Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS200 > week 1, lecture 2 > Flashcards

week 1, lecture 2 Flashcards

1
Q

do obese people use more or less calories than lean people in situations when not trying to lose weight?

A

more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

satiety signals (5)

A

leptin, GLP1, CCK, PYY, vagal afferents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hunger signals (1)

A

ghrelin (released by stomach during fasting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where do the satiety and hunger signals act on

A

different nuclei in the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

arcuate nucleus of hypothalamus neurons. which increases and which decreases food intake

A

POMC reduce food intake and increase energy expenditure

AGRP increase food intake and reduce energy expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what effect do non-esterified fatty acids have on insulin resistance?

A

increase it (by inactivating the insulin receptor via serine phosphorylation)

released from central fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do adipokines (hormones in fat cells) effect the insulin receptor?

A

increase sensitivity of insulin receptor and increase activity of enzymes that oxidize non-esterifired fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Anti-hyperglycemic adipokines vs Hyperglycemic adipokines

A

Anti-hyperglycemic adipokines: leptin, adiponectin (drops in T2DM)

  • Hyperglycemic adipokines: resistin, retinol-binding-protein 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pro inflammatory cytokines secreted by fat cells do what to insulin receptor sensitivity?

A

decrease it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

visceral adiopcytes

A

recruit macrophages and activated them –> inflammatory cytokines (TNF alpha, IL6) –> increase CRP in liver

insulin resistance –> increase free fatty acids –> activate DAMPs and increase pro inflammatory cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

effects of obesity + inflammation

A

lipids cause ROS and free fatty acids circulating bing PAMP-R in adipocytes producing IL6 and TNFalpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is a cause of singaling inhibition of insulin resistance

A

serine phosphorylation of receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

overweight vs obesity BMI

A

overweight >25
obese >30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

waist: hip ratio for obestiy

A

men: >0.9
women >0.85

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

energy expenditure

A

total amount of energy we expend, measured in kcal/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is energy expenditure composed of

A

resting metabolic rate + diet-induced thermogenesis + activity-related energy expenditure (exercise activity thermogenesis + non exercise activity thermogenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

RMR resting metabolic rate

A

metabolism of an individual
at rest
* Energy requirements of respiration, circulation, etc.

energy expenditure in an individual that is at rest and has not recently eaten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

AEE activity-related energy expenditure

A
  • Exercise activity thermogenesis (EAT) – energy used during “dedicated exercise”
  • Non-exercise activity thermogenesis (NEAT) – energy used when an individual is moving, but “not exercising” ! much larger component of AEE (i.e. fidgeting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

diet induced thermogenesis DIT

A

increase in metabolic rate associated with ingestion of food and post-absorptive heat production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how much of energy expenditure does resting metabolic rate make up>

A

60-75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the main determinant of resting metabolic rate

A

fat-free mass
(main component is skeletal muscle) (also includes bone, visceral organs, ECF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how much does resting metabolic rate vary in the same individual

A

varies from 2 – 10% in the same individual
▪ time of day, temperature season, etc. as well as errors in
measurement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

resting metabolic rate varies how much between individuals

A

8-18%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what makes up the majority of total energy expenditure

A

resting metabolic rate >non exercise activity thermogenesis > diet induced thermogenesis >exercise activity thermogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

basal metabolic rate (BMR)

A

▪ Completely rested subjects in the morning, after 8 hours of sleep, fasting for 12 hours, and at a room temperature of between 22 – 26 Celsius
▪ 80% of variations in BMR are due to FFM variations (same as RMR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

NEAT

A

“portion of daily energy expenditure resulting from spontaneous physical activity that is not specifically the result of voluntary exercise”

▪ variation can be up to 2000 kcal/day in two similar- sized individuals

▪ differences in occupations, leisure activities, molecular/genetic factors, seasonal effects

