Week 7-Appetite Flashcards
What is the Model of Appetite Control adapted from Higgs et al., 2017)
The environment + signals from gastro-intestinal (GI) tract relating to ingestion of food affects:
-Cognitive control (Prefrontal cortex, Hippocampus)
-Homeostasis (Hypothalamus)
-Reward - liking and wanting (Dopamine and opioid system)
Define Homeostasis
The ability to maintain a relatively stable internal state
Define metabolism
The process by which your body converts what you eat and drink into energy
Define Hunger
The drive to consume, elicits a behavioural response (eating) to a biological need
Define Satiation
Processes during a meal that generate negative feedback leading to its termination (within-meal inhibition)
Define Satiety
The end state of satisfaction. The further suppression of the drive to consume and post-meal intake (between-meal inhibition)
Define peripheral appetite control
Includes motor functions of the stomach (e.g., rate of emptying) and release of peptides and hormones from the gut and fat tissue
Define Central appetite control
Brain and central nervous system
What are the Negative feedback systems and Energy Balance?
NF: Feedback from changes in one direction elicit compensatory changes in the opposite direction. The act to maintain homeostasis - a stable environment.
EB: Energy Intake (EI) minus energy expenditure (EE).
In an ideal homeostatic energy system an organisms energy intake should equal energy expenditure.
What is the Homeostatic control of energy?
-A biological need to maintain the body’s energy stores
Depletion of energy stores –> drive to eat
Repletion of energy stores –> negative feedback to terminate eating
-Co-ordinated by the hypothalamus
-Harrold et al. (2012) + Berthoud et al. (2017)
How is the homeostatic control of energy asymmetric?
-Defends well against energy deficit. However defence against energy excess is weaker
->More sensitive to under-eating than over-eating
->We can gain weight more easily than losing weight
-“Eat more” command is dominant over the “Stop eating” command
-Harrold et al. (2012) + Berthoud (2004)
What hormones starts a meal?
Ghrelin: A peptide hormone released by the stomach
-High conc. during breakfast, lunch and dinner then massive drop but levels off after 8pm
What ends a meal?
Gastric Distension which is a potent satiety signal that terminates intake and promotes initial post-meal satiety
-Stretch-receptors signal gastric distension
What is Duodenal’s brake?
CCK’s (Cholecystokinin) response to fat in the duodenum
Decreases the rate of gastric emptying
Satiation and early satiety
What is Ileal Brake?
Occurs further down the small intestine than Duodenal Brake
GLP-1 (Glucagon-like-peptide-1)
Post-meal satiation and reduced hunger at the next meal
What is leptin?
-Plays a long term role in the controlling of appetite and is produced by the adipose tissue (the body’s fat stores) when full
-It results in reduced food intake
-It’s a long term (“tonic”) signal
-Mice with genetic obesity (ob/ob) cannot produce leptin because they are born without the required gene code
What evidence is there that people with obesity have a weaker regulatory control?
-Weaker gastric distension (enlargement of stomach to signal satiety) (Geliebter, 1988)
-Blunted satiety hormone response to eating (PYY, GLP-1) (Lean & Maklova, 2016)
-Rare cases of human obesity where leptin cannot be produced due to gene defect
-However, most people with obesity do not possess a leptin deficiency. In fact, they produce excess leptin. Is obesity therefore due to leptin insensitivity or leptin resistance?
What new drug treatment has been used to cause weight loss?
-Semaglutide aka Wegovy is a GLP-1 receptor agonist
-It works by suppressing appetite and increasing feelings of fullness
-It’s associated with sustained, clinically relevant reductions in body weight
How is the CNS involved in appetite control?
-CNS regions receive signals from the body (e.g., gut, liver)
-The receptors within the CNS can also detect circulating levels of nutrients
-Substances such as glucose can cross the blood-brain barrier
-Specific neuronal populations recognise and integrate multiple energy-relevant signals and act in a network to determine energy intake and expenditure
Which 2 Lower CNS structures are involved in appetite regulation and how?
- Vagal nerve: Afferent (inwards/towards) fibres from gastrointestinal tract and liver –> brainstem
- Brainstem (Hind Brain): Relays afferent vagal signals associated with eating to the hypothalamus
- Nucleus Tractus Solitarius - NTS
- Area Postrema - AP (adjacent to NTS)
What are the 4 key hypothalamic sites in the Higher CNS structures involved in appetite regulation? (Harrold et al., 2012)
- Arcuate Nucleus (ARC)
- Ventro-Medial Hypothalamus (VMH)
- Lateral Hypothalamus (LH)
- Paraventricular nucleus (PVN)
What does the ARC do?
-It contains functionally discrete populations of neurones:
- Orexigenic (stimulates food intake)
-Neuropeptide Y (NPY)
-Agouti-related peptide (AGRP) - Anorexigenic (inhibits food intake):
-Pro-opiomealonocortin (POMC)
-Cocaine and amphetamine-regulated transcript (CART)
-The ARC has extensive reciprocal connections with other hypothalamic regions including the PVN, VMH, and LH
-These regions receive afferent information via the NTS/AP
What Mechanisms create Satiety in the CNS?
-5-HT aka Serotonin is a key CNS satiety signal in the short-term (“episodic”) regulation of food intake
-5-HT drugs are successfully used as appetite suppressants to treat obesity
-The 5-HT drug Lorcaserin was hailed by the media as a “magic bullet” (but caution is needed as risk of heart problems)
(Harrold et al., 2012)
What reasons do we enjoy eating?
-Eating for pleasure (to feel better)
-Eating to feel better (takes something negative away)
-Cues associated with the intake of tasty food (e.g., the sight and smell of food) acquire strong motivational properties and become highly wanted
-This is because eating is highly rewarding and reinforcing