Exam 2 Flashcards
Digestive system
Series of organs coordinated to facilitate nutrient intake and uptake
Mouth
Saliva
Moisten food
Mucus
Amylase
Stomach
Acidic
Protease enzymes (pepsin)
Gastric lipase (FA)
Intrinsic factor (B12)
Contractions grind and mix food
Gastric emptying
Regulated movement from stomach to SI
Small intestine
Primary site of digestion and absorption
Bile acids
Muscles (longitudinal, circular)
Rich blood supply
Microvilli
Liver
Produce bile acids (stored in the gallbladder)
Process nutrients
Pancreas
Produce digestive enzymes and insulin
Release bicarb
Swallowing
Reflex initiated by movement of food from mouth to pharynx
Reflex closes the epiglottis over the larynx
Want to prevent food from ending up in airways or nasal passages
Upper esophageal sphincter
Closes off upper esophagus
Lower esophageal sphincter
Closed distal end of the esophagus
Blocks reflux of the stomach contents back into the esophagus
Chyme
Stomach digested food
Gastroesophageal reflux disease
Lower esophageal sphincter is loose
Stomach contents reflux back up into esophagus (constant)
Acid content irritates lower esophagus
Can wear away the lining, detrimental
Drugs for GRD
Antacid neutralizes the acid
Block acid secretion
Proton pump inhibitor
Lumen
Inside of small intestine
Where the food/contents are
Collectively called the mucosa
Villi
Small folds
Rich blood supply
Lined with a single layer of epithelial cells
Increase surface area
Increases interaction with food
Crypt cells
Complex organization of cells as a result of the villi structure
Crypts of cells that do not project out into the lumen
Stem cells that replenish them are at the bottom of the crypt
Cells migrate from crypt up the lumen
Enterocytes
Majority of cells
Digestion and absorption
Goblet cells
Secrete mucin
Enteroendocrine cells
Hormone selection
Paneth Cells
Immune monitoring
Large intestine
Receives food residue from small intestine
Large population of bacteria
Absorb water and minerals
Beginning to form fecal matter
Regularity depends on
Microbiome
Food intake
Genetics
Autonomic nervous system
Regulates function of visceral organs
Unconscious functions
GI hormones
Small polypeptides
Released in response to meals
Travel to different regions of the digestive system to regulate GI function
What do hormones do
Regulation of GI motility
Epithelial cell growth
Regulated to maintain homeostasis
Secretion of various chemicals
Peristalsis
Sweeping motion
Propels food forward
Sequential contractions
Swallowing, stomach, small sections of small intestine
Segmentation
Circular muscle in small intestine
Closely spaced contractions in discrete areas of the intestine
Increase contact with mucosal surface
Mass movement
Large intestine
Contractions that occur over a large area of intestine
Move waste towards the rectum
Salivary glands
Release saliva in the mouth
Easies swallowing, breaks down some carbs
Gastric glands
Produce gastric juice in the stomach
Uncoil proteins, enzymes break down proteins, mucus protects stomach cells
Pancreas excretion
Produces pancreatic juice
Bicarb neutralizes acidic gastric juices
Enzyme break down carbs, fats, proteins
Liver’s job
Produce bile for the gallbladder
Gallbladder
Release bile to the small intestine
Emulsify fat
Intestinal glands
Product intestinal juice
Enzymes break down protein, fat, lipids
Mucus protects intestinal wall
Carb digestion
Starts in the mouth
Salivary amylase
Break down alpha 1,4 bonds
Carb digestion SI
Uses amylase from the pancreas
Converts amylose and amylopectin to dextrins (broken down by brush border)
Brush border
Organization of microvilli on enterocytes
