Over-nutrition (F2 15/12)

Question 1

LO’s

Answer 1

• Describe the factors affecting the control of appetite
• Describe the consequences of over-nutrition
• Describe the role of obesity in causing insulin resistance

Question 2

Give examples of appetite effectors

Answer 2

• Habit: always eat when go past fridge
• Cognitive: seeing food
• Hormones
• Sensory Input: smell
• Energy stores/ Ergostat
• Lipidstores/ Lipostat
• Nutrient Status

Question 3

How is the hypothalmus involved in appetite control, and how do we know?

Answer 3

• Hypothalmus controls eating and drinking automatically.
• It contains the arcuate nucleus which has two zones (one is the NPY/AgRp and POMc) sends information about appetite to the paraventricular nucleus, which then regualtes appetite and energy balance.
• We know the hypothalmus is involved in hunger because damage to it can cause hyper/hypo phagia (eating).

Question 4

Describe the arcuate nucleus

Answer 4

• It has two zones made of two different types of neurones.
• One zone is made up of NPY neurones, which stimulate appetite.
• The other zone has POMC nurones that suppress appetite.
• Both zones respond to insulin (which says your full) and leptin (which says your fat stores are full so you stop eating).

Question 5

Name the four Appetite Stimulators

Answer 5

• Neuropeptide Y, (NPY)
• Agouoti Related Peptide, (AgRP)
• Ghrelin, a gut hormone, secretion inhibited by stretch of stomach
• Orexin (hypocretins)

Question 6

Name all the Appetite Suppressors

Answer 6

• Leptin, a lipostat hormone, released by adipose tissue
• Peptide YY, a gut hormone (PYY)
• Glucagon like peptides, (GLP-1)
• Melanocortin
• Endorphins
• TNF, CRH inflammatory mediators
• Many others probably
• All interact with many functions

Question 7

How does the eat/don’t eat response work?

Answer 7

The two domains of the arcuate nucleus receive messages:

• When the stomach is empty it produces ghrelin and stimulates the NPY AgRp (which stimulates appetite).
• Peptide YY is released from the colon in response to eating. Reduces appetite and inhibits NPY AgRp.
• Leptin is released from adipose cells and insulin is released from the pancreas, after eating. They both inhibit the NPY AgRp and stimulate the POMC.
• The two domains of the arcuate nucleus (the NPY AgRp and the POMC then send the message to the paraventricular nucleus which regulates a response).

Question 8

Is there any genetic basis to obesity?

Answer 8

• There is a polygenic predisposition to obesity
• Moving from genetic predisposition to obesity itself generally requires some change in diet, lifestyle, or other environmental factors.
• But there are two Monogenic Elements:
  
  • Ob: produces leptin
  • FTO: is associated with weight gain
• Monogenic obesity (eg leptin deficiency) is rare.

Question 9

Describe Leptin

Answer 9

• Produced by the ob gene
• Secreted by adipose cells
• More Fat Cells = More Leptin
• Measures status of fat stores
• Used by hypothalamus to regulate fertility

Question 10

What is insulin resistance?

Answer 10

• Cells fail to respond adequately to insulin
• Results in hyperglycaemia
• β-cells increase insulin production
• Can lead to type 2 diabetes
• Obesity and insulin resistance often co-exist

Question 11

Why do obesity and insulin resistance often co-exist?

Answer 11

1. Mass: β-cells make a finite amount of insulin at any one time. Increase mass and this dilutes, so less effective.
2. Molecular: the insulin receptor is a tyrosine kinase class receptor, these are bistable switches that under physiologic conditions for certain types of cells, and insulin response may be a threshold phenomenon. That is the receptor does not respond to excess insulin in hyperglyceamic state (think of it as becoming desensitised).
3. Leptin Resistance: Fructose is converted into fat in liver. This can disrupt the leptin signalling so the individual becomes prone to further overeating, weight gain, and insulin resistance.