▪ The most variable aspect of energy expenditure on a population basis

  • 6-10% of EE in individuals with a sedentary lifestyle
  • up to 50% in highly active individuals (often those that are standing or constantly moving around in their occupation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

impact of overfeeding on NEAT

A

minority of people, NEAT increases

majority of people, NEAT does not increase, but today EE does still increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

impact of underfeeding on NEAT and RMR

A

RMR and NEAT decreases

i.e. if loosing weight, EE decreases (mostly due to losses in FFM)

Studies suggest that those that undergo exercise regimens with underfeeding will not suffer as large a decrease in NEAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

models of energy expenditure

A
  • Independent model of energy expenditure:
    ▪ changes in EE are independent of the energy you “budget”
    for a behaviour (NEAT, EAT)
    ▪ Therefore, if you increase your NEAT & EAT, your total EE goes up… and it’s “easier” to lose weight
  • Compensation/allocation model of energy expenditure
    ▪ if you increase the energy expenditure in one area (EAT for example), you decrease the expenditure in another (RMR or NEAT)
30
Q

compensator vs non-compensator

A

▪ Compensator – if a compensator is overfed, then spontaneous physical activity (NEAT) increases

▪ Non-compensator – with overfeeding, less increase in EE, mostly due to less of an increase in NEAT

31
Q

effect of weight loss from caloric restriction on skeletal muscle

A

skeletal muscle becomes more efficient

decrease SNS activity

switch to isoforms of myosin heavy chain to expend less ATP

RMR decreases from thyroid hormone decrease and SNS decrease

32
Q

what GLUT transport does exercise impact

A

GLUT4 –> improve glucose transport from blood to muscle and decrease insulin resistance

33
Q

homeostatic pathway

A

stimulate eating when energy stores are low

34
Q

peripheral players that sense nutrients in homeostatic pathway to modulate appetite and EE

A

adipose tissue, stomach, intestine, liver, pancreas, endocrine signals

35
Q

central players that sense nutrients in homeostatic pathway to modulate appetite and EE

A

nerves and CNS nuclei

Vagus nerve, brainstem, hypothalamic nuclei, cortex, aspects of the limbic system

36
Q

2 nuclei of the hypothalamus that regulate feeding in the homeostatic model

A

arcuate nucleus (ACN) and paraventricular nucleus (PVN)

37
Q

presence vs absence of food in homeostatic model

A

presence of food: POMC –> ACN –> MSH –> PVN –> reduce eating and increase EE

also AGRP neurons are inhibited

satiety is mediated by increased MSH signaling, either directly (MSH release) or indirectly (inhibition of AGRP release)

38
Q

serotonin signalling in the homeostatic pathway. where are they found in the brain? what does increased signalling do?

A

in midbrain (raphe nucleus) and project to the arcuate nucleus (ACN) in hypothalamus

increased serotonin signalling activates MSH and inhibit AGRP therefore reducing food intake and increasing energy expenditure

39
Q

hedonic model of eating; which brain areas?

A

food intake driven by reward pathways in the brain (esp in absence of hunger)

Lateral hypothalamus, ventral tegmental area, nucleus accumbens (part of ventral striatum), limbic system nuclei
* Major neurotransmitters implicated are dopamine as well as the endogenous opioids (enkephalins, endorphins, etc.)

40
Q

CNS portion of the hedonic model

A

lateral hypothalamus projects to VTA in midbrain where dopaminergic neurons are and which diffusely project to the nucleus accumbens, amygdala and prefrontal and orbitofrontal cortex

41
Q

reward deficiency hypothesis

A

lean people have better activation of reward pathway

obsess are reward deprived; stratal dopamine release is impaired and decreased receptor activation

also obese have greater corticolimbic activation in presence of yummy looking food

Increased reward expectation + decreased reward upon eating! increased eating behaviour

42
Q

what hormone in the pancreas effects eating

A

insulin

43
Q

which hormones in the GI effect eating

A
  • Stomach – ghrelin (orexigenic)
  • Rest of the GI tract: GLP-1, CCK, peptide YY, oxyntomodulin
44
Q

which hormones are in adipose tissue that effect eating?

