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SEM2 > BIOL1080 lectures 15-onwards > Flashcards

BIOL1080 lectures 15-onwards Flashcards

1
Q

What is the gastrointestinal (GI) tract?

A

vast body surface area exposed to external environment, long tube going through the body that starts with mouth and ends with anus

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1
Q

What is the purpose of the GI tract and what mechanisms does it use to deal with it?

A

Sees food as well as potentially toxic substances/infectious agents
- senses and expels noxious substances (vomit, diarrhea)
- specialized populations of T cells localized to the intestinal mucosa (ex: Peyer’s opatches)

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2
Q

What do muscular sphincters and valves do for the GI tract?

A

partially segregate function within the tube

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2
Q

Name some unique properties of the GI tract

A
  • ~28 ft long (has to be folded extensively in the abdominal cavity)
  • Large luminal surface area of ~200-400 m2 due to many villi/microvilli
  • Houses resident gut microbiome (bacteria, etc.) which protects against pathogenic microbes that enter/reside in the tract
  • Intrinsic (i.e. enteric) nervous system controls & coordinates function (e.g. opening & closing of sphincters)
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3
Q

What are the 4 basic processes of the GI tract?

A

motility (peristalsis), secretion, digestion, absorption (of water and nutrients)

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4
Q

Where does chemical and mechanical digestion begin?

A

In the mouth

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4
Q

What helps with secretion in the GI tract?

A

saliva, mucous, antibodies (IgA), digestive enzymes, bile, bicarbonate

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5
Q

Expand on the small intestine and accessory organs

A
  • Enzymes released from pancreas in inactive form e.g. trypsinogen
  • Activated in small intestine by enterokinase in brush border of duodenum e.g. trypsin is important protein digestion
  • Gallbladder stores bile produced by liver for fat digestion
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6
Q

What is the cephalic phase of digestion and absorption?

A

digestion starts in mouth: chewing (mechanical) (mastication)
- Secretions in response to sensory stimuli (sight, smell, taste) prepare GI tract for food processing
- Salivary secretion under autonomic control
- Stimulated by sympathetic & parasympathetic nervous systems
- Softens & lubricates food
- Provides enzymes: amylase & some lipase (no protein digestion)

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7
Q

Expand on the gastric phase of digestion and absorption (what it is, what it does)

A
  • swallowed food + semidigested proteins activate gastric activity
  • Secretory cells of the gastric mucosa
  • Influence of parasympathetic nervous system (i.e. rest & digest)
  • Increases intestinal & gland activity
  • Relaxes sphincter muscles in the GI
    tract
  • Digestion of protein & fat, but not carbohydrate in the stomach
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8
Q

What is the main contributor of digestive enzymes?

A

pancrease

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9
Q

What can increases absorption in small intestine?

A

Small intestinal mucosa has villi, increases surface area to promote nutrient absorption

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10
Q

What secretes into the lumen of small intestine?

A

upon opening of pyloric sphincter & food (chyme) entering the upper duodenum
1. Bicarbonate – from cells in the intestinal epithelium & in pancreatic secretions
2. Digestive enzymes – from the pancreas
3. Bile acids (as bile fluid) – from the liver/gallbladder

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11
Q

What types of digestive enzymes help with absorption in the small intestine?

A

anchored on the luminal surface of small intestine epithelial cells
1. Disaccharidases
2. Amino peptidases

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12
Q

What breaks down in mouth?

A

carbs and lipids, proteins DO NOT

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13
Q

What types of transport can move sugars across the brush border into the blood stream?

A

Active (ATP), faciliated (no ATP)

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13
Q

What do amylase and lipase break down?

A

ONLY carbs, NOT proteins

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14
Q

What breaks down carbs?

A

their each respective enzyme, secreted by the brush border, enzymes break disaccharides, break them down into single sugar monosaccharides

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14
Q

What happens to blood glucose when you have a carb heavy meal?

A

it increases

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14
Q

What do villi do?

A
  • on the brush border on the end of enterocytes, they increase surface area to increase digestion and nutrition absorption
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15
Q

How are the monosaccharides glucose, galactose, and fructose absorbed?

A

glucose and galactose: active transport
fructose: faciliated

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15
Q

What disease may lactose intolerance be related to?

A

Celiac’s

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16
Q

What results in lactose intolerance?

A

deficiency in lactase enzyme

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17
Q

Explain the 3 steps in which peptide and amino acids are transported

A
  1. Proteins broken down into smaller peptides
  2. Epithelial cells secrete peptidases to break down larger peptides into individual amino acids
  3. Transported throughout body in blood stream to produce energy or protein synthesis
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18
Q

How are proteins broken down in the stomach?

