Carbohydrate. Carbohydrate molecules made up of mono-, di- tri- and poly-saccharides...

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Transcript of Carbohydrate. Carbohydrate molecules made up of mono-, di- tri- and poly-saccharides...

  • Slide 1
  • Carbohydrate
  • Slide 2
  • Carbohydrate molecules made up of mono-, di- tri- and poly-saccharides multi-hydroxylated 5- (ribose) and 6-carbon (glucose, fructose, galactose...) cyclic molecules. Some monosaccharides
  • Slide 3
  • Some Disaccharides
  • Slide 4
  • Mammals store glucose as glycogen (humans store approximately 350g in muscle; 90 g in liver) Plants store glucose as starch, build cellulose for structure
  • Slide 5
  • Tissue Stores ~g Days Days Minutes StarvationWalkingMarathon Running Adipose TG 9,000 34 10.8 4,018 Liver Glycogen 90 0.15 0.05 18 Muscle Glycogen 350 0.6 0.2 71 Blood Glucose20 0.03 0.01 4 Body Stores of Energy
  • Slide 6
  • Carbohydrates primary NRG source for C&PNS NRG for moderate/stressful activities ribose/deoxyribose (RNA/DNA/ATP) muccopolysaccharides (mucus/synovial) glycoproteins (cell membranes) D-galactosamine (collagen/cartilage)
  • Slide 7
  • DRI 130 g/day 45% to 65% of total calories (4 kcal/g) IOM recommend 1 hour of moderately stressful exercise every day NRG for moderately stressful exercise is 50 80% carbohydrate... 6 7 mph ~ 600 800 kcals @ 50% ~ 300 400 kcals ~ 75 100 g additional CHO Therefore, a logical minimum DRI would be more than the IOM recommendation ~ 200g/day would be a reasonable estimate
  • Slide 8
  • - Mastication in mouth Bolus w/ saliva/mucus Salivary -amylase - Pancreatic enzymes pancreatic -amylase - Brush border saccharidases: maltase sucrase lactase
  • Slide 9
  • Slide 10
  • Monosaccharides are absorbed via sodium co-transporters
  • Slide 11
  • Carbohydrates are transported to the liver through the portal vein and are picked up by the liver (and the rest of the bodys cells for those that the liver doesnt get) for processing... Liver stores glucose as glycogen (so does the kidney) & releases glucose to the venous circulation and it is transported to the rest of the body through the arterial circulation..........
  • Slide 12
  • Regulation of glucose levels in the blood is very important Normal Fasting (Serum) ~ 70 100 mg/dl Elevated = Diabetes Low = Hypoglycemia Insulin from pancreas stimulates uptake of glucose into muscle cells and fat cells by activating the GLUT4 transporters. After eating a meal, glucose levels increase in the blood and trigger an insulin response. Within a1 to 2 hours, glucose levels decline back to normal. With insulin resistance, or diabetes, glucose levels remain elevated for prolonged periods of time and the enhanced levels of glucose in the blood greatly increase risk for a variety of chronic diseases. When serum levels of glucose decrease too much, then the pancreas releases glucagon to stimulate the liver and kidney to break down glycogen to glucose and release glucose into the blood (glycogenolysis). And the liver will automatically enhance synthesis of glucose from amino acids. Adrenals will release cortisol if levels stay too low for prolonged periods of time to enhance breakdown of protein in muscles to release amino acids so the liver can pick up the amino acids and make them into glucose (gluconeogenesis). This breakdown however, only occurs in non-exercising muscles. Because there always is a ready supply of amino acids in liver (even without breakdown of muscle protein), rates of gluconeogenesis range from 3 to 4 grams glucose produced/hour. Unfortunately, this rate is less than the amount of glucose necessary for optimal brain function and as a result, we have a minimum requirement for carbohydrates (source of the nutrient: glucose) in our diet.
  • Slide 13
  • Glycemic Index and Glycemic Load: Glycemic Index: A relative measure of how rapidly the digested carbohydrate appears in the blood as glucose relative to the same amount of pure glucose over time. A 50 g amount of glucose would have a GI of 100 while a 50g amount of other carbohydrate sources would be expressed relative to the glucose GI. GI is 70 or more is high GI of 56 to 69 is medium GI of 55 or less is low.
  • Slide 14
  • Glycemic Index and Glycemic Load: Glycemic Load: A measure of total amount of glucose appearing in the blood over time based on the total amount of digestible carbohydrate in the food. GL = GI / 100 x g GL of 20 or more is high GL of 11 to 19 is medium GL of 10 or less is low Because some high GI foods may contain relatively little total carbohydrate (or visa versa), calculating a glycemic load based on both GI and total CHO can make sense: Wonder enriched white bread: GI = 73, GL = 10... Betty Crocker chocolate cake: GI = 38, GL = 20...
