THE GROWTH HORMONE DEPENDENT INCORPORATION OF SULPHATE INTO THE COSTAL CARTILAGE OF OBESE-HYPERGLYCAEMIC MICE OF DIFFERENT AGES

ABSTRACT The in vivo incorporation of sulphate into costal cartilage was measured in both lean and obese-hyperglycaemic mice of different ages. In 2–10 months old obese mice the sulphate incorporation was found to be markedly increased as compared with lean controls. After a peak value at the age of 4–5 months there was a gradual fall in the sulphation activity. In the lean litter mates a decrease in the sulphation activity was already observed after the first month of life. These findings are considered against the background of the metabolic changes characteristic of the syndrome and the current concepts of the actions of insulin and growth hormone. A possible role of growth hormone in the aetiology of the obese-hyperglycaemic syndrome is discussed.

ENDOCRINE ACTIVITY OF THE TESTIS IN OBESE-HYPERGLYCAEMIC MICE

ABSTRACT The endocrine activity of the testis in relation to hyperglycaemia and obesity was investigated by using hereditary obese-hyperglycaemic mice (AO-mice). The AO-mice had smaller testes and hypoplastic seminal vesicles. The occurrence of atrophic interstitial Leydig cells was a conspicuous feature in these animals. However, a positive reaction for steroid 3β-ol dehydrogenase was also obtained in these interstitial cells. The Leydig cells of the AO-mice represented an endocrine organ with a total volume of only half that in the normal litter mates (AN-mice). Although there was a slight decrease in the number of spermatozoa, all stages of a normal spermatogenesis were identified. The signs of reduced endocrine activity of the testis in the obese-hyperglycaemic syndrome are discussed in the light of previous data on reproduction anomalies in diabetes and obesity.

THE METABOLISM OF VARIOUSLY LABELLED GLUCOSE IN FATTY LIVERS FROM MICE WITH CONGENITAL HYPERGLYCAEMIA AND OBESITAS

ABSTRACT The in vitro utilization in liver slices of 14C-glucose, labelled in the C1 or C6 positions, was studied in mice of the American variety of the hereditary obese-hyperglycaemic syndrome. Those obese-hyperglycaemic animals (AO-mice), which exhibited a macroscopically obvious fatty liver (liver fat content 32.6 ± 2.7 %), were compared with lean normoglycaemic litter mates (AN-mice) (liver fat content 15.7 ± 0.9%). The incorporation of glucose into all the fractions of the livers analysed tended to be lower in the AO-mice. Thus after incubation in 14C6-glucose the CO2 was significantly lower (P < 0.001), while for lipids, the corresponding difference was only probable (P < 0.05). For the insoluble residue after extraction with trichloracetic acid and alcohol-ether the difference was significant at the 1 % level for 14C1-glucose and at the 0.1 % level for 14C6-glucose. Only with CO2 was there a difference between AO- and AN-mice (lower in the AO-mice; significant at the 5 % level) for the ratios of the radioactivities derived from the glucose labelled in the C6 and C1 positions.

THE OCCURRENCE OF ARGYROPHIL CELLS IN THE ISLETS OF LANGERHANS OF AMERICAN OBESE-HYPERGLYCAEMIC MICE

ABSTRACT Distinct argyrophil islet cells were found in thin paraffin sections of pancreas both from normal mice and from those with the American variety of the obese-hyperglycaemic syndrome. In the obese animals the relative proportion of argyrophil cells was only about half as great as in their thin litter mates. In both groups the argyrophil cells were mainly localized to the periphery in the larger islets. The results are discussed in the light of the hypothesis put forward by Mayer et al. (1953), that hyperglycaemia in the obese strain results from excessive secretion of glucagon from the A cells.