Fermentation by  bacteria- flatulence (methane, hdrogen, CO2)
    • Osmotic diarrhea
    • Breath hydrogen test to diagnose
  17. How is lactose intolerance tested?
    Breath hydrogen test
  18. Is lactose intolerance an immune disorder?
    Not immune related
  19. What is primary lactose non-persistance?
    • Decreased lactase production after weaning
    • 70% of adults worldwide but varies with population
    • Mutation for lactase persistance (autosomal dominance- Single-Nucleotide-Polymorphism in intron)
    • Dairy farming cs malaria hypothesis
  20. What is secondary lactose intolerane?
    • Caused by some injury to the small intestine
    • eg. Parasite infection, celiac disease, pathology, malnutrition
  21. What is congenital lactose intolerance?
    • Non-functioning protein
    • Uncommon
    • Infants, lactase-free formula (unable to digest breast milk)
    • Same as lactose intolerance after infancy
  22. What is a milk allergy?
    • Not the same as lactose intollerance
    • Protein, or peptides in milk
    • IgE antibodies
    • Mast cell degranulation
    • Massive histamine response
    • Anaphalaxis
    • Involves immune reaction
  23. How is galactose absorbed?
    • SGLT-1 (sodium-glucose transport proteins) and GLUT-2
    • First pass removal by liver
    • Preferential conversion to glycogen
  24. How is fructose absorbed?
    • GLUT5 facilitated diffusion agains concentration gradient into cell
    • GLUT5 or GLUT2 to exit cell
    • First pass removal by liver (GLUT2)
    • Rapid oxidation (faster than glucose)
    • Preferential conversion to fatty acids, triglycerides
  25. How is glucose homeostasis maintained?
    • Dietary CHO from stomach delivered to small intestine
    • Glucose and other monosaccharides transported through the bloodstream to the liver
    • Galactose and fructose are converted to glucose
    • Blood levels of glucose maintained for brain and other body cells
    • Glucose transported to muscle
    • Glucose is stored as glygocen in both liver and muscle
    • The glycogen stored in the liver maintains blood glucose between meals
    • Muscle glycogen provides immediate energy to the muscle during exercise
  26. What stimulates glucose synthesis?
    Plasma glucose
  27. How is glycogen degraded?
    • Glycogen Phosphorylase --- glucose-1-P
    • Phosphoglucomutase---glucose-6-P (glycolysis)
    • glucose-6-phosphatase---glucose

    • BUT:
    • glucose-6-phosphatase is only in liver- this means only the liver and kidney can make glucose from glycogen
  28. Why can only the liver and kidney make glucose from glycogen?
    Glucose-6-phosphatase (the enzyme that converts glucose-6-P into glucose) is only in the liver and kidney
  29. What is the brains glucose requirement?
    120 g/day
  30. What is the hepatic glycogen availability?
  31. What is gluconeogenesis?
    production of glucose from non-carbohydrate carbon substrates
  32. What are the precursors for gluconeogenesis?
    Amino acids, pyruvate, gycerol
  33. What stimulates gluconeogenesis?
    Stimulated by glucagon and glucocorticoids when plasma glucose is low
  34. What happens as a result of gluconeogenesis?
    Protein breakdown is high
  35. What is ketogenesis?
    • Fatty acid beta-oxidation in the basence of glucose
    • No anaplerosis of TCA cycle
    • Causes acetyl-CoA to accumulate
    • Beta-hydroxybutyrate and acetoacetate are products (ketones)
    • Ketone bodies are an alternate fuel for the brain (do have negative impact)
  36. What is ketoacidosis?
    • Beta-oxidation of fatty acids in absence of glucose
    • TCA cycle intermediates depleted for gluconeogenesis
    • Acetyl-CoA accumulates
  37. What are the components and breakdown of total energy expenditure?
    • 67%- Basal Metabolic Rate
    • 10%- Diet-Induced Thermogenesis
    • 23%- Activity
    • ?%- Adaptive Thermogenesis
  38. What are the facilitative glucose transporters?
    SLC2A1-5- Solute carrier family 2 members 1-5

    • GLUT1- RBCs, brain (blood brain barrier), kidney
    • GLUT2- Liver, B-cell, kidney, smal intestine
    • GLUT3- Brain (neurons)
    • GLUT4- Muscle, heart, adipose tissue
    • GLUT5- Small intestine (fructose transporter)
  39. How do insulin receptors interact with GLUT4?
    • Insulin binds to receptors starts many protein cascades
    • Protein cascades result in translocation of GLUT-4 to the plasma membrane
    • Influx of glucose
    • Glycogen synthesis, glycolsis, and fatty acid sythesis
  40. Why is glucose transport important?
    • Glucose-6-phosphatase is only in liver (and kidney)
    • Muscle can't export glucose derived from glycogen
    • Peripheral cells can't synthesize glucose from glycogen of gluconeogenic precursors
