Exam 3 - Nutrition Flashcards
Metabolism
- refers to the chemical processes and reactions involved in maintaining life
- enable us to release energy from carbohydrate, fat, protein, and alcohol
- permit us to synthesize new substance and excrete wast products
- a metabolic pathway is a group of reaction that occur in a progression
what does the kidney excrete
urea in urine
one liver function
converts ammonia to urea
Adenosine Triphosphate
- ATP
- only energy in ATP can be used to make new compounds, contract muscles, conduct nerve impulses, pump ions across membranes
ATP
made of adenosine bound to 3 phosphate groups, bonds contain energy
Derivatives of niacin and riboflavin transfer…
hydrogens from energy yielding compounds to oxygen in metabolic pathways
Ethanol metabolism
- High NADH leads to greater fatty acid synthesis which can lead to fatty liver
Niacin
- nicotinic acid, vitamin B-3
- component of nicotinamide adenine dinucleotide
- NAD+: oxidized
- NADH: reduced
Riboflavin
- vitamin B-2
- component of flavin adenine dinucleotide
- FAD: oxidized
- FADH2: reduced
Job of lactate dehydrogenase
Requires the electron from NADH to convert lactate to pyruvate
Aerobic cellular respiration
- molecules from food are oxidized to form ATP with O2 as the final electron acceptor
- creates 30-32 molecules of ATP per glucose
Anaerobic metabolism
- insufficient O2 present
- incomplete breakdown of glucose
- creates 2 molecules of ATP per glucose
Glycolysis
- glucose is oxidized to form: 2 pyruvate, 2 NADH+, 2 ATP
- occurs in the cytosol
- role is to break down carbohydrates to generate energy and produce building blocks for other compounds
- does not require oxygen
Transition reaction
- synthesis of Acetyl-CoA
- Also makes: NADH and CO2
- occurs in mitochondria
- requires oxygen
- irreversible reaction
Citric acid cycle
Acetyl-CoA enters the citric acid cycle
- per molecule of glucose: 6 NADH, 2 FADH2, 2 GTP, CO2
Electron transport chain
- oxidative phosphorylation: energy carried by NADH and FADH2 is used to form ATp
- oxygen is the final electron acceptor: allows regeneration of NAD+ and FAD, oxygen combine with hydrogens to form water
Anaerobic metabolism
- pyruvate is produced during glycolysis and converted into lactate
Cori Cycle
- the absence of oxygen, muscle produces lactate from pyruvate
- Lactate leaves the muscle via blood and enters the liver
- liver enzymes convert lactate to glucose using ATP
- Glucose returns to the muscle
Lipolysis
breakdown of triglycerides into free fatty acids and glycerol
fatty acid oxidation
- breakdown of fatty acids for energy production
- fatty acids broken down with oxygen as electron acceptor
- occurs in the mitochondria
ATP production from fats
- triglycerides stored in adipose
- during fasting, triglycerides are broken down into fatty acids by hormone-sensitive lipase: activity is increased by glucagon, growth hormone, and epinephrine, decreased by insulin
- fatty acids are taken up by cells and shuttled into mitochondria from cytosol by carnitine
Beta-oxidation: ATP production from fats
- almost all naturally occurring fatty acids are made up of an even number of carbons ranging from 2-26
- to transfer energy from fatty acids: carbons are cleaved off in pair, NADH and FADH2 made, carbons are used to make acetyl-CoA that enters the citric acid cycle
More beta-oxidation
- fatty acids contain many more carbons than glucose
- fatty acids also store more chemical energy per carbon than glucose (less oxygen)
- fats yield more energy than carbohydrates
Carbohydrate aids fat metabolism
- some citric acid cycle compounds are used for other purposes
- cells can use pyruvate (from glucose) to replenish supply of oxaloacetate
- there is no pathway to make carbohydrates from fatty acids
- fats burn in a carbohydrate flame
Ketosis and Ketoacidosis
production of ketoacids results in metabolic acidosis: the depletion of bicarbonate
fasting ketosis
- acidosis is mild
- self limiting: ketosis increases insulin sensitivity, resulting in decreased fatty acid release and increased glucose uptake
