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mechanisms 2 Flashcards

1
Q

what is catabolism

A

large to small

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2
Q

what is anabolism

A

small to big

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3
Q

3 macronutrients

A

carbs

protein

fats

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4
Q

2 micronutrients

A

vitamins

minerals

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5
Q

what are nutrient sensing pathways

A

growth and development needs nutrients

pathways monitor and respond to nutrient availability in the environment

nutrients used to generate energy and building blocks of cells

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6
Q

what is the AMPK pathway and how does it work

A

AMP-activated kinase pathway

nutrient sensing pathway - senses energy balance (AMP or ADP to ATP), relays to mitochondria

if energy lvls dec, AMPK activates pathways to generate ATP and inhibit ones that consume it - inc catabolic switches off anabolic

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7
Q

what is GCN2 pathway and how does it work

A

general amino acid control non-depressible 2

nutrient sensing pathways

senses uncharged tNRAs that accumulate upon amino acid deprivation

attentuates translation, which consumes amino acids and is energy demanding (terminates this basically)

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8
Q

what is TOR/mTOR and how does it work

A

target of rapamycin
mechanistic target of rapamycin

nutrient sensing pathway

many inputs including AMPK (energy) and GCN2 (amino acids)

most attention on nutrients and growth factors

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9
Q

mitochondria and ROS

A

mit. produce ROS

these have key role in inflammation, metabolism, etc

if accumulate, can be hella bad

counteracted by antioxidants

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10
Q

antioxidant strategies - 3

A

SOD in mitochondria

gluthione peroxidase

catalase in peroxisomes

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11
Q

what is SOD in mitochondria and how worky

A

antioxidant

converts O2+ to H2O2

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12
Q

what is gluthione peroxidase and how worky

A

antioxidant

converts +OH to H2O2 and then to water and oxygen

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13
Q

what is catalase and how worky

A

antioxidant

in peroxisomes, convert H2O2 to water and oxygen

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14
Q

migranes and mitochondria

A

brain energy deficits in people with migranes

suggests energy metabolism impairment

inc energy intake by hyperexcitable brain or dec energy supply due to mitochondrial impairment

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15
Q

causes of oxidative stress

A

alcohol

diet

smoking

medication and treatments

air and water pollutants

stress

lack of good nutrition

lack or excess exercise

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16
Q

effects of oxidative stress

A

dna damage

lipid peroxidation

mitochondrial dysfunction and apoptosis

extracellular matrix depletion

fucked inflammation

alterations in nucleus structure

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17
Q

mitochondria and ageing effects

A

inc in free radicals released from mito

damaged cell, damaged mitochondria

reduced ATP production

changes neutrient sensing pathways

cellular senesence

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18
Q

what is cell senescence

A

normal cell, wont divide itself / cell cycle arrest

in response to environmental signals intrinstic or extrinsic

dynamic process, remain viable but undergo changes to metabolic activity and gene expression - to senensence associated secretory phenotype

upreg of anti apoptotic pathways, compromise repair and regen, accelerates ageing effects

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19
Q

what are the intrinsic and extrinsic factors that drive a cell to senescence

A

dna damage

reactive metabolites

oncogenes

inflammation

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20
Q

how is cell senesence good - 3

A

for embryonic development

wound healing and regen

tumour suppression

21
Q

how is cell senesence meh

A

reprograms il-6

22
Q

how is cell senesence bad - 1

A

tumour development, stem cell exhaustion

23
Q

what is the senesence associated secretory phenotype and what does it cause

A

pro inflammatory, tissue destructive

contributes to inflammation, metabolic dysreg, stem cell dysfunction, ageing phenotypes, chronic disease, geriatric syndromes, loss of resilience

24
Q

what does SASP acc do

A

inc cytokines, chemokines, growth factors

ROS

bioactive lipid metabolites

proteases

microRNA, DNA fragments, nucleic acids

25
what is trained immunity
cells of our innate immune system can be trained to respond to one exposure to make a diff response on a subsequent exposure e.g. beta glucan, BCG, diet (oxidised LDLs) changes monocytes and macrophages in particular - inc response to second threat vs first
26
western diet and trained immunity
triggers systemic inflammation, augmenting cellular responses epigenetic effect on cells e.g. due to inc oxidised LDLs in diet inc trained immunity
27
what is a microbiome
microbial community that occupies well defined habitat and has distinct properties - microorganisms and theater of activity/ host tissues
28
what is a microbiota
commmunity of microorganisms that occupy a particular site/ habitat
29
what is dysbiosis
imbalances in microbial communities in or on body. associated with many diseases
30
microbiota role in barrier function + tissue homeostasis
microbiota modify epithelial and systemic immune responses germ free animals - no microbiota - have underdeveloped lymphoid structures and immune responses mucosal epithelial cells modify their phenotype in response to the microbiota host epithelium and immune system can alter composition and function of the microbiota
31
impact of fibre-enriched diet and fibre deficiency
supports healthy microbiota microbiota ferments fibres and makes short chain fatty acids e.g. acetate and butyrate important for epithelial function and repair esp in colon fibre deficiency = dysbiosis can cause collitis
32
respiratory microbiome
lung is not sterile not due to contamination of sample from nose or mouth during sampling the diversity of micoorganisms drive homeostasis of tissues
33
examples of diseases that have evidence for a role of gut microbiota
asthma depression diabetes non alcoholic fatty liver disease inflammatory bowel disease colon cancer heart disease
34
microbiota and rheumatoid arthritis
inflammation of joints normal gut microbiota, intact gut barrier, local inflammatory cells normal, normal homeostasis dysbiosis = damage to gut barrier, local inflammation, no homeostasis, inflammation in other tissue types systemically
35
gut-brain axis
short chain fatty acids act on gut epithelium, maintaining integrity and homeostasis dysbiosis = sends signals into circulation, crosses blood brain barrier can cause neurodegenesis
36
what is adipose tissue
central metabolic organ in regulating whole body energy homeostasis secretes adipokines and controls systemic energy balance by regulating appetite related signals
37
what are adipokines
hormones, cytokines, metabolites
38
adipose tissue and an unhealthy diet
dynamically remodeled in response to nutritional status - changes to structure linked to changes to function
39
main 3 things associated with chemicals in tobacco
immunomodulatory toxins carcinogenic toxins addictive toxins
40
effects of toxins in tobacco - 3
inc cell metastases, proliferation and invasion thus modifying immune response
41
what is ALD
alcoholic liver disease
42
harmful chronic use of alcohol effects
liver oxidative stress and inflammation sleep disturbance further driving - neg feedback
43
physical inactivity harmful effects
dec microbiotal diversity inc inflammation and oxidative stress alt skin and mucosal microbiome inc likelihood of NCDs
44
what mediates beneficial effects of exercise
myokines
45
examples of myokines
il-6 il-8 il-5, etc
46
extreme physical activity results
massive fibre damage, inflammation, TNFa, etc tend to be acute
47
what drives loss of adipose tissue when exercising
il-6 if no il-6, no fat loss -- it only drives fat loss, not ability to exercise
48
how can il-6 be blocked (med)
tocilizumab

341 (17 decks)

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