Eating Flashcards
Homeostasis and Energy Balance
Food provides energy for synthesis and repair of tissue
Negative feedback system satisfies hunger Drive
Behaviour is a major role in weight gain (low activity, and over consuming)
Food regulation is complicated- need a balanced diet and nutrients
Appetite = st anticipation, early sensing systems and lt feedback
Biological control
Digestion
Lipids, amino acids, glucose are stored as fat, glycogen and protein
Insulin (pancreas) promotes use of glucose and the conversion of bloodborne fuel to forms that can be stored (glycogen in liver)
Fasting = low insulin, glucose saved for brain (low insulin = diabetes)
Mayer, 1995
Glucostatic theory
St regulation that states eating is regulated by a system to make sure glucose is at a set point
Low levels - hunger
High level - satiety
Lipisatic theory
Same for fat and lt regulation
Too simplistic
Not driven to eat due to deficit but anticipation of deficit
Pleasure and reward is critical
Episodic appetite regulation
Satiety is an end state of satisfaction, the drive to consume is suppressed
Satiation - processes that generate neg feedback = termination of eating
Blundell (1991) satiety cascade allows conceptualisation of processes (1984)
EAR
Starting a meal
Wilkinson et al (2012)
We try a lot of food, experience allows estimation of satiating potential, expected satiation determines energy intake
Rozin et al (1998)
Patient RH had bilateral damage to temporal lobe = amnesia
Could eat 3 meals, refused 4th due to stomach feeling tight - couldn’t remember he’d eaten - memory major in deciding what to eat
Higgs (2005)
Large number of studies of neurologically intact pps showed memory of recent eating influenced eating later
Role of gherlin
Peptide hormone which increases eating, acts on NTS and AP complex in the brain which effects need and desire as well as producing the cephalic salivary response (anticipation of food prepares he body for digestion)
Sensation of hunger from low glucose and leptin lead to eating, pleasure = further consumption
EAR
Post-ingestive processes
Gastric distension
Potent satiety signal, terminates intake. Intake after this has short lived impact on subsequent energy intake
Stretch receptors signal distension up the vagal nerve to the hypothalamus
Geliebter (1998)
Food intake was significantly reduced (p< 0.01) by a ballon up to 400ml. Stretch receptors via the vagus nerve to hypothalamus
Distension contributes partly to termination of intake
Gut hormones
Carbs suppress gherlin (hunger hormone) = satiety
Protein and fat = CCK which acts as the duodenal brake and travels up vagal nerve to hypothalamus- satiety!
Lleal brake works in same way but GLP-1 to fat
Lewis (2015)
Gut hormone response differs for portion sizes (released to detecting nutrients) GLP-1 and PYY blunted by small portion - satiety not signalled
EAR
Post-absorptive processes
Nutrients undergone digestion and pass through the intestinal wall to blood - these are metabolised in tissues or organs or enter the brain directly
Key glucose and fat sensing mechanisms exist in the liver - absorbed nutrients go here and this sends signals and. Glucose levels to the hypothalamus
Glucose responsive neurons in the brain adjust engery requirements
Tonic appetite regulation
Body stores energy as fat and these form layers called adipose tissue around internal organs
Leptin (protein produced by adipose tissue) acts in a negative feedback system to reduce food intake and acts as a natural adiposity signal
Found in a strain of mice, which when injected with blood of Lean mice lost weight. Didn’t have leptin, couldn’t produce it due to mutation
Farooqui (2001)
Congenital leptin deficiency in humans - children excessive weight gain, huge appetite. Administration of leptin reverses condition
Most obese people don’t have this, in fact they have excess leptin - insensitive or resistant?
CNS control of eating
Brain integrates signals (gut- distension, chemoreceptors, liver - metabolic receptors) via vagal nerve as well as detecting nutrients in the periphery and substances that cross blood brain barrier
Nuclei in the hypothalamus (NTS AND AP) receive and relay signals to key areas in the hypothalamus and are identified with appetite
ARC, VMH, LH AND PVN are key sites in the hypothalamus
ARC contain neurones that are oxexigentic - stimulate intake (NPY and AGRP) and some that are anorexigenic (POMC, CART)
CNS - serotonin
Short term regulation
Fat and carbs trigger peripheral signals - release CCK which activates the serotonin system
Increased S = reduces intake and weight in rodents and humans
Drugs that stimulate serotonin and injecting S into the PVN = inhibits food intake
Rodents who’s serotonin doesn’t function properly over eat
Halford (2005)
Serotonin drugs that increase S are successful in treating obesity
Serotonin acts on POMC nurones which are anorexgenic so inhabit intake
Act on inhibitory receptors on NPY neurons which inhibit normal orexigentic effect
Obesity
Health survey England (1993-2012)
Obesity has increased - higher in women
Obesegentic environment - easy access, energy dense foods
Behaviour is determined by culture and own concerns (want to be healthy, want to be full)
Price - healthy food ££
Portion sizes are larger
Social - Christmas birthdays
A variety of food - want to try it all
Obese people tend to demonstrate weaker regulatory control. Overwhelmed by cues to over consume.
Evidence that obese people eat quicker and fail to develop satiety during a meal
However is this a consequence of body fat or a cause??
Lean and Malkova (2016)
Meta analysis - obese people GLP-1 and PYY levels are reduced (satiety signals)
Lower self control and greater response to cues, addicted to food