  41. What is the Cori cycle?
    • Lactic acid cycle
    • Glucose in muscle is converted to 2 pyruvate (uses 2 ATP)
    • 2 pyruvate is converted to 2 lactate
    • Lactate goes to liver
    • 2 lactate is converted back to 2 pyruvate and back into glucose (requires 6 ATP)
  42. How does athletic performance depend on glucose?
    • Requireent for gucose increases with exercise intensity
    • Marathon: glycogen for 1-3 hours
    • CHO loading to maximize glycogen
  43. What is type-I Diabetes mellitus?
    • Blood sugar above normal levels- spilled in the urine (glucosuria)
    • Cell-mediated autoimmune Beta cell distruction
    • Genetic predisposition
    • 5-10% of all cases of diabetes
  44. How is T1DM diagnosed?
    • Glucosuria/Ketonuia- urinalysis
    • Fasting plasma glucose concentration >7.00mmol/L (normal 5mmol/L)
    • Oral glucose tolerance test- plasma glucose >11mmol/L
    • Glycated hemoglobin (hemoglobin A1c) >6.5% (normal range 3.5-5.5%)
  45. Simplified version of T1DM
    • Stomach converts food to glucose
    • Glucose enters the blood stream
    • Pancreas produces little or no insulin
    • Glucose unable to enter body effectively
    • Glucose levels increase
  46. What are the consequences of untreated diabetes?
    • No glucose in cells- Ketoacidosis
    • Hyperglycemia- dehydration
  47. How is T1DM managed?
    • Insulin injections (pump, nasal, islet transplant)
    • Balance intake, activity, insulin
  48. How is insulin synthesized?
    • Signal peptide is translated and translocated into the ER lumen
    • Folding, oxidation and signal peptide cleavage
    • ER export, Golgi transport, vesicle packaging 
    • Protease clevage liberatoes C-peptide
    • Carboxypeptidase E produces mature insulin
  49. How is insulin secreted?
    • GLUT2 allows an influx of glucose
    • Glucose and respiration produce ATP
    • An increase in the ATP:ADP ratio closes the K-ATP channel, causing depolarisation
    • Voltage-gated calcium channels cause an influx of Ca2+ 
    • Ca2+ activate insulin gene expression via CREB (Calcium responsive element binding protein)
    • Exocytosis of stored insulin
  50. What is the peak age of T1DM onset?
  51. What is microangiopathy?
    • High glucose in some non-insulin sensitive tssues damages cells
    • Accumulation of AGEs (advanced glycation end products)
  52. What is nephropathy?
    • Thickening of glomerulus
    • Results in micralbuminuria
    • Dialysis, transplant
  53. What are the risk factors for T2DM?
    • Heredity- multigenic disorder
    • Obesity (visceral)
  54. T2DM mechanism
    • Stomack converts food to glucose
    • Glucose enters bloodstream
    • Pancreas produces sufficient insulin but it is resistant to effective use
    • Glucose unable to enter body effectively
    • Glucose levels increase
  55. What happens to GLUT4 peripheral tissues in T2DM?
    • Fat-based economy
    • Low muscle glycogen
    • Increased muscle proteolysis for gluconeogenic AAs
    • Cori cycle
  56. What happens in the liver in T2DM?
    • Gluconeogenesis
    • Lipogenesis, increased VLDL
    • Non-alcoholic fatty liver disease
  57. How is drug treatment used to treat T2DM?
    • Metformin (a biguanide)
    • Decrases hepatic gluconeogenesis
    • Increased peripheral insulin sensitivity
    • Increases GLUT4 mediated glucose uptake
    • Increases fatty acid oxidation
  58. How does metformin work?
    • Metformin activates AMPK (AMP activated protein kinase)
    • AMPK increases muscle glucose transport and decreases hepatic glucose production
    • AMPK can also decrease acetyl-CoA carboxylase activity, hence decreasing hepatic FA, VLDL synthesis and increasing hepatic FA oxidation
    • AMPK also decreases SREMP-1 expression and activity, which results in a decrease in hepatic gene expression and also leads to a decrease in hepatic FA, VLDL synthesis
    • All of these pathways resul in a decrease in plasma glucose and plasma triglycerides
  59. How is T2DM monitored?
    • Urinalysis
    • Fasting plasma glucose (FPG) and insulin
    • Oral glucose tolerance test (OGTT)
    • Glycated hemoglobin (HbA1c)
  60. What is a catabolic response to surgery?
    • Inflammatory response and neuro-endocrine response can lead to insulin resistane and hyperglycemia
    • Insulin resistance and hyperglycemia lead to loss of body protein
    • Loss of body suppression can lead to immunosuppression (delayed wound healing) or muscle wasting (delayed convalescence)
  61. How is insulin resistance and hyperglycemia caused by neuro-endocrine response combated during surgery?
    Epidural analgesia
  62. How is loss of body protein during surgery combated?
    Proper nutrition