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BMS200 > Obesity > Flashcards

Obesity Flashcards

1
Q

MAFLD diagnostic criteria

A

hepatic steatosis and 1 of 3:
- T2D
- obesity/overweight
- if normal weight, need 2 of 7 risk factors: (increased WC, hypertension, elevated plasma TG, elevated LDL, prediabetes, HOMA-IR, increased CRP)

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2
Q

what is the main difference between MAFLD and NAFLD

A
  • MAFLD is unrelated to the presence of absence of other liver disease - significant because there appears to be compounded damage in those with viral hepatitis/other liver damage
  • MAFLD correlates better with non-metabolic problems better than NAFLD (lung conditions - covid mortality; chronic kidney disease/reduced eGFR)
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3
Q

what is included in “liver function tests”

A

ALT, AST, alkaline phosphatase (ALP), bilirubin

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4
Q

what do liver function tests report on & not report on?

A

they do not report on function - ONLY if there is damage

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5
Q

when can ALP be elevated?

A

liver damage
bone, intestine, kidney damage
gall bladder damage

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6
Q

when can bilirubin be elevated?

A

liver damage
gallbladder problems

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7
Q

what can we use to assess liver function?
why?
will these be high or low in acute liver failure?

A

INR and albumin
- INR measures clotting ability (prothrombin protein which is synthesized by the liver)
- albumin is also synthesized by the liver
acute liver failure: albumin can be low; low prothrombin resulting in elevated INR

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8
Q

what enzymes will be elevated when there is hepatocellular injury/liver disease?
what is the threshold for liver damage?
what is the threshold for Wilson’s disease?

A

AST and ALT are elevated
liver damage: 5x the upper limit of normal
Wilson’s disease: AST:ALT ratio of 2 and ALT:bilirubin <4

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9
Q

T/F: Anorexia nervosa and bulimia are complex eating disorders with a single factor contributing to their etiology

A

F: multiple factors contribute to their etiology

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10
Q

physical factors contributing to etiology of eating disorders

A

OCT traits
cognitive rigidity
emotion sensitivity
impulsivitiy
stress/trauma early in life
challenging interpersonal relationships
body dissatisfaction

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11
Q

biological factors contributing to etiology of eating disorders

A

50% are due to multiple genetic effects
dysfunction in serotonin, dopamine, NE, opioid and CCK systems
hypothalamic regulation
peripheral satiety changes (leptin, ghrelin, hormones, etc.)
malnourishment and exacerbate comorbid psychiatric conditions that further disordered eating behaviours

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12
Q

describe an instance where amenorrhea can precede weight loss

A

eating disorder - we would expect someone to stop menstruating once they have lost weight, but women can stop menstruating before they lose weight which implicates involvement of hypothalamus because it regulates the reproductive organs

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13
Q

sociocultural factors contributing to etiology of eating disorders

A

idealization of thin-ness

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14
Q

what are some common triggers for eating disorders

A

dieting
illness leading to weight loss - especially for anorexia

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15
Q

complications of eating disorders that are independent of weight

A

vitamin and mineral deficiencies
stunted growth if across lifespan
reduced gastric motility

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16
Q

complications of eating disorders that are consequences of malnutrition

A
  • bradycardia, hypotensis, orthostasis, hypothermia
  • metabolic alkalosis, hypochloremia, increased bicarbonate
  • osteopenia
  • myopathies
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17
Q

complications of eating disorders that are consequences of purging

A
  • esophageal tears, intractable vomiting (can’t control once you start vomiting), hematemesis
  • metabolic acidosis (abusing laxatives), hypokalemia
  • cardiomyopathies (specific vomit inducers)
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18
Q

what is included in the microbiota-gut-brain axis
draw it out

A

ANS, ENS, spinal nerves, HPA axis, immune system, enteroendocrine cells, microbiome, vagus nerve

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19
Q

how is LPS related to gut microbiota and obesity?

A

change in gut microbiota seen in obesity -> increased gut permeability which allows LPS to enter circulation and trigger pro-inflammatory state within adipocytes, promoting insulin sensitivity

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20
Q

how are SCFAs related to gut microbiota and obesity?

A

enteroendocrine cells modify their secretions (digestive hormones) in response to microbial metabolites (like SCFAs)
SCFAs have been connected to regulating satiety

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21
Q

how is the vagus nerve related to gut microbiota and obesity?