Microvilli membrane is studded w/ glycosidases
Food pushes against the border during contractions
Carb absorption
Only absorb monosaccharides
GLUT2
Basal transporter
Moves monosaccharides out of the enterocyte and into the blood
Facilitated transport
SGLT1
Transport glucose and galactose
Active transport
Need NRG
GLUT5
Transport fructose
Faciliated transport
Protein digestion
Starts in the stomach
HCL uncoils
Pepsin breaks into pieces
Protein digestion SI
The pancreas secretes digestive enzymes and bicarb
Hydrolyze peptide bonds → oligopeptides
Protein absorption
Brush border peptidases hydrolyze oligopeptides (AA, mon/di/tri peptide)
Transported across the intestinal cell membrane
Active and facilitated transport
Transporters move the AA and small peptides out of the basal region + into the blood
Lipid digestion
Starts in the stomach
Gastric lipase (TG –> FFA + monoglycerides)
Lipids SI
Bile acids and lecithin from gallbladder
Pancreatic lipases work with protein co-lipase to hydrolyze TG
Emulsification of fat droplets gives lipases access
Micelles
Form from monoglycerides and FFA surrounded by bile acids
Give lipids access to epithelial cells
Vitamin absorption
Anabolic reactions
Make glycogen, triglycerides, protein
Require NRG
Catabolic reactions
Breakdown glycogen, triglycerides, protein
Releases NRG
Glucose used for
Metabolism
Stored as glycogen
Convert to fat for storage
Distribute to the rest of the body
Glycolysis
1 glucose → 2 pyruvate
Cell uses 2 ATP to go through glycolysis
Gains 4 ATP (2 Net) per glucose
Fats (cell level)
TG broken down and absorbed as FA
Packaged as lipoproteins
Processed through the liver
Beta oxidation
Proteins (cellular)
Broken down and absorbed as single AA
Processed through the liver
Don’t generally use for NRG
Citric acid cycle
All NRG yielding nutrients can be broken down to acetyl CoA
Acetyl CoA can enter CAC or be used to make fat
Electrons are carried to electron transport chain
Feasting
Person eats excess of NRG needs
Body stores glycogen and fat
Fasting
Nutrients from a meal are no longer able to provide NRG
2-3 hours after a meal
Body draws on glycogen and fat stores
Fasting beyond glycogen depletion
Glycogen stores dwindle
24 hours of starvation
Break down protein sources to synthesize glucose
Liver convert fats to ketone bodies
Caloric restriction
Decrease in food intake from what an organism would eat on its own
Increase lifespan
Model of delayed aging
Neutral balance
Energy in = energy out
Maintain weight
Consumed = burned
Positive balance
Energy in > energy out
Gain weight
Primarily stored as fat
Negative balance
Energy in < energy out
Lose weight
NRG stores
Gain weight: stored as fat b/c it is essentially endless storage
Adipose tissue TG = greatest tissue depot of NRG
Gross NRG
From bomb calorimeter
Digestible NRG
Gross NRG - fecal NRG loss
Metabolizable NRG
Diegstable NRG - urinary and gaseous NRG loss
Caloric content of macronutrients
Protein/carb = 4 kcal/g
Fat = 9 kcal/g
Non biological factors (NRG in)
Accessibility
Geographical
Socioeconomic, income
Culture
Family
Climate
Time
Etc
Biological factors (NRG in)
Hunger
Satiation
Appetite
Satiety
Hunger
Physiological response (to nerve signals and hormones) after a lack of sufficient food
Satiation
Sensation that prompts the cessation of eating during a meal
Feel full while you are eating, acute
Appetite
Desire to eat
Satiety
Feeling of fullness and satisfaction that persists after a meal
Feeling between meals, occurs over time
CCK
Protein hormone
Station response
Stimulate gallbladder to contract → bile acids
GLP1
Released from SI
Satiation signal
Release insulin independent of blood glucose levels