A
  • whole proteins chewed and swallowed into stomach
  • HCl acid denatures proteins, unfolding 3D structure to reveal polypeptide chain
  • enzymatic digestion by pepsin forms shorter polypeptides
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19
Q

After broken down in the stomach, how do proteins get digested in the small intestine?

A
  • trypsin, chymotrypsin, and proteases continue enzymatic digestion, forming tripeptides, dipeptides, and amino acids
  • in enterocytes, tripeptides and dipeptides are further broken down into amino acids, which are absorbed into the bloodstream
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20
Q

How is fat emulsified?

A

Mouth (lingual lipase) → stomach (gastric lipase) → small intestine (pancreatic lipase)

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21
Q

When can lipases act on lipids?

A

when the lipids are broken down

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22
Q

What does bile do and what is its function?

A

makes fat soluble
* Produced in liver, stored in gall bladder
* Aids digestion of lipids through emulsification (large lipid globules broken down and distributed in chyme)
* Lipids are hydrophobic but bile salts are amphipathic (hydrophilic & lipophilic) i.e. hydrophilic side interfaces with water & hydrophobic side interfaces with lipids

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23
Q

How do fat droplets break down into smaller droplets (micelles)?

A

they are stabilized by bile salts, in the process of being digested by pancreatic lipase
- Inside is hydrophilic, outside is hydrophobic (how the droplets can be broken down into smaller droplets

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24
Q

What is the ileal chyme?

A
  • Ilium, duodenum, jejunem
  • chemical- & particle- rich liquid
  • comes in from ileum (via ileocecal valve
  • Any unabsorbed nutrients
  • Hormones & chemical messengers * Soluble fibre
  • Insoluble fibre
  • Microbes
  • Cellular debris
  • Excretion products from the liver
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25
Q

How do lipids absorb and transport?

A
  • Absorbed as fatty acids & monoglycerides (which are broken down and then moved across the brush border into the blood stream)
  • Reassembled into triglycerides & packaged as chylomicrons (type of lipoprotein)
  • Chylomicrons are too large to cross capillary wall – first absorbed into lymphatic system
  • Will re-enter circulation through thoracic duct near heart
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26
Q

What is the large intestine made of?

A

cecum and colon

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27
Q

Elaborate on the large intestine

A
  • Colonic epithelium absorbs water & simple ions (sodium, potassium, magnesium, & calcium)
  • Resident microbes digest & absorb what chemicals they can in the process of fermentation
    Short-chain fatty acids produced as end-products
  • Resident microbes produce some vitamins (vitamin K, some B vitamins) as a by-product of their metabolism
  • Some end-products can have hormone-like activity
  • Resident microbes produce gases during their digestion & consumption of ileal chyme (carbon dioxide, methane, hydrogen sulfide)
  • Newly-arriving, live microbes (probiotic or other) seek to get a foothold in the microbial ecosystem & multiply
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28
Q

What is hedonic hunger/eating?

A

the drive to eat to obtain pleasure in the absence of an energy deficit

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29
Q

What is homeostatic hunger/eating?

A

increased motivation to eat following depletion of energy stores

30
Q

What is the Ellyn Satter foundation and what does it promote?

A

both homeostatic and hedonic eating
- feed yourself faithfully, give yourself permission to eat, notice as you learn and grow

(eating should be joyful, bodies know how much to eat and grow, meals are foundation for trust (eating alone or in big groups), understanding and supporting positive eating is the key for avoiding struggles, believe that people are healthier in all ways when they eat and feed with practicality, trust and enjoyment)

31
Q

What is energy in biology?

A

the capacity to do work

32
Q

What is ATP?

A

medium of energy exchange, the energy currency of the cell

32
Q

What is the difference between ATP and ADP?

A

ATP: 3 phosphate groups
ADP: 2 phosphate groups

33
Q

What generates ATP?

A
  • glucose and fatty acid metabolism generates most
  • some generated by glycolysis and Kreb’s cycle
  • relatively little from amino acids
34
Q

What is glycolysis?

A

transforms glucose into pyruvate, the free energy released is used to form ATP, as it also gives reducing equivalents (NADH, FADH2, that help produce ATP)

35
Q

What produces the reducing equivalents NAHD and FADH2?

A

glycolysis, beta oxidation, Kreb’s cycle

36
Q

What does NAHD and FADH2 do?

