Appetite regulation and obesity essential reading week/lecture 1 (Speakman et al., 2011 - models of adiposity)

Question 1

what is body fatness regulated by?

Answer 1

• Body fatness is regulated via mechanisms that control intake and energy expenditure.
  ○ Correspondence between energy intake and expenditure over time and the apparent protection of the level of body adiposity in face of energy balance led to this idea.

Question 2

set point model

Answer 2

○ Physiology, genetics and molecular biology
○ Active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point (encoded in the brain?)
○ Model consistent with biological aspects of energy balance
○ Struggles to explain environmental and social influences on obesity, food intake and physical activity.
○ Doesn’t effectively explain the obesity epidemic

Question 3

settling point model

Answer 3

○ Passive feedback between the size of the body stores and aspects of expenditure.
○ Accommodates the social and environmental characteristics of energy balance.
○ Struggles to explain some biological and genetic aspects

Question 4

failures of set and settling point models

Answer 4

• These models reflect their failure to address the gene-by-environment interactions dominating regulation of body weight.

Question 5

general intake model

Answer 5

○ Components of set point and settling point models
○ Food intake affected by wide range of physiological, environmental, social, psychological and dietary factors.
○ Sorts factors into 2 sets (uncompensated and compensated - environmental and physiological)
○ Compensated factors have negative feedback loops with intake but uncompensated factors affect but aren’t affected by intake.
○ Can explain changed in body weight that occur throughout the lifespan.
○ Only focuses on the regulation of intake, subsuming expenditure as one of the compensated factors.

Question 6

dual intervention point model

Answer 6

○ Not a single set point but upper and lower boundaries that define the points at which active physiological regulation becomes dominant and between which is where there is only weak or no physiological regulation of weight and/or fatness.
○ Argument that this is a more realistic version of set point model.
○ No defined target
○ Two intervention points are regulated independently so could be quite wide and vary between individuals
○ Allows for the inter-individual susceptibility to weight gain in a common environment
○ Consistent with results of studies showing a genetic contribution to variance in BMI.
○ Combines the set point model involving active regulation based on fatness, which would operate outside of the upper and lower intervention points with the settling point model of passive regulation operating in between them.
○ Nature of the intervention points is unclear and might be determined by a combination of genetic and environmental factors acting in concert