Obesity and diabetes are two of the most prevalent health conditions in industrial nations. Recent studies suggest that a gut derived peptide, gastric inhibitory polypeptide (GIP), may be involved in the pathogenesis of type 2 diabetes and obesity induced by overnutrition.^1,2 The “thrifty genotype” hypothesis suggests that those who are prone to obesity have been favoured by natural selection in the past because they possess genes that promote the efficient storage of ingested food as body fat for use in periods of undernutrition. However, with the sedentary lifestyle and year round plentiful food supply of modern society, the tendency is to accumulate fat. Miyawaki et al have shown that GIP directly links overnutrition to obesity and may be a potential target for antiobesity drugs.²

GIP was initially discovered and named for its gastric inhibitory properties. In 1886, Ewald and Boas showed that olive oil mixed with a meal inhibited both gastric emptying and acid secretion. In 1930 Kosaka and Lim proposed that this mixture liberated a chemical from the small intestine and went on to show that gastric acid secretion and gastric emptying could be inhibited by intravenously infused extracts of intestinal mucosa.³ They named the chemical “enterogastrone”. Later, this factor was isolated and found to be localised to the duodenum and jejunum in specific endocrine cells …