A

supply protons (H+) & electrons (e-) to the electron transport chain where most of the ATP is made

37
Q

Explain the pathway NAHD and FADH2 do to create ATP

A

-they donate electrons along chain, causing gradient of H+
-high in mitochondrial intermembrane, low in matrix of mitochondria
- the movement of protons from gradient activates ATP synthase that phosphorylated ATP, which is the usable energy molecule

38
Q

Explain the products of Kreb’s cycle

A

reduction equivalents are produced, helping to produce ATP in innermitochondrial membrane

39
Q

How can ATP be generated without O2?

A

anaerobically
* Phosphocreatine (PCr) degradation
* 9-10 seconds worth
phosphocreatine decreases quickly in anerobic as it is all being used up to make more ATP during exercise

ATP → ADP + Pi
PCr + ADP + H+ → ATP + Cr
* ATP is rebuilt by adding a phosphate to ADP

40
Q

Give an example of anaerobic respiration

A

sprints

41
Q

What is the end product of anaerobic ATP production?

A
  • glycolysis continues to produce ATP
  • end product is lactate in anaerobic conditions
42
Q

Where can energy be stored?

A

fat, carbs, protein

43
Q

How is energy stored in carbs?

A

liver, muscle, blood
* Stored as glycogen in liver (~150g) – most concentrated since liver is only ~2kg
* Stored as glycogen in muscle (~350g) – ~40% body mass is muscle
* Only ~30g of glucose found in blood i.e. not much

43
Q

How is energy stored in fat?

A

as triglycerides in adipocytes

44
Q

When will energy in protein be used?

A

Protein is not often used for energy, only for emergencies
- Large potential energy source
* Protected but will be used in starvation or caloric restriction

45
Q

Explain the pros and cons of carbohydrates as fuel

A
  • Aerobically, can generate ATP slightly faster than fat
  • Can generate ATP anaerobically (3x faster than aerobic)
  • Holds a lot of water i.e. heavier & less energy-dense than fat
  • why sports drinks are high in carbs
46
Q

Explain the pros and cons of fats as fuel

A
  • Doesn’t hold water i.e. more than 2x as energy-dense as carbohydrate
  • Most abundant energy reserve
  • Can’t provide energy anaerobically i.e. must have oxygen
47
Q

What is the absorptive state of energy homeostasis?

A
  • First 3-4 hours after a meal
  • Energy (macronutrients) are
    stored i.e. anabolism
  • Excess macronutrients stored i.e. anabolic state
  • Glycogen (carbohydrate) stored in liver & muscle
  • Triglycerides (fat) stored in adipose tissue, liver, & muscle
  • Excess calories in the form of glucose or amino acids converted to fat
47
Q

What is the postabsorptive state of energy homeostasis?

A

fasting
* Stored macronutrients are mobilized for energy i.e. catabolic state
* Glucose is spared for nervous system

48
Q

What is the normal fasting blood glucose?

A

~4 – 5.5 mmol/L (very narrow range)

48
Q

How are blood glucose levels regulated?

A
  • Contrasts with free fatty acids (other major circulating fuel), which varies from 0.2 – 2 mmol/L (10 fold range)
49
Q

What is fasting hyperglycemia and hypoglycemia

A

fasting hyperglycemia- glucose > 7 mmol/L
fasting hypoglycemia- glucose ~< 3.5 mmol/L

50
Q

Why is blood glucose maintained so tightly?

A
  • Many cells require glucose
  • Maintain osmotic balance (i.e. optimal concentrations of electrolytes & non-electrolytes)
  • Hyperglycemia can cause glycosylation of amino acids in kidneys, peripheral nerves, & lens of the eye, causing damage
50
Q

How is glucose regulated?

A
  • Insulin released when blood glucose is elevated e.g. after a meal
  • Glucagon released when blood glucose is low e.g. fasting
  • Reciprocal changes in the two hormones very important i.e. not just the change in one at a time
51
Q

Why is substrates used during exercise?

A
  • Prolonged, lower intensity exercise relies more on plasma- derived substrates, particularly free fatty acids but also some blood glucose
  • As exercise intensity increases, increased need to mobilize energy stores (substrates) within the muscle itself i.e. glycogen & triglycerides
  • Muscle glycogen is the predominant fuel used during high intensity exercise
52
Q

Explain the major contributing fuel for walking, slow jogs

A

Prolonged, low intensity
Mainly blood glucose & fatty acids; some triglycerides & glycogen

53
Q

Explain the major contributing fuel for cycling, jogging/running at 60-90% VO2 max

A

Moderate to high intensity
Mainly muscle glycogen & triglycerides; blood glucose & fatty acids

54
Q

Explain the major contributing fuel for sprinting, weightlifting i.e. large anaerobic component

A

Very high intensity
Muscle glycogen, phosphocreatine (PCr)

55
Q

Why do we age?