Leptin
Protein hormone released from adipose
Interact w/ receptor in hypothalamus
Satiety signal
Concentration related to concentration of adipose
Ob/ob mice
Mutation in gene that encodes leptin
Don’t produce leptin
Have a receptor and can respond
Db/db mice
Mutation in gene responsible for coding leptin receptor
Produce leptin
Can’t respond
Gas exchange
Most accurate and most complicated
Measure O2 consumed and CO2 expelled to digest macronutrients
Works b/c different macronutrients require different amounts of CO2 and O2
Gas exchange comparisons
Fat = most O2, CO2
Carbs = equal CO2 and O2
Protein = 2nd most O2, least CO2
EER
Only works for people ≥ 19 years old
Different inputs for men and women
Derived from population data, uses averages
EER factors
Age (NRG expenditure decreases)
Physical activity (NRG expenditure increases)
Weight (NRG expenditure increases)
Height (NRG expenditure increases)
Fitness wearables
Uses velocity and heart rate measurements
20-90% margin of error
Cool to look at
Physical activities
Everything above basal metabolism
Chewing gum to all out competitive sports
Basal metabolism
NRG required to exist, keep the lights on
Breathing, heart rate
Homeostatic regulation of core body temp
Core needs to resist temp changes
Heat and cold
Cold but not freezing
NST
Adaptive thermogenesis players
Metabolic rate increases, don’t depend on shivering
Mediated by adipocytes
ST
Metabolic rate increases
Use shivering (muscle contraction) to generate heat
White adipocytes
NRG storage depot
Not cool
Brown adipocytes
Start out as a different cell → brown adipocytes
Very special, very cool
Brite or beige adipocytes
Come from white adipocytes
Gain extra functions
Used to not be cool → become cool
Brown and beige adipocytes
Have increased mitochondrial density
Uncouple the electron transport chain
BMI equation
weight (kg) / height^2 (m^2)
Underweight
BMI < 18.5
Normal
18.5 - 24.9
Overweight
25-29.9
Obese
30-34.9
Extremely obese
BMI > 35
Obesity has been continuously increasing in the US
Obesity is a driver of every chronic disease
Public health systems will be more burdened
Hydro densitometry
Weight of person in water compared to on land
Difference provides a measure of the body volume
Not as accurate as other methods
Air displacement plethysmography
Measure air displaced by a person’s body
Can tell body fat
Bioelectric impedance
Measures body fat using electric current
Leaner the person = less resistance
Look at conduction of tissues
Dual X-ray absorptiometry
Uses X-rays to differentiate lean body mass from fat and bone tissue
Precise measurement of total fat and distribution
Gold standard
Skinfold
Estimate body fat
Gauge thickness of a fold of skin
Compare with standards
External only
Fed state
Insulin > glucagon
Favor NRG storage
Blood glucose is elevated
Glycogen storage increases
Postabsorptive state
Insulin decreases
Glucagon increases
Blood glucose decreases
Liver glycogen breakdown
Increase use of FA for NRG
Fasting state
Glucagon > insulin
Liver glycogen = depleted
Gluconeogenesis
TG broken down, use FA for NRG
Ketone formation, ketogenesis
Type 1 diabetes
Decreased insulin production
Increased glucose due to low insulin
Muscle unable to use glucose
Behaves as if there is low glucose
Type 2 diabetes
Failure to respond to insulin
Sufficient insulin secreted
Muscle unable to use glucose due to insulin resistance
Insulin
Secreted from the pancreas (beta cells)
Response to elevated blood glucose levels
Glucagon
Secreted from alpha cells
Response to low blood glucose
Glycogenolysis
Glycogen breakdown; glucose production
Glycolysis
Glucose breakdown; forming two molecules of pyruvates
