Nutr - Topic 3

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  1. what is type II diabetes?
  2. what are the different functions of glucose?
    • Converted to glycogen to store energy
    • Converted to fat to store energy
    • Oxidized for energy: for the brain, RBCs, Mammary glands, fetus, spermatogenesis (notably not the gut)
    • Glycoproteins
    • Precursor of amino acid C-skeleton
    • Prevent ketosis
  3. what organs use glucose for energy?
    • Brain
    • RBCs
    • Mammary glands
    • Fetus
  4. can you synthesis glucose from AA?
  5. where do we get get CHO from our diet?
    • Fiber
    • Starch
    • Sugars
    • Plant based foods + milk
  6. what is the AMDR for carbs?
  7. what are monosaccharides?
    • Monomers Cn (H2O)n
    • Hexoses C6H12O6
  8. what are disaccharides?
  9. what are starches?
    glucose polymers
  10. what is amylose?
    alpha(1-4) chains of glucose
  11. what is amylopectin?
    • alpha(1-4) chains of glucose with alpha(1-6) branches
  12. what are the three types of fibre?
    • soluble
    • insoluble
    • functional
  13. what is soluble fiber?
    Forms a gel in water, pectins (found in fruits)
  14. what is insoluble fibre?
    • Hemicellulose, cellulose
    • Have beta bonds, which we cannot digest
  15. what is functional fibre?
    psyllium added to foods
  16. what are the features of soluble fibre?
    • Viscous gel
    • Delays gastric emptying
    • Glycemic control
    • Binds Cholesterol and bile acids
    • Fermended by colonic bacteria
    • Low GI
  17. What are the features of insoluble fibre?
    • Bulk (laxitive effect)
    • Delays gastric emptying
    • Some glycemic control
    • Binds cations
    • Minor fermentation by colonic bacteria
  18. how are CHO digested?
    • Mouth: salivary amylase
    • Small intestinal lumen: pancreatic amylase, glucoamylase
    • Small intestinal brush border: sucrase-isomaltase, lactase
  19. GI circulation?
  20. what is lactose intolerance?
    • β-galactocidase (gene family) deficiency in adults
    • Lactose not digested in small intestine and reaches colon
    • It is fermented in the colon by bacteria producing flatulence (methane, hydrogen, CO2)
    • Osmotic diarrhea
    • Breath hydrogen test to diagnose
    • Not immune related
  21. 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 (SNP) in intron)
    • Dairy farming VS malaria hypothesis
  22. what is secondary lactose intolerance?
    • Caused by some injury to the small intestine
    • Eg. Parasite infection, celiac disease, pathology, malnutrition
  23. what is congenital lactose intolerance?
    • Non-functioning protein
    • Uncommon
    • Infants, lactase-free formula (unable to digest breast milk)
    • Same as lactose intolerance after infancy
  24. what is a milk allergy?
    • Not the same as lactose intolerance
    • Protein, or peptides in milk
    • IgE antibodies
    • Mast cell degranulation
    • Massive histamine response
    • Anaphalaxis
    • Involves immune reaction
  25. how is galactose absorbed?
    • SGLT-1 (sodium-glucose transport proteins) and GLUT-2
    • First pass removal by liver
    • Preferential conversion to glycogen
  26. 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
  27. what stimulates glucose synthesis?
    • plasma glucose
    • rapid response = relaying on activation of enzyme rather than new glucose
  28. how is glycogen broken down ?
  29. explain the degradation of glucose
  30. what is the cori cycle (lactic acid cycle)?
  31. what is the fasting plasma glucose?
    • 5mM
    • so  if the molecular weight of glucose is 180g/L
    • then 180g/l x 5 = 90 g/d
  32. what is the brains glucose requirement?
  33. what is the hepatic glucose requirement?
  34. what is gluconeogenesis?
    Production of NEW glucose from non-carbohydrate carbon substrates
  35. what are the precursors for gluconeogenesis?
    Amino acids, pyruvate, glycerol
  36. what stimulates gluconeogenesis?
    Stimulated by glucagon and glucocorticoids when plasma glucose is low
  37. what happens as a result of gluconeogenesis?
    Protein breakdown is high ↑
  38. how do glucose levels affect an athletes performance?
    • Requirements for glucose ↑ with exercise intensity
    • Marathon: glycogen for 1-3 hours
    • Carbohydrate loading to maximize glycogen
    • More later with protein metabolism
  39. Glucose Homeostasis - Long term fast
  40. what is ketogenesis?
    • Fatty acid β-oxidation in the absence of glucose = ↑ rate of generation of Acetyl CoA
    • No anaplerosis (building up of TCA cycle, build up of acetyl CoA) of TCA cycle
    • Causes acetyl-CoA to accumulate
    • β-hydroxybutyrate and acetoacetate are products (ketones)
    • Ketone bodies are an alternate fuel for the brain (do have negative impact)
    • But: ketoacidosis, impact on brain