  • Slide 15
  • GL / GI per serving of some common foods (adapted from: Low GIMedium GIHigh GI - 55 56 - 69 70 100 Grapes 8 / 46Pineapple 7 / 59Watermelon 4 / 72 LowApples 8 / 42Cantaloupe 4 / 65Popcorn 8 / 72 GLPeanuts 1 / 14Beets 5 / 64Wheat bread 8 / 71 0 - 10Corn 9 / 54Sugar 7 / 68White bread 10 / 70 Baked beans 7 / 48Rye bread 8 / 58Waffles 10 / 76 Honey 10 / 55 Bananas 12 / 52Life cereal 16 / 66Cake donuts 17 / 76 MediumNavy beans 12 / 38Potatoes 12 / 57Cheerios 15 / 74 GLSourdough bread 15 / 54Wild rice 18 / 57Shredded wheat 15 / 75 11 - 19Parboiled rice 17 / 47Sweet potatoes 17 / 61Gatorade 12 / 78 Apple juice 12 / 40Coca Cola 16 / 63Bran flakes 13 / 74 HighLinguine 23 / 52Couscous 23 / 65Baked potatoes 26 / 85 GLMacaroni 23 / 47White rice 23 / 64Cornflakes 21 / 90 20+Spaghetti 20 / 42Power bar 24 / 56Dried dates 42 / 103 Note that complex carbohydrates form the basis of both high glycemic and low glycemic foods; indicating that the simplified concept that complex carbohydrates are better than simple carbohydrates doesnt make a lot of sense. Another note: when eaten in combinations, then the GI/GL is completely different than the tabled values indicating that actually applying the GI/GL information to a mixed-diet is very difficult
  • Slide 16
  • The concern with glucose relates only to sustained high levels in the blood. Both glucose (and fructose) can exist in a closed-ring structure (as shown on the second slide) and also as an open-chain structure. In the open-chain configuration, the aldehyde of glucose and the ketone of the fructose can form a reversible Schiff base with any free amino group of any phospholipid, protein, and even on DNA; ultimately leading to the formation of Advanced Glycation End-products (AGEs). Once formed, the AGEs can activate inflammatory processes in the local tissues in which they are formed and the inflammatory process lead to additional tissue dysfunction and various disease such as retinopathies, peripheral vascular disease, atherosclerosis, and stroke. (~3-6 h to equilibrium) (> weeks to form) Glucose Schiff base Amadori Products various dicarbonyls AGEs Fructose Schiff base Heyns Products various dicarbonyls AGEs Removal of glucose from the blood is largely dependent on insulin while removal of fructose is not; as a result glucose levels in the blood are typically 500 times greater than those of fructose; indicating that glucose is the molecule we need to be concerned with in regard to chronic disease and that fructose is a relatively minor player. Because the freely reversible Schiff bases need to be present for several weeks (or more) to rearrange into stable Amadori / Heyns products; only chronically elevated levels of glucose can lead to elevated risk for disease. With a rate of reversion that reaches equilibrium in approximately 3 to 6 hours, additional Schiff bases formed because of elevated glucose (or fructose) levels following a meal will essentially be back down to normal levels following a customary overnight fast. Because it takes weeks of elevated glucose to lead to additional AGE formation even a weekend of gluttony should not have a great effect as long as normal eating behaviors are followed in subsequent days. Thus, those individuals with normal insulin function have nothing to worry about when it comes to carbohydrate consumption. Only those with insulin resistance (pre-diabetes) or diabetes need to be concerned and to try and avoid high glycemic loads throughout the day to minimize the additional risks of prolonged periods of elevated glucose (additional issues on the cause of insulin resistance & diabetes are discussed in the PPt on CAD and Cancer).
  • Slide 17
  • Because of the enhanced formation of AGEs in those with insulin resistance (pre-diabetes) or diabetes, they also have a greater risk for chronic diseases than those with normal insulin responses; essentially as shown below in relation to clinical norms
  • Slide 18
  • The Schiffs bases are freely- reversible and will equilibrate with glucose levels in approximately 3 to 6 hours. Their conversion into AGEs requires a sustained elevation in glucose levels over several weeks. With the traditional timing of eating meals based essentially on work schedules - a timing that includes an overnight fast; normal risks for chronic disease are produced (top graph). Sustained elevation in glucose levels because of insulin-resistance (middle graph) or diabetes (bottom graph) will produce an elevated risk for chronic diseases.
  • Slide 19
  • Because it only takes approximately 3 to 6 hours for Schiffs-base levels to equilibrate with the glucose- levels (regulated to be 70 100 mg/dl) it is highly doubtful that even with an early breakfast and late dinner eating pattern (with multiple snacks) there will be an elevated risk for AGE formation (to produce an insulin-resistant pattern and the