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Appetite hormones matter because body weight is regulated by a hormonal feedback loop, not by willpower alone. Leptin, released from fat tissue, and ghrelin, released from the stomach, are the two central signals. Leptin tells the brain 'stores are full, stop eating', while ghrelin tells the brain 'stores are low, start eating'. For example, imagine a patient with severe anorexia nervosa (an eating disorder with dangerously restricted food intake) and very low body fat: leptin levels fall sharply, which is part of why periods also stop (amenorrhoea). In practice, most common obesity reflects leptin resistance, not leptin deficiency, so simply giving more leptin does not reliably treat it.

Leptin is released by fat (adipose) tissue in proportion to fat stores. It acts on the arcuate nucleus, a hypothalamic region, to signal satiety (fullness) and suppress appetite. Falling leptin at very low body weight, as in anorexia nervosa or starvation, is part of the mechanism behind loss of periods (amenorrhoea) in these states. Ghrelin is released mainly by the stomach and rises before meals to drive hunger, then falls after eating, the opposite timing to leptin. PYY (peptide YY) and GLP-1 (glucagon-like peptide-1), both released from the gut after food intake, add to leptin's satiety signal. GLP-1 is also the biological basis for newer weight-loss drugs that mimic it. Take a patient about to eat lunch: ghrelin has been rising through the morning, then PYY and GLP-1 rise after the meal to end the eating episode. Most obesity reflects leptin resistance, high leptin levels the brain no longer responds to, which is why leptin replacement does not treat typical obesity.

• Leptin crosses into the brain and acts on a hypothalamic region containing the first-order neurons that sense energy stores. Which nucleus is this principal target?
• Within the hypothalamusA small brain structure that controls basic functions like hunger, temperature, sleep and hormone release.Read more →, one population of neurons powerfully drives feeding and is switched off when energy stores are plentiful. Which neurons are these?
• A long-distance runner with very low body fat stops having periods, with low luteinising hormone. Falling levels of which hormone signals the brain that energy stores are inadequate?
• Besides stimulating appetite, the stomach-derived hunger peptide has a second endocrine action reflected in its receptor's name. Which hormone does it also release?

• Leptin, released from fat tissue to signal satiety, unlike ghrelin's stomach-derived hunger signal.
• Ghrelin, rises before meals to drive hunger, whereas leptin and PYY rise with fullness.
• Leptin resistance, the mechanism in most common obesity, rather than a true leptin deficiency.
• Anorexia nervosa, low leptin from depleted fat stores drives amenorrhoea, unlike the high leptin resistance seen in obesity.

• That nucleus makes vasopressin and oxytocin rather than sensing energy stores.
• That nucleus is the master circadian clock, not an appetite sensor.
• Those neurons drive the stress hormone cascade rather than feeding.
• Those neurons govern thyroid hormone release, not appetite drive.
• Those neurons govern reproductive hormone release rather than feeding.

• Localise the clue to the relevant anatomical level, cell type, pathway or molecular process.
• Map that structure or process to its normal function.
• Predict the deficit or clinical sign produced when it is disrupted.
• Reject options that belong to a neighbouring structure, pathway or level of explanation.