Neural + hormonal mechanisms involved in the control of eating

Lashley (1938) - believed neural mechanisms involved in making decisions on when to eat. Thought must be brain mechanism involved in motivation to eat - research showed hypothalamus to play key role. Lateral hypothalamus (LH) - hunger centre (initiated eating), ventromedial hypothalamus (VMH) - satiety centre (fullness - cessation of eating).

Hypothalamus - body's control centre, plays crucial role in many bio functions eg emotions. Maintains body's homeostasis - receives messages from diff parts f body + makes appropriate responses. Became known as dual control theory (DCT), based on idea of homeostatic perception of hunger + satiety, whereby when level of glucose is low, liver sends signals to LH, creates hunger, motivates to eat. When eaten, glucose released, activates VMH, produces satiety, stops further eating.

Hypothalamus helps maintain constant internal environment (homeostasis). Which foodstuffs eaten in response to low glucose factors depends on several factors eg usual diet, culture etc. Problems w/ theory arose eg fact rats able to each satiety even if satiety centre removed + hunger centre removed - still became hungry.

Solution to inability of DPT to explain LT effects of lesions to LH abd VMH - set point theory (SPT). Suggest everyone has individual metabolic set point, certain weight body shaped towards, determined by rate calories consumed.

Set points alter depending on factors eg eating patterns + exercise. When diet, leptin levels increase -> hypothalamus triggering 'hunger pangs'. Set point for obese individuals higher than for healthy individuals, lower for underweight individuals.

Nucleus of hypothalamus role in controlling eating behaviour - diff types nerve cells, one which manufactures neuropeptide NPY, (appetite simulator). Neuropeptides minute proteins encoded by genes, work as chemical messengers b/ween neurons/fat deposits of body + brain. Fat hormone leptin neuropeptide produced from fat cells + released into blood to signal to H calorific storage too high - associated w/ decreasing appetite. H detects drop in leptin, believes lack of calories, generates sensation of hunger, stimulates to eat more.

NPY neurons also activated by ghrelin - hormone secreted from lining of stomach, concentration in blood falls after each meal, rises progressively until next. Action of G upon H to increase sensation of hunger -> stimulate eating. May be L helps regulate G levels.

Coleman (1973) - Parabiois, technique that unites separate animals physiologically, used in order to pair up diff genetic strains of mice + surgical joining of 2 mice. 2 forms of mice used - 'ob' mice + 'db' mice.

When 'ob' mice paired w/ normal, obese lost weight. When 'db' mice paired w/ normal, normal starved to death after 1 week, blood-sugar concentrations declined to starvation levels. 'Db' paired w/ 'ob', 'ob' lost weight - blood-sugar starvation. Survival - 20-30 days.

'Db' produce blood-borne satiety factor so powerful, induces normal mice to starve. 'Ob' mice recognise + respond to circulating factor provided by db/db partners. Db have circulating factor that stops eating, in ob + normal, db resistant. When w/ normal, ob get circulating factor from N, lose weight - decrease in hunger. But, CF in insufficient amounts to be lethal. Db circulate factor that satiety centre in VMH doesn't response to, ob have normal satiety, but produce inadequate levels of satiety signal. Circulating satiety factor (leptin) blood-borne hormone, function in neg feedback loop to control fat tissue by modulating appetite. L produced in fatty tissue, w/ L receptor expressed mainly in H.

Supports lipostatic theory, displays complexity of mechanisms involved in regulation of eating.

Confirms key role of leptin. 

Conducted on enimals - ethical constraints. Justified by hoping would lead to effective treatments for diabetes.

Animals - generalisation to humans.

Hetherington + Ranson (1940) found lesions to VMH -> hyperphagia + weight gain. Anad + Brobeck (1951) found lesions to LH -> aphagia + weight loss. Supports DCT.

Stellar (1954) found stimulating VMH decreased eating, but when lesioned increased eating, while LH when stimulated + lesioned produced opp effects. Indicates (as predicted by DCT) - 2 brain areas are feeding + satiety centres.

Powley + Keesey (1970) found rats that lost weight through starvation + had lesions made to their LH didn't lose more weight, supports as shows rats had slimmed to new set point before lesions created.

Perceiving LH as 'feeding centre' - oversimplified, as poss to recover from LH lesions, which also produce disruptions in aggression levels, sexual behaviour etc. Lesions to NST can on own produce aphagia + adipsia.

Most research done on animals, can't generalise to humans. 

Baicy et al (2007) found leptin binds to NPY neurons in nucleus brain area, decreases activity of neurons, signals to H to produce feeling of satiety. Illustrates key role L plays in controlling eating.

Shiiya et al (2002) found G levels in blood plasma lower in obese participants + higher in AN participants than normal. G levels increased under conditions of low energy balance + decreased under conditions of high energy balance, supports idea of G being involved in stimulation of appetite + feeding.

Identifying L as important factor in control of eating brought hopes that L therapy could be developed to treat obesity. But, L injections, not proven to be universally effective treatment. R's believe need to identify mechanisms at molecular levels L works at if therapy to be of use. 

Mechanisms not fully understood. Eg not clear how G + L reach targets in brain. Degree to which L + G working independently/ in conjunction also not understood.