Physiology of Eating - L1
Spring 21
Spring 21
Kartei Details
| Karten | 13 |
|---|---|
| Sprache | English |
| Kategorie | Biologie |
| Stufe | Universität |
| Erstellt / Aktualisiert | 06.05.2021 / 06.06.2021 |
| Weblink |
https://card2brain.ch/box/20210506_physiology_of_eating
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| Einbinden |
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Pro's Translational Approach of Research
1. Physiological Mechanisms of energy balance regulation are well conserved
2. Methodology/Ethics
3. Control of variables like environment, genetic variation, placebo effects
4. Repeatability
5. cost
Cons Translational Approach Research
1. Mice are not rats and not humans
2. moslty male animals are used
Measures of obesity
1. WHR
2. BMI
- widely used
- does not take the body composition into account -> great disadvantage
- however, correlations are still seen between BMI & health risks
Causes of obesity (2)
1. Energy intake & energy expenditure
2. Genetics & Environment
Energy expenditure (&energy intake)
Brown Adipose tissue -> UPC1 (uncouples ATP to produce heath without using muscular activity)
-> NO convincing evidence yet that BAT as viable pharmacological target for BW loss (activation through pharmacological might even lead to increased heart rate and systolic blood pressure)
Beta-2 Adrenoceptor = main target for pharmaceuticals to target BAT
Does excess caloric intake lead to an activation of BAT as means of preventing obesity?
NO! No evolutionary reason why such a mechanism should have been developed -> unnecessary energy waste
Energy expenditure (&energy intake) -> Thyroid hormones
- cold environment & eating increase thyroid hormone secretion (they increase the metabolism in general)
. Specifially increase heat production through an uncoupling effect: "endogenous uncouplers"
Genes & Environment
Is obesity monogenetic?
NO! Polygenic: independent & interacting effects of genetics, epigenetics & the environment
(monogenic diseases in relation to bodyweight are mostly related to leptin deficiency - but only makes up 5% of obesity cases)
Environment & body weight
(+Twin experiment)
We are more susceptible to obesity in our current environment than in our past environment.
Monozygotic twin experiment: received + 1000kcal/d for 100 d -> between groups substantial variances in BW gain, but within groups only slight differences (Environment plays a big role)
Collateral fattening
BW changes -> FM establishes faster than FFM -> leads to lower EE -> feedback loop activated to compensate for lean mass which leads to excess caloric intake -> excess fat deposition
Ultra-processed foods
lead to increased energy intake & weight gain:
Mechanisms? (Proposals)
1. disconnection of gut-brain communication
2. Eating rate
3. Protein leverage hypothesis
Sleep + obesity
endocrine changes -> higher food reward -> lower thermogenesis & PA -> more fatigue -> higher EI & lower EE
Consequences of obesity (3)
1. health care costs due to comorbidities
2. comorbidities (heart attack, fatty liver disease, diabetes..)
3. negative stigma + people are blamed for their condition