    • β-oxidation of FA ---> generates Acetyl CoA
  41. how does ketone synthesis work?
    • β-oxidation of FA in absence of glucose
    • TCA cycle intermediates depleted for gluconeogenesis during fasting
    • Acetyl CoA accumulates ↑
    • HMG-CoA lyase increased ↑ in fating (glucagon:insulin ration)
  42. use of ketone bodies in preripheral tissues???adbasjbcjkdskvjacdruaehvkuH
  43. what is ketoacidcosis?
    • Ketone bodies are strong acids and they lower blood pH
    • Acidification is bad because it impairs the ability of hemoglobin to bind to oxygen
    • Eventually resulting in a coma
  44. what is the respiratory quotient (RQ)?
    RQ = CO2 produced/O2 consummed

    • Substrate utilization:
    • if burning CHO --> RQ = 1 (during fed state)
    • if burning FAT --> RQ = 0.7 (during fasting)
  45. add
  46. what are the components of total energy expenditure?
    • 67% - Basal Metabolic Rate (BMR)
    • 10% - Diet-Induced Thermogenesis
    • 23% - Activity
    • %- Adaptive Thermogenesis
  47. what is the BMR for males?
    • For a 70 kg male:
    • 1.0kcal/kg/h --> 1700kcal/day
  48. what is the BMR for females?
    • For a 55kg woman:
    • 0.9kcal/kg/h --> 1200kcal/d
  49. what happens when there is low blood glucose?
    Hypoglycemia, isnulin shock (hypoglycemia coma) due to lack of enough glucose to meet the brains needs
  50. hwhat happens when you have a high blood glucose?
    Hyperglycemia, dehydration, ketoacidosis, cerebral edema (diabetic coma)
  51. how much is the glucose levels found in our blood?
  52. what happens when there is high blood glucose?
    • Pancreas --> secrete insulin by the beta ells
    • Insulin --> stimulates glucose oxidation, storage  (in skeletal muscle) and conversion to fat (in the liver)
    • Insulin --> also inhibits glucose production

  53. what are major facultative glucose transporters?
    • high affinity for glucose
    • good at picking all glucose
  54. what is an example of a major facultative
    glucose transporter?
    • SLC2A1-5 (solute carrier family 2 members 1-5)
    • GLUT1- RBCs, brain (blood brain barrier), fetus (increase at low glucose concentration)
    • GLUT2- Liver, B-cell, kidney, smal intestine (high capacity of glucose uptake)
    • GLUT3- Brain (neurons), palcenta (high affinity at low concentration)
    • GLUT4- Muscle, heart, adipose tissue (insulin mediated / sensitive to insulin)
    • GLUT5- Small intestine (fructose transporter)

    • Glucose transporter (GLUT2) to exit (facilitative transport)
    • SGLT1 in intestine; SGLT2 in kidneys for re-uptake of glucose
    • High concentration of glucose found in urine and feces
  55. how does the regulation of insulin secretion by the β cells work?
    • 1. Glucose enters the beta cell through GLUT2 (glucose 2 transporter) and ATP production ↑
    • 2. ATP blocks the exit of K from the cells through K channels thus ↑ cellular K concentration
    • 3. ↑  K  concentrations causes the plasma membrane to open Ca channels thus allowing Ca to enter the beta cells
    • 4. ↑ Ca in β cells causes insulin containing granules to be released by the β cells
  56. how do insulin receptors interact with GLUT4?
    *anabolic effects of insulin that are mediated by the insulin receptors**
    • 1. Insulin binds to the α subunit of the insulin receptor
    • 2. That ↑ glucose transport and autophosphorylation of the β subunit of the receptor
    • 3. That will activate tyrosine kinase activity
    • 4. Tyrosine phosphorylation will activate a cascade of intracellular signalling proteins that mediate the effects of insulin on glucose, fat and protein metabolism
  57. what are incredins?ihwdqhdiwh
  58. what is type 1 diabetes (TD)
    • Diabetes mellitus: "sweet urine"
    • Blood sugar levels above normal levels --> spoiled in urine
    • Metabolic disorder - carbs (glcuose), protein and fat
    • 10% of total diabetes cases
    • Cell mediated autoimmune β cell destruction
    • Genetic predisposition + precipitating event
    • Autoimmune disease: pancreatic β cells are destroyed by body's immune system
    • Lab tests for antibodies to glutamic acid decarboxylase (GAD), a protein found in pancreatic cells
    • GAD catalyses the decarboxylation of glutamate to --> γ-aminobutyric acid, a neurotransmitter
    • Autoimmune disease could be also caused by viral infection
  59. what are the stages in developing TYPE 1A diabetes?
    • 1. Genetic presupposition
    • 2. Overt immunologic abnormalities & normal insulin release - Antibodies attacking beta-cells)
    • 3. Progressive loss insulin release & glucose normal -  Remainder beta-cells secrete more insulin
    • 4. Overt diabetes & C-peptide present
    • 5. No C-peptide -  Due to complete beta-cell destruction / C-peptide is a part of the inactive form of insulin (precursor of insulin)
  60. what happens if no insulin is produced?
  61. how is the metabolism during untreated type 1 DM?
    • GLUT4 peripheral tissues
    • Not getting any insulin
    • Have to rely on: Fat Based economy, Low muscle glycogen, Increased muscle proteolysis for gluconeogenic AAs, Cori cycle

