This case report addresses the problem of underreporting negative results and adverse side effects in animal testing. We present our findings regarding a hyperphagic mouse model associated with unforeseen high mortality. The results outline the necessity of reporting detailed information in the literature to avoid duplication. Obese mouse models are essential in the study of
obesity,
metabolic syndrome and
diabetes mellitus. An experimental model of
obesity can be induced by the administration of
gold thioglucose (GTG). After transcending the blood-brain barrier, the GTG molecule interacts with regions of the ventromedial hypothalamus, thereby primarily targeting
glucose-sensitive neurons. When these neurons are impaired, mice become insensitive to the satiety effects of
glucose and develop
hyperphagia. In a pilot study for optimising dosage and
body weight development, C57BL/6 mice were treated with GTG (0.5 mg/g
body weight) or saline, respectively. Animals were provided a physiological amount of standard diet (5 g per animal) for the first 24 hours
after treatment to prevent
gastric dilatation. Within 24 hours after GTG injection, all GTG-treated animals died of gastric overload and subsequent circulatory
shock. Animals developed severe attacks of
hyperphagia, and as the amount of provided chow was restricted, mice exhibited unforeseen
pica and ingested bedding material. These observations strongly suggest that restricted feeding is contraindicated concerning GTG application. Presumably, the impulse of excessive food intake was a strong driving force. Therefore, the actual degree of suffering in the GTG-induced model of
hyperphagia should be revised from moderate to severe.