The Hunger Satiety Cycle

Question 1

Thermodynamic approaches to weight control: why are we putting on weight as a population? Support from WWII? Allostasis?

Answer 1

• Calories in= calories out to maintain weight
• Although intakes have decreased since the 1970s, we are putting on increasing weight because our outputs are much lower
• allostasis: concept of increased set points, food industry are posing an allosteric pressure, increasing weights so people need more food to maintain weight
• Support from WWII: increase in energy intake despite rationing, which lead to a weight gain of 1 kg

Question 2

What are the 3 main phases involved in initiation of eating?

Answer 2

1) Cephalic phase: sight and smell of food leads to pancreatic secretions (including NaHCO3, enzymes such as cholecystekinin, insulin) to prepare the GI system
2) Gastric phase: starts upon eating: nutrient sensing and stomach distention
3) Absorption of nutrients in GI system: satiety

Question 3

Drivers for hunger: exercise or the circadian rhythm?

Answer 3

• exercise has been shown to be a poor indicator of increased hunger
• Circadian rhythms may have a greater effect

Question 4

Homeostatic control of appetite

Answer 4

• Satiety: POMC neurons in the arcuate nucleus of the hypothalamus are activated by PYY (released from intestinal L cells). GLP1 and oxyntomodulin also slows gastric emptying, increase satiety. PYY and oxyntomodulin are secreted in proportion to caloric load
• Hunger: ghrelin, NPY activation of NPY/AgRP in arcuate nucleus
• these regions can communicate with the paraventricular nucleus which comminucates with higher brain regions

Question 5

Role of the vagal nerve in appetite regulation

Answer 5

• vagus nerve responsible for gastric emptying and parasympathetic control of the gut
• VN also causes insulin, enzyme and juice release from pancreas, along with release of cholecystekinin and ghrelin (important in the cephalic phase)
• in vagotomy: may lead to increased feelings of satiety due to reduced gastric emptying. Vagus nerve isn’t needed for duodenal or ileal brakes (these are hormone controlled). May be a potential mechanism for weight loss approach (less invasive than bariatric surgery)

Question 6

Gastric phase of feeding

Answer 6

• after cephalic phase, when nutrient sensing starts and abdominal distention
• in humans, having fizzy xantham gum drink increased satiety

Question 7

The need for the cephalic phase in NGT feeding

Answer 7

• healthy volunteers develop diarrhoea within 90-120 minutes post-NGT
• BUT when give cephalic phase (i.e. sight, smell, a morsel of food), bolus feeding or SCFA this effect ceased
• there is a need for ‘priming’ of the gut to reduce caecal water secretions

Question 8

Are ultra-processed foods (UPF) to blame for the obesity crisis?

Answer 8

• with every 1% increase in UPF, there is a 0.25% increase in obesity
• also OR for obesity is similar for unprocessed foods, when volunteers go on a diet of UPF they weigh more and put on more fat due to eating more
• they also are eating faster- perhaps as needs less chewing?

Question 9

Anorexia of illness hypothesis

Answer 9

• one of the common sickness behaviours is to lose appetite and fluids when ill
• this may increase autophagy and repair: clearance of damaged cells

Question 10

Using gut hormone drugs in the treatment of obesity

Answer 10

• could address the gap between Orlistat and dietary approaches with bariatric surgery
• Semiglutide (GLP1 analog) has the capacity to slow gastric emptying and increase satiety, data shows there is a 16% weight loss on this drug over 68 weeks