    • Liver (GLUT2)
    • Gluconeogenesis = ↑ rate due to FA synthesis
    • Lipogenesis = ↑
    • VLDL - fat metabolism
    • NAFLD - fat droplet accumulating in the liver

    • Other non GLUT4 peripheral tissues
    • Glucose/Glycogen excess

  62. 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%)
  63. how does DM1 work?
  64. what are the consequences of untreated diabetes?
    • No glucose in cells        Hyperglycemia (↑ blood glucose)
    •            ↓                                ↓
    •   Ketoacidosis                 Dehydration
  65. what are 2 types of chronic type 1 diabetes ?
    • Microvascular (↑ hexokinase)
    • retinopathy
    • nephropathy
    • neuropathy

    • Macrovascular
    • artherosclerosis (more dominant in T2DM)
  66. what is microangiopathy?
    • High ↑ glucose in some non-insulin sensitive tssues damages cells
    • Accumulation of AGEs (advanced glycation end products)
  67. what is retinopathy?
    • Destroyed
    • Leading cause of blindness
  68. what is nephropathy?
    • Thickening of the glomerulus
    • Results in microalbuminuria - small levels of protein in the blood
    • Dialysis, transplant - can cause kidney failure
  69. what is neuropathy?
    Nerve damage in periphery because of impaired blood flow
  70. how do we manage T1DM?
    • Insulin injections (pump, nasal, islet transplant)
    • Balance intake, activity, insulin
  71. what are the risk factors for T2DM?
    • Age of on set: generally over 40 years
    • Risk factors 
    • heredity - multigenic disorder
    • obesity (visceral)
  72. what is the T2DM prevalence in Canada?
    • More than 2 million Canadians have diabetes
    • By the end of decade, number expected will be 3 million
    • Why? the population is aging, obesity rates are ↑, Canadian lifestyle = sedentary
    • Indigenous poeple in Canada are 3 x to 5 times more likely than the general population to develop T2DM
    • 30% of American children born in 2000 forcast to develop T2DM
  73. what is type 2 Diabetes mellitus?
    • Typically overproduction of insulin
    • there is an insulin resistance
    • central obesity
    • Followed by β cells exhaustion
    • need for insulin
  74. what is hyperinsulinemia and hyperglycemia?

    Hyperinsulinemia: normal insulin metabolism and normal intracellular glucose

    Hyperglycemia: insulin resistance and low ↓ intracellular glcuose
  75. what are symptoms and clinical findings of T2DM?
    • Glucosuria
    • Dehydration***
  76. what is glucosuria?
    • Blood glucose 10mml/L --> blood sugar flushed out via kidneys
    • Frequent urination and excessive thirst (polyuria and polydipsia)
  77. t2dm and glut 4
  78. how does de novo lipogenesis work?
  79. how is T2DM monitored?
    • Urinalysis
    • Fasting plasma glucose ≥ 7 mmol/L (FPG)
    • Insulin
    • Oral glucose tolerance test (OGTT)
    • glycemic response to 75 glucose load
    • plasma glucose > 11-2 hours after load
    • Glycated hemoglobin (HbA1c) ≥ 7%
  80. what are the stages of development of T2DM?
    • Normal
    • FPG < 5.6 mmol/l
    • high ↑ insulin sensitivity
    • moderate plasma insulin
    • low plasma glucose

    • Prediabetes
    • FPG 5.6-6.9 mmol/L
    • low insulin sensitivity
    • high ↑ plasma insulin - compensatory hyperinsulinemia and progressive β cell failure
    • increasing plasma glucose

    • Diabetes
    • FPG > 6.9mmol/L
    • lower insulin sensitivity
    • extremely high plasma glucose - hyperglycemia
    • very low plasma insulin - failed β cells
  81. what are some T2DM drug treatments?
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Nutr - Topic 3
2016-12-02 18:01:36
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