Neural and hormonal mechanisms involved in the control of eating…

The idea

Eating is homeostatic: the body defends a fairly stable store of energy, and the hypothalamus is where the signals are read. The classic dual-centre model makes the lateral hypothalamus the on switch and the ventromedial hypothalamus the off switch - lesion the ventromedial area in a rat and it overeats into obesity, lesion the lateral area and it starves. Hormones carry the news. Ghrelin is released by the empty stomach lining, acts on neuropeptide Y cells in the arcuate nucleus, and rises sharply in the minutes before a meal then falls once food arrives, as Cummings showed with repeated blood sampling. Leptin is secreted by fat cells in proportion to fat stored and tells the hypothalamus there is enough; mice bred without it eat until grossly obese.

What earns the marks

• AO1: establish homeostasis and the hypothalamus as the control centre before naming any structure.
• AO1: the lateral hypothalamus initiates feeding and the ventromedial hypothalamus inhibits it, evidenced by aphagia and hyperphagia after lesioning in rats.
• AO1: ghrelin is a short-term hunger hormone from the stomach lining acting via the arcuate nucleus, rising before meals and falling afterwards.
• AO1: leptin is a long-term satiety hormone from adipose tissue signalling the size of fat stores to the hypothalamus.
• AO3: the dual-centre model is oversimplified - ventromedial lesions also damage the paraventricular nucleus and fibres of passage, so the overeating may not be caused by that nucleus at all.
• AO3: biologically reductionist - it cannot explain eating for pleasure, boredom or social occasion, when people eat although satiety signals say stop.
• AO3: application - leptin replacement cures congenital leptin deficiency but fails in common obesity, where leptin is already high and receptors are insensitive, which supports leptin resistance.

Common mistakes and how to put them right

• Swapping the two hypothalamic centres, or writing that the lateral hypothalamus stops eating.

• Saying ghrelin and leptin 'cause hunger and fullness' without naming where each is made and where it acts.

• Reporting rat lesion findings as though they were human evidence, with no comment on extrapolation.

• Describing leptin as a meal-to-meal signal.

  Put it right: It tracks stored fat over long periods, which is why it is the long-term signal.

Exam tips

• A frequent stem describes someone who has lost weight and cannot stop feeling hungry; apply falling leptin and rising ghrelin rather than discussing motivation.
• Name each hormone's source, target and direction of effect in one sentence apiece - that structure banks the knowledge marks quickly and leaves room for evaluation.
• 'Neural and hormonal' means both; an answer that is all hypothalamus and no hormones is only half a response.