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FSHN 350- Unit 2

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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