A

Leptin, adiponectin, resistin, retinol- binding protein 4 (RBP-4), FGF-21

45
Q

white fat

A

predominant form of adipose tissue

stores triglycerides and visceral adipose tissue

endocrine organ

46
Q

brown fat

A

decreases with age

role in thermogenesis

mitochondria burn fat (beta oxidation) via ATP

regulated by catecholamines (dopamine, epinephrine (adrenaline), and norepinephrine (noradrenaline))

47
Q

white fat into brown fat via?

A

exercise, cold, sympathetic stimulation

48
Q

white vs brown fat

A

white for energy storage

brown for energy expenditure

49
Q

leptin; where its found and what its secreted and inhibited by

A

secreted by white adipocytes when insulin present,

inhibited by catecholamines

increases post prandially

50
Q

how is leptin anorexigenic?

A

suppresses NPY and AGRP, increases MSH secretion from arcuate nucleus of hypothalamus

51
Q

obese people and leptin

A

Obese subjects tend to have elevated leptin levels and the hypothalamus is resistant to leptin

52
Q

where is insulin secreted and in response to what?

A

by pancreatic beta cells in response to elevated blood glucose

53
Q

where are insulin receptors in the brain and what hormone is increased

A

ventral stiatium

linked to increased dopamine signalling (increase hedonic pathway)

54
Q

what is the only orexigenic hormone

A

ghrelin

55
Q

what cells in the brain release ghrelin

And where is gastric found in the stomach

A

gastric fundus (in response to fasting)

stimulates hunger pathways (amplify AGRP and NPY, inhibit MSH) via stimulating vagus nerve

56
Q

obesity and ghrelin

A
  • Fasting levels of ghrelin are negatively correlated with BMI
  • Obese patients might not suppress ghrelin as effectively after a meal
57
Q

CCK, GLP1 and PYY effects in GI tract

A

CCK in duodenum (SI) - slows gastric emptying and increases satiety

GLP1 and PYY are more distal in the intestine but also slow gastric emptying and increases satiety

GLP1 also for insulin secretion

58
Q

adiponectin

A

mostly in white adipose tissue

as visceral fat and insulin resistance increase, adiponectin decreases

increases insulin sensitivity

decrease fat accumulation

59
Q

resisting and retinol binding protein 4 (RBP4) have what effect on insulin resistance

A

increase it

60
Q

adiponectin has what effect on insulin sensntivity

A

increases insulin sensitivity (opposite to resisting and RBP4)

61
Q

SLIDE 45 and 46 chart

A

xx

62
Q

HPA axis and gut microbiota via which hormone

A

chronic cortisol elevations

63
Q

vagus nerve impact on gut microbiome

A

intestinal distention via mechanoreceptors and vagal chemoreceptors via entereoendocrine cells

64
Q

obesity and gut microbiome

A

increased gut permeability allows LPS to enter circulation = inflamed and insulin insensitive

enteroendocrine cells (serotonin, ghrelin, CCK, GLP1, PYY) alter secretions in response to SCFAs

vagus nerve

65
Q

what does gut microbiome produce

A

dopamine, serotonin, GABA,

SCFAs regulate satiety (increase PYY and GLP1, stimulate vagus nerve, induce anorexigenic signals, increase leptin, induce thermogenesis)

66
Q

bifidobacterium and lactobacillus relate to leptin and ghrelin how

A

positive to leptin (satiety) and negative to grhrelin (hunger)

67
Q

h pylori eradication increases

A

certain bacteria that correlate with decreased gremlin (hunger)

68
Q

CCK impacts food intake how via vagus nerve

A

reduces it

69
Q

where is GLP 1 released

A

intestinal epithelia enteroendriceine cells in small intestine and large intestine

70
Q

function of GLP1

A

increase insulin, reduce glucagon, delay gastric emptying, regulate appetite

71
Q

do obese humans have more or less SCFA produced

A

Increased energy harvest! increased fermentation! increased production of short chain fatty acids (SCFA’s)
Obese humans have elevated SCFA production

BMS200 (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions