Appetite regulation

Question 1

Settling point regulation model

Answer 1

system reaches ‘settling point’ where input is equal to output so if input increased, adiposity increases until new settling point reached and output matched again

Question 2

Limitations of set point regulation model (Speakman et al 2011)

Answer 2

doesn’t explain increasing prevalence of obesity over past 40 years (Flegal et al 2010)
set point regulation seems to occur over weeks/months but signals fluctuate throughout the day so time scales don’t match
ignores socioeconomic and environmental factors

Question 3

Evidence for set point regulation model (Speakman et al 2011)

Answer 3

consistent with high contribution of genes on BMI and role of biology in weight regulation (Segal & Allison 2002)
consistent with people’s tendency to regain lost fat after dieting (Anderson et al 2001)

Question 4

Set point regulation model (Speakman et al 2011)

Answer 4

fat produces signal, sensed by brain, compared to a target level of body fatness and any discrepancy triggers changes in intake/expenditure
simple concept of negative feedback loop

Question 5

Socioeconomic factors of obesity

Answer 5

Money - affects quality of food, places it can be bought from
Physical geography - can’t afford transport, food dessert (deprived areas where food is hard to come by)
opportunity - geography, growing own food
access - flats can’t grow food, can’t get to other places
deprived areas have more fast food outlets
less PA - more time on tv/internet so more advertising for food choices

Question 6

Obesity effects on health

Answer 6

reduced life expectancy, cardiovascular disease, type 2 diabetes, cancer, liver disease, respiratory disease, psychological effects

Question 7

Fullness definitions

Answer 7

Satiation - within-meal process, stop eating during meal even if more food available
Satiety - between-meal process, inhibits intake after meal so don’t seek more food
Satiety cascade - sensory -> cognitive -> post-ingestive (body processes) -> post-absorptive

Question 8

Leptin evidence

Answer 8

Mice engineered to not have leptin gained more weight, when injected with leptin had dramatic weight loss
high fat diet may cause them to become leptin resistant and put on weight (but they are more basic than humans)

Question 9

Hormones in appetite regulation

Answer 9

Leptin = satiety
Grehlin = hunger (stimulating ghrelin in someone’s stomach means they eat more in their next meal)
Cholescystokinin = satiety signal released by stretch receptors in stomach (signal to stop eating) (might be less in those that binge)

Question 10

Appetite regulation

Answer 10

Homeostatic principle - eat to restore homeostasis to maintain absence of hunger

Question 11

Mechanisms in appetite regulation

Answer 11

Central - hypothalamus, brainstem, endocannabinoids
Peripheral - episodic factors: stomach, intestines, blood, hormones

Question 12

Limitations of settling point model

Answer 12

Environmentally determined settling point can’t explain inter-individual differences
doesn’t account for impact of genes

Question 13

General model of intake regulation (de Castro & Plunkett 2002)

Answer 13

combines components of set and settling point - suggests food intake is affected by physiological, environmental, social, psychological and dietary factors sorted into uncompensated (environmental - not affected by intake) and compensated (negative feedback loops affecting/being affected by intake)
not set points - suggests level for intake/body weight is quite malleable

Question 14

Limitations of general model of intake (de Castro & Plunkett 2002)

Answer 14

focuses only on regulation of intake, leaving expenditure as one of the compensated factors

Question 15

Dual intervention point model (Herman & Polivy 1984)

Answer 15

no single set point, instead upper and lower bounds to define points where active physiological regulation becomes dominant
between bounds there is weak/no physiological regulation