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FSHN 350- Unit 2

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