A

our genes
- genetic variation in “longevity” genes may influence lifespan

56
Q

How many SNPs exist in the human population?

A

10 million, 1 every 300 nucleotides

57
Q

What are SNPs?

A

A difference in a single DNA building block (nucleotide)

58
Q

Are SNPs the only source of genetic variation?

A

No, but represents major source that distinguishes one individual from another

59
Q

What is precision nutrition?

A

system that uses information of the characteristics of an individual (sex/gender, and omics markers) to make personalized recommendations for preventing/treating disease

60
Q

What are nutrigenetics?

A

polymorphisms (genes to nutrients)
- studies the different response to diet depending on the genotype of individual

61
Q

What are nutrigenomics?

A

gene expression (nutrients to genes)
- focuses on mechanisms through which that different response to the diet depending on the genotype takes place

62
Q

What is molecular nutrition?

A

“nutrient-gene interaction”
(combination of genes and nutrients)

63
Q

What is aging associated with?

A
  • an increase in inflammatory cytokines that contribute to various age-related disorders
  • Alzheimer’s, cardiovascular disease, arthritis
64
Q

What is Interleukin-6 (IL-6) and how does it affect mortality?

A

an inflammatory cytokine
* Plasma levels positively correlated with greater mortality

65
Q

What promotes IL-6 and what does it cause?

A
  • SNP
  • associated with an increase in IL-6 & an increased mortality rate
  • Promoter = region of DNA that initiates transcription of a particular gene
66
Q

What is a polymorphism

A

a DNA sequence variation that is common in the population

66
Q

What is mitochondrial DNA damage?

A
  • Mitochondria contains genes e.g. components of the electron transport chain
  • Damage due to generation of reactive oxygen species (ROS) * Highly reactive chemical species containing oxygen
  • E.g. peroxides, superoxide, hydroxyl radical, singlet oxygen
67
Q

How often does damage to the mitochondrial genome occur?

A

10x more frequently than nuclear genome

68
Q

What does DNA polymerase gamma do?

A

replicates & proofreads/repairs mitochondrial DNA

69
Q

Explain the relationship between aging and mitochondrial DNA damage

A
  • Errors in replication become more frequent with age
  • Accumulating mutations in mitochondrial DNA accelerates aging
  • DNA polymerase gamma corrects errors less effectively
70
Q

Explain a mouse model for aging and mitochondrial mutations

A
  • Mice genetically engineered to carry mutations in mtDNA polymerase gamma
  • mtDNA replication error-prone & proofreading activity lost
  • Mice show accelerated signs of aging evident by 25 weeks (young adult stage), weight loss, hair loss, curvature of spine i.e. reduced lifespan
  • Causative link between mtDNA mutations & aging phenotype
71
Q

Can exercise reduce effects of aging (mice study)?

A
  • Pol-G mice lack mtDNA error correction & show increased mtDNA mutations & overall advanced aging
72
Q

What is healthy aging?

A

since aging is inevitable, it is lifestyle choices that can help individuals stay healthy as they age

73
Q

Give examples of healthy aging lifestyle choices.

A

healthy eating, physical and mental activity, social connections, routine screenings, regular eye/dental care

74
Q

Explain the results of a caloric restriction on healthy aging for animals and on humans

A
  • Generally refers to 20 – 40% reduction in daily energy intake without malnutrition
  • Originally reported in 1935: severe food restriction extended healthy lifespan in rats
  • Demonstrated in yeast, worms, fruit flies, mice, rabbits, dogs, & monkeys
  • No conclusive evidence in humans
75
Q

How does exercise compare to drugs that are used to improve the ability of muscle to respond to insulin (i.e. insulin sensitivity)? (study info)

A
  • 3234 diabetes-prone participants (i.e. diagnosed with prediabetes) studied over 4 years
  • 2 groups:
    1) Metformin (given as preventative drug)
    2) Lifestylemodification
  • Lifestyle recommendations
  • 150 min/week moderate exercise
  • Encouraged to follow Food Pyramid*
  • Target was to lose ~7% of initial body weight
76
Q

How does exercise compare to drugs that are used to improve the ability of muscle to respond to insulin (i.e. insulin sensitivity)? (key findings of study)

A

Incidence of diabetes blunted the best by lifestyle intervention
* Metformin reduced the incidence of diabetes by 31% compared to the placebo
* Lifestyle changes reduced the incidence of diabetes by 58% compared to the placebo

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