ATP production without oxygen (anaerobic energy metabolism)
Lipolysis
Breakdown of triacylglycerol (triglyceride) to fatty acids and
glycerol
Beta-oxidation
Breakdown of fatty acids to acetyl-CoA
Proteolysis
Breakdown of protein to amino acids
Transamination/Deamination
Transfer/ removal of amino group from the amino acids
Citric Acid cycle
A central metabolic pathway, oxidizing acetyl-CoA to CO2 and
generating reducing equivalents (NADH + H, FADH2), and GTP
(ATP)
Oxidative phosphorylation
A series of coupled processes in which reducing equivalents are
oxidized, and the resulting proton gradient enables ATP
production
Gluconeogensis
Glucose synthesis from noncarbohydrate sources
Ketogenesis
Formation of ketones from acetyl-CoA
Glycogenesis
Formation of glycogen
Lipogenesis
Synthesis of fatty acids and formation of triacylglycerol
Protein breakdown products
AA –> pyruvate, acetyl CoA, CAC
TG breakdown
Glycerol –> pyruvate
FA –> acetyl CoA
Alcohol –> acetyl CoA
Dietary Factors modulating glycemic responses
Quality
Quantity
Glycemic index/load
Type and amount of carvs
Fiber
Fat, protein
Timing
Host Factors modulating glycemic responses
Digestion and absorption
Insulin sensitivity
Insulin secretion
Physical activity
Lean body mass
Previous meal
Microbiome
Enzymes
Catalysts of metabolic reactions
Substrate binds to active site → complex → transformation → release
Cofactors and coenzymes
Derived from vitamins and minerals
Combines with the enzyme to form an active enzyme
Epiglottis
Blocks the larynx
Protects airways during swallowing
functions of muscles in the digestive system
Segmentation
Peristalsis
Sphincter contractions
Water soluble nutrients
Absorbed across enterocytes
Released into the blood
Deliverd to the liver
via the portal vein
Secretion and motility coordinated by
Hormonal system
Nervous system
Starch enzyme
Pancreatic amylase
Dextrins enzyme
Isomaltase
TG enzyme
Lipase
Protein enzyme
Pepsin
Nutrient with largest diff btwn gross and metabolizable NRG
Vitamins
Orlistat
Decreases digestible NRG
of foods with fat
Insulin decreases blood glucose by
Increase uptake in adipose
Increase uptake in muscle
Increase lipogenesis
Increase glycogenesis
FA can be made from
AA
Glucose
Acetyl CoA
Ethanol
Overexpression of UCP1
Increase NRG expenditure
Catabolic reactions to generate ATP
In all cells
Break down macronutrients
Consume O2
Release ATP, CO2, H2O
Anabolic reactions to store NRG
Glycogenesis
Lipogenesis
Anabolic during catabolic states
Gluconeogenesis
Ketogenesis
Long term fasting
Glycolysis
Split glucose into 2 x pyruvate
Generate ATP and NADH
Cori cycle
Liver produces pyruvate via glycolysis
Convert pyruvate to lactate to regenerate coenzyme
Lactate in muscle → liver → convert to glucose → return to muscle
Lipolysis
Glycerol can be used to make pyruvate
FA can be turned into Acetyl CoA
Beta oxidation
Need carnitine and CoA
Cleave FA into 2 carbon units
Each cleavage = 1 NADH + 1 FADH2
Glucogenic AA
Used to synthesize glucose
Or can enter the citric acid cycle directly
Ketogenic AA
Converted directly to acetyl CoA
Transamination
Keto acid + AA → keto acid + AA
Deamination
Make ammonia + keto acid
Alcohol digestion
Absorb as early as stomach
Liver catabolizes
Alcohol → acetyl CoA
CAC
Acetyl CoA = input
Oxaloacetate = needed to bring Acetyl CoA in
ETC
Passing e- releases NRG to pump H+
H+ gradient powers ATP synthase
Water formed
Glycogenesis
Liver and muscle
Lipogenesis
Liver and adipose
Take any substrate
Can be made from proteins, carb, fat
Gluconeogenesis substrate
Lactate
Glycerol
AA
Need oxaloacetate
Ketogenesis
Start with acetyl CoA
Builds up due to gluconeogenesis
