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The putative satiety hormone PYY is raised in cardiac cachexia associated with primary pulmonary hypertension
  1. C W le Roux1,
  2. M A Ghatei1,
  3. J S R Gibbs2,
  4. S R Bloom1
  1. 1Department of Metabolic Medicine, Hammersmith Hospital, Imperial College, London, UK
  2. 2Department of Cardiology, Hammersmith Hospital
  1. Correspondence to:
    Professor Stephen R Bloom
    Department of Metabolic Medicine, Hammersmith Hospital Campus, Imperial College, London W12 0NN, UK;

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Weight loss greater than 6% independently correlates with reduced survival in patients with congestive heart failure (CHF).1 Cardiac cachexia is a gradual and graded process, with wasting affecting muscle, bone, adipose tissue and the heart.1 Reduced appetite has been proposed as a important factor for weight loss caused by cardiac cachexia.2

The mechanism of cardiac cachexia remains largely unclear. Gastric myoneural inhibition and gastrointestinal hypomotility with delayed gastric emptying is commonly observed, and gut hormones may also play a role, because the anorexia is often characterised by a premature feeling of fullness and loss of hunger.2 The gut hormone ghrelin stimulates hunger, increases food consumption. and was previously shown to be raised in patients with cardiac cachexia and CHF.3 Ghrelin is produced from the stomach and usually rises in anticipation of a meal and then falls after the ingestion of nutrients.

The gut hormone PYY3–36, acting as a terminator of hunger, is produced by the L cells in the distal gastrointestinal tract; it reduces appetite and 24 hour food intake by binding to the neuropeptide Y Y2 receptor in the hypothalamic arcuate nucleus.4

Severe pulmonary hypertension results in a low cardiac output and neurohumoral activation. Patients frequently report loss of appetite and weight, and since it occurs in a young population …

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