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FSHN 350- Unit 2
| Question | Answer |
|---|---|
| how many pounds of sugar to Americans consume per year? | 130 |
| photosynthesis | 6CO2 + 6H2O -> C6H12O6 + 6 O2 |
| two categories of CHO | simple and complex |
| three monosaccharides | glucose, fructose, galactose |
| two types of complex carbohydrates | oligosaccharides, polysaccharides |
| how many monosaccharides on oligosaccharides? | 3-10 |
| three types of polysaccharides | starch, glycogen, fiber |
| homopolysaccharide | composed of only 1 type of monosaccharide *most foods |
| heteropolysaccharide | composed of >1 type of monosaccharide |
| amylose vs amylopectin | amylose straight chain (1-4 bonds only) amylopectin branched (some 1-6 bonds) |
| glycogen | primary CHO storage; highly branched |
| dietary fiber | found naturally in plants |
| functional fiber | can be manufactured for derived from plants |
| soluble fiber | fermentable by intestinal bacteria |
| insoluble fiber | cannot be fermented by bacteria |
| lactose | glucose + galactose |
| sucrose | fructose + glucose |
| maltose | glucose + glucose |
| CHO digestion in stomach | none |
| amylose small intestine digestion | pancreatic amylase turns it into maltose |
| diagnosis of lactose intolerance | hydrogen breath test, stool acidity test (excess H as byproduct of intestinal bacteria) |
| what happens when SGLT 1 is overloaded | GLUT-2 can pass glucose and galactose into the enterocyte |
| Glucose-Galatose malabsorption disorder | genetic mutation of SGLT-1 (they eat more fructose) *glucose stays in blood and lowers risk of diabetes |
| which GLUT transporter is insulin dependent? | glut 4 |
| which GLUT transporter in liver, pancreatic beta cells, and intestine? | glut 2 |
| which GLUT transporter in heart, skeletal muscle, and fat? | glut 4 **insulin dependent |
| which GLUT transporter in brain? | glut 3 |
| glycemic index | AUC for 50g food/AUG for 50g glucose |
| glycemic load | another index normalized to serving standards |
| 4 functions of insulin | promotes glucose uptake, promotes glycogenesis, promotes protein synthesis, promotes fat synthesis |
| glucose 6 phosphate and hexokinase | allosteric inhibitor |
| glucose 6 phosphate and glucokinase | DOES NOT inhibit (excess glucose taken up by the liver) |
| insulin and glucokinase | indirectly induces glucokinase |
| insulin and glycogen synthase | activates (dephosphorylates!) |
| glucagon/epinephrine and glycogen synthase | deactivate it |
| glucagon and glycogen phosphorylase | activates it |
| epinephrine and glycogen phosphorylase | activates it (skeletal muscle) |
| AMP and glycogen phosphorylase | activates in (ATP deactivates it) |
| most of glycogen in the body is found | in the muscle (75%- just b/c there is more muscle in the body) |
| 3 regulatory enzymes of glycolysis | hexokinase/glucokinase; PFK, pyruvate kinase |
| PFK inhibition/activation | inhibited by ATP; activated by AMP and ADP |
| pyruvate inhibition/activation | inhibited by acetyl-coA; activated by fructose 1,6 biphosphate, activated by insulin (exception to insulin being anabolic) |
| two fates of pyruvate | lactate -> CORI cycle acetyl CoA -> TCA cycle |
| transport of pyruvate and NADH into mitochondria | pyruvate: mitochondrial pyruvate carrier NADH: shuttle systems |
| intermediates in TCA cycle | citrate, isocitrate, a-ketoglutarare, succinyl coA, succinate, fumarate, malate, oxaloacetate |
| what is made in TCA cycle? | 6 NADH, 2 FADH, 2 GTP |
| other sources of NADH in CHO metabolism | 2 in glycolysis, 2 in converting pyruvate to acetyl coA |
| regulation of TCA cycle (3) | -low intermediates slows down the cycle -high NADH:NAD slows down the cycle -high ATP:ADP slows down the cycle |
| gluconeogenesis: what instead of pyruvate kinase? | pyruvate carboxylase-> oxaloacetate -> PEP carboxylase |
| gluconeogenesis: what instead of PFK? | fructose 1,6 biphosphatase |
| gluconeogenesis: what instead of hexokinase? | glucose 6-phosphatase |
| three irreversible enzymes (differences for gluconeogenesis) | hexokinase, PFK, pyruvate kinase |
| lipemia and fructose | elevates triglyceride levels for longer and higher than other sugars |
| type 1 diabetes cause | autoimmune disorder destroys pancreatic beta cells |
| diabetes 1 and 2 percentages | 5%= type 1, 95%= type 2 |
| type 1 diabetes remedies | pump, injection, or inhalation |
| risk factors for type 2 diabetes | aging, genetics, obesity, sedentary lifestyle, high blood lipids, high blood pressure, women who had gestational diabetes, certain racial groups |
| three tests to diagnose diabetes | A1C test, fasting plasma glucose, glucose tolerance |
| diabetic A1C cutoff | 6.5% or above |
| diabetic fasting plasma glucose cutoff | 126 or above (mg/dL) |
| diabetic oral glucose tolerance test | 200 or above (mg/dL) |
| biological effects of insulin (4) | increase fat uptake/synthesis, increased glycogen synthesis, increased protein synthesis, increased vasodilation |
| biological effects of insulin resistance (4) | ^ lipolysis, ^ hepatic glucose output, decreased glycogen synthesis, decreased vasodilation |
| 3 potential treatments for diabetes | lower glucose absorption, improved insulin action, improved insulin secretion |
| GD risks to baby | high glucose levels during in utero, initial low blood sugar, obesity, type 2 diabetes, macrosomia |
| GD risks to mother | difficult delivery, pre-eclampsia (high BP), increased risk of type 2 diabetes |
| GD natural phenomenon? | it's good to become a little insulin resistant to secure glucose for the growing fetus |
| glucose travels through placenta via | glut 3 |
Created by:
melaniebeale
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