A

vagus nerve connects to the gut nucleus of the solitary tract which connects to the hypothalamic arcuate nucleus (involve in energy balance/satiety)
vagotomy assoc with changes in body weight

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22
Q

how can SCFAs regulate satiety? (6)

A
  • increase PYY and GLP-1 secretion
  • stimulates vagus nerve
  • passing though BBB and inducing anorexigenic signals
  • reduces fat accumulation in adipocytes
  • increases thermogenesis and energy expenditure
  • increases leptin production
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23
Q

what effect does SCFA supplementation have on weight?

A

intervention studies failed to show benefit of supplementary SCFAs on weight in metabolic syndrome

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24
Q

main differences between homeostatic and hedonistic pathways

A

homeostatic: regulates maintaining calories, satiety and biological aspect of food

hedonistic: eating for pleasure of food
- no direct connection between mesolimbic dopaminergic system (reward system) and gut microbiota has been established

25
Q

what are some specific ways gut microbiota influence weight

A
  • bifidiobacterium and lactobacillus positively correlate with leptin and negatively with ghrelin
  • after eradicating H. pylori, the increased Bacteriodetes:Firmicutes ratio correlates with reduced ghrelin concentration
26
Q

how is GLP-1 connected to the microbiota-gut-brain axis?

A

in the LI, GLP-1 release is induced by the microbiota
GLP-1 functions:
- increase insulin and decrease glucagon
- delay gastric emptying
- regulate appetite via vagus nerve - SCFA acting on enteroendocrine cells to stimulate GLP-1 which acts on hypothalamus to reduces food intake

27
Q

how does the vagus nerve contribute to the microbiota-gut-brain axis?

A

CCK promotes reduced food intake via the vagus nerve

28
Q

how are microbiota connected to glucose and insulin metabolism?

A
  • transplant of microbiota from healthy patients into patients with metabolic syndrome increases insulin sensitivity
  • intestinal dysbiosis associated with low grade inflammation in obesity and insulin resistance
29
Q

what is the effect of microbiota on energy harvesting?

A
  • gut microbiome genes present in obese condition appear to be involved in energy harvesting (get more energy out of your food from polysaccharides)
  • fecal transplant from obese mice to germ-free mice results in transfer of obese phenotype
30
Q

what is the correlation between Bacteriodetes counts and insulin sensitivity?

A
  • obese humans seem to have reduced Bacteriodetes counts and germ0free mice are leaner but once exposed to bacteria, increase body fat by 50% and reduce insulin sensitivity
31
Q

how are gut microbiota connect with lipogenesis?

A
  • increased energy harvest -> increased fermentation -> increased production of SCFAs
  • obese humans have elevated SCFA production
  • mice deficient in SCFA receptors are leaner than controls
32
Q

which bile acids are primary bile acids?
secondary bile acids?

A

primary: cholic acid, chenodeoxycholic acid

secondary: deoxycholic acid, lithocholic acid

33
Q

which microbial enzymes are involved in bile acid synthesis and metabolism? how?

A
  • bile acid hydrolases - deconjuggation of primary bile acids
  • hydroxysteroid dehydrogenases - oxidation of bile acids
  • dehydroxylation of unconjugated bile acids
34
Q

how are bile acids connected to the microbiome and obesity?

A
  • reduced TG synthesis in liver, increased LPL activity for better clearance
  • reduce hepatic gluconeogenesis
  • increase BAT activity and increased BMR
  • promote GLP-1 and PYY release (reduce food intake, decrease gastric emptying)
  • promote insulin secretion
35
Q

what receptor is involved with bile acid metabolism and obesity? how?

A

FXR receptor - reduces TGs in liver, reduce hepatic gluconeogenesis, promotes insulin secretion
FXR deficient mice experience leaky gut

36
Q

what are the components of energy expenditure

A

RMR - resting metabolic rate
AEE - activity related energy expenditure
DIT - diet induced thermogenesis

37
Q

resting metabolic rate definition
how is it affected by age?
how is it affected by sex?
is it affected by genetics?
is it different from REE?

A
  • mainly influenced by metabolically active tissues (fat free mass: skeletal muscle, bone, ECF)
    males > females
    young adults > elderly
  • genetics accounts for 40% of RMR
  • we consider it the same as resting energy expenditure (REE) though there are slight differences
38
Q

activity related energy expenditure definition

A

affected by:
- exercise activity thermogenesis
- non-exercise activity thermogenesis (NEAT)

39
Q

what is non-exercise induced thermogenesis (NEAT)?

A

energy expenditure during all PA excluding sport like exercise
ex. walking, fidgeting, writing, body posture, dancing

40
Q

diet induced thermogenesis definition

A

increase in metabolic rate associated with ingestion of food resulting in post-absorptive heat production
aka. the thermic effect of food

41
Q

basal metabolic rate definition
factors that affect BMR?
when do you measure BMR?