Diabetic ketoacidosis
- more serious metabolic acidosis
- seen in type 1 diabetics with absolute insulin deficiency
Diabetic ketoacidosis steps
- absolute or relative insulin deficiency
- hyperglycemia
- glucosuria: urinary loss of water and electrolytes
- dehydration and hypovolemia
- can lead to increased lactate
- can lead to acidosis
- increased counter regulatory hormones: glucagon, cortisol , growth hormone, and epinephrine
Protein metabolism
- amino acids being used for fuel must first be deaminated: requires vitamin B6, results in carbon skeleton that enters citric acid cycle or creates acetyl-CoA or pyruvate
Glycogenic amino acids
use carbons from carbon skeleton to form glucose
ketogenic amino acids
use carbons to form acetyl-CoA
Glycolysis review
- glucose to pyruvate
- occurs in cytosol of cells
- all organs do it
Transition reaction review
- pyruvate to acetyl-CoA
- occurs in mitochondria of cell
- occurs in all organs
Citric acid cycle review
- acetyl-CoA to CO2
- Occurs in mitochondria
- occurs in all organs except red blood cells, parts of the kidney, and brain
Gluconeogenesis
- begins in the mitochondria then moves to cytosol
- mostly liver, a lesser extent in the kidneys
Beta-oxidation
- fatty acid to acetyl-CoA
- occurs in mitochondria
- occurs in all organs
Glucogenic amino acid oxidation
- amino acids to pyruvate
- occurs in the cytosol
- liver and to a lesser extent kidneys
Non-glucogenic amino acid oxidation
- amino acids to acetyl-CoA
- occurs in mitochondria
- liver and to a lesser extent kidneys
Alcohol oxidation
- ethanol to acetaldehyde to acetyl-CoA
- It occurs in Cytosol and Mitochondria
- done by liver
regulation of energy metabolism
- the liver plays a major role in metabolic pathways
- regulation involves: ATP concentrations, enzymes, hormones
Insulin and metabolism
- low level of insulin promote: gluconeogenesis, protein breakdown, lipolysis
- increased insulin promotes synthesis of: glycogen, fat, protein
Fasting and feasting
- energy sources used during fasting vary depending on the length of the fast
- depletion of lean mass to about 50% is fatal
- other problemsL depletion of electrolytes due to diuretic effect of ketone bodies, buildup of urea due to protein catabolism
Postprandial fasting (0-6 hours)
order of digestion: 1. Carbohydrates, 2. Proteins, 3. Fats
Short term fasting (3 to 5 days)
carbohydrates are depleted
- order of digestion: 1. Protein (gluconegenesis), 2. fat/ketones
feasting
- excess energy intake from any source will result in fat storage
- excess dietary fat can be stored with minimal processing
- excess carbohydrates: maximize glycogen, use as energy, convert to fat (small amount), spare fat from lipolysis
- excess protein: mostly converted to glucose, very small amount storage, potentially increased muscles protein synthesis if combined with intense exercise
inborn errors of metabolism
- genetic conditions that affect a metabolic pathway
- often enzyme mutation leading to decreased activity
- symptoms are often not very specific. but in some cases management needs to start immediately
- newborn screening to look for 30+ conditions
Phenylketonuria
- insufficient phenylalanine hydroxylase activity
- cannot convert phenylalanine to tyrosine
- instead form toxic metabolites
Phenylketonuria management
- special formula at birth
- low-phenylalanine diet for life
- fruits, vegetables, and breads generally can be eaten
- dairy products, eggs, meats, nuts, and aspartame must be avoided
Galactosemia
- cannot convert galactose to glucose
- must switch to soy formula at infancy
- throughout life must avoid: dairy products, butter, organ meats, some fruits and vegetables
glycogen storage disease
- liver cannot convert glycogen to glucose
- leads to: poor physical growth, low blood glucose levels, liver enlargement
- management: must consume frequent meals and cornstarch in between meals
energy balance
- the relationship between energy intake and energy expenditure
energy equilibrium
when calories consumed matches the amount of energy expended