The sand-rat (Psammomys obesus) is an animal model for the study of human
maturity onset diabetes which appears to be controlled by caloric intake. In the present investigations, these animals have been studied in relation to the influence of low- and high-energy diets on
body weight, plasma
insulin and
blood glucose levels, and on insulin secretion from the perfused pancreas and the secretion of
corticotropin-like intermediate lobe peptide (CLIP, ACTH18-39) and the
insulin secretagogue beta-cell-tropin (beta-CT, ACTH22-39) from the pituitary neurointermediate lobe. The sand-rats maintained on the high-energy diet all became obese. Insulin secretion from the perfused pancreas of the obese sand-rat in the presence of 5.6 mM
glucose was significantly higher than in the lean controls maintained on low-energy diets. Increasing the
glucose concentration to 16.7 mM only produced a small stimulation of insulin secretion in the obese animals, and the difference between the two groups was not significant. Stimulation of insulin secretion by beta-CT was variable, but the obese animals appeared to be more responsive. Pituitary neurointermediate lobes were incubated for 4 h to measure the secretion of the
ACTH related
peptide. These were separated by gel filtration and the concentrations measured by radioimmunoassay with a
CLIP antiserum and a
CLIP standard. In all experiments beta-CT was 4-6 per cent of the total
CLIP immunoreactive material. In these experiments the obese animals maintained on a high-energy diet were divided into two groups, those with plasma
insulin levels less than 500 mu u/ml and those with
insulin levels greater than 500 mu u/ml. The latter group had a significantly higher
blood glucose level, presumably due to the
insulin resistance resulting from the severe hyperinsulinaemia. It was also observed that
CLIP-IRM and beta-CT secretion was lower in this group than in the animals maintained on low-energy diets or those on high-energy diets with moderate hyperinsulinaemia. This suggests a possible feedback inhibition by
insulin on the secretion of beta-CT.