A

minimal amount of energy expended to maintain all vital processes at REST
- mainly influenced by LBM (80% of BMR) which includes skeletal muscle and lipids coming from skeletal muscle
- measured in the morning after 8 hours of sleep, fully awake and fasted 10-12 hours

42
Q

do carbs, fats, or proteins have the greatest thermic effect?

A

proteins have the greatest effect, then carbs, then fats

43
Q

describe the pathophysiological relationship between BMR/RMR and obesity

A
  • absolute energy expenditure is higher in obese patients
  • increased FFM is paralleled by increases in fat mass
  • RMR is positively correlated with weight
  • obesity is associated with increased sedentary behaviour
44
Q

why don’t we use exercise activity thermogenesis (EAT) as much as NEAT when looking at weight loss?

A

it accounts for a small portion of energy expenditure in those who are not regularly physically active and since most people don’t exercise, it prompted researchers to look at NEAT

45
Q

what is metabolic efficiency?
what does a high and lower metabolic efficiency relate to?

A
  • nutrients transported to ATP and that ATP used to support tasks
46
Q

high vs low metabolic effiiciency? what does this mean for weight gain?

A

high metabolic efficiency: less energy is wasted on thermogenesis
- people who are more efficient can put their energy into activity, not producing heat

low metabolic efficiency: lower amount of nutrients obtained and more energy is lost in thermogenesis and so less energy is available for ATP conversion into TG for weight gain

47
Q

what happens to NEAT with overfeeding?
does this apply to all individuals?

A
  • observation that 10% increase in bodyweight -> greater total energy expenditure (60% of which was due to NEAT) from more spontaneous PA
  • increased caloric overfeeding results in increased NEAT - but not enough to prevent weight gain
  • there seems to be a great difference between individuals
48
Q

what is the effect of caloric restriction on long term weight?

A
  • lower energy intake results in compensatory reduction in all energy expenditure components
  • loss of FFM
  • reduced RMR: changes in HPAT axis (thyroid function), and lower sympathetic activity (slows SNS which slows metabolism)
49
Q

results from biosphere 2 experiment

A
  • weight loss over 2 years resulted in reduced energy expenditure and reduced spontaneous PA
  • even after weight regain, impact on energy expenditure and spontaneous PA remained - applicable to yo-yo diets
50
Q

what is the effect of combining calorie restriction and exercise vs just calorie restriction?

A

weight loss in both cases but:
- weight loss without exercise results in reduced energy expenditure (including NEAT)
- weight loss with exercise results in reduced RMR but not NEAT (good)

51
Q

how are GLUT4 transporters and carbohydrate metabolism affected by exercise?

A

exercise causes GLUT4 transporters to move into skeletal muscle cell membranes independent of insulin
this persists for several hours after exercise
regular exercise routines have been shown to help recover lost insulin sensitivity

52
Q

50% of variability of spontaneous PA is believed to be a result of ___?

A

genetics

53
Q

independent model vs allocation model

A

independent model - exercise has an independent additive impact on total energy expenditure
- ie. more exercise = greater EE

allocation model - exercise results in compensatory reduction in other components of EE (such as NEAT)

54
Q

compensators vs non-compensators

A

compensators: in response to overfeeding, will increase spontaneous PA
- are less susceptible to obesity

non-compensators: are unable to response to overfeeding with an increase in NEAT, and they are therefore more susceptible to obesity; less likely to lose weight from calorie restriction

55
Q

what happens at the level of skeletal muscle that might affect someone’s ability to continue to lose weight?

A

reduced activity related muscle thermogenesis: those who lost 10% body weight were able to spend fewer calories to perform the same tasks that used to require more calories at their previous weight
- possibly due to reduced SNS stimulation (less NE stimulating muscle) -> change in MHC isoforms to more energetically economical/efficient type

56
Q

what are the 2 main mechanisms that account for insulin resistance as a complication of obesity?

A
  1. increased weight -> increased macrophages and inflammatory cells with in adipose tissue -> greater release of pro-inflammatory cytokines that disrupt insulin’s action -> insulin resistance
  2. as obese adipose tissue fills up, the excess calories are stored as ectopic fat in muscle and liver (which aren’t designed for this) and ultimately leads to defective glucose handling -> insulin resistance
57
Q

homeostatic vs hedonsitic pathways
- centers
- what they stimulate

A

make a table

58
Q
A

BMS200 (3 decks)

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