AbstractThe obese hyperglycemic mouse colony was set up and established at this institution. Since the radioinununoassay of insulin was still a recent method, it was fraught with many inherent difficulties. It was thus investigated and aligned with our special requirements.
The sequential development of the inherent obese hyperglycemic syndrome has been studied in these animals by investigating the relationship between the grovth rate, blood sugar and serum insulin changes with regard to age.
A close relationship was observed in these three parameters.
There vere primarily three phases in the development of the syndrome:
(a) the dynamic phase until about week 24 characterized by an increased growth, hyperglycemia and increased serum insulin.
(b) a static phase when weight gain was minimal and the weights of the animals were stable. Hyperglycemia too was fairly stable within its own limits and serum insulin concentrations were reduced with time...
(c) this third phase was characterized by a reduction in all three parameters. However this apparent amelioration of the disease terminated in ketosis.
The results of the investigations strongly suggest that obesity is prcbably a secondary manifestation of tissue resistance to insulin. This "abnormality" is present to an exaggerated degree in the obese animals thus resulting in hyperglycemia, excessive insulin production, and accretion of adipose tissue. This state of affairs is brought to a conclusion when an insufficiency of insulin production results and the animals succumb to diabetes per se.
This tissue resistance was made even more evident during the course of studies involving primarily potassium and glucose uptake "in vivo". The investigations were carried out in animals between 16 and 20 weeks of age using the conventional glucose tolerance test under conditions of potassium surplus and deficiency. The importance of potassium was stressed in that further impairment in glucose tolerance was observed in animals maintained on a potassium deficient diet, and an improvement was apparent in animals fed on high potassium diet. This is partially explained by an increased serum insulin and therefore presumably an increased secretion of insulin. Sodium and potassium were measured in tissue, serum and urine. The obese and normal animals on the control 41B diet did not show much variation in these parameters. The glycogen content of liver and pancreas was much higher and that of muscle was much lower in the obese. The various changes of the parameters on the experimental diets have been discussed in the text.
|Date of Award||1972|
|Supervisor||A. J. Matty (Supervisor)|
- obese hyperglycemic syndrome