The Influence of Obesity on Serum Insulin Measured by Three Methods

Abstract

It has been suggested that there is close relationship between obese subjects and maturity onset diabetes from William's and Ogilvie's reports.
In the present study, this relationship between obesity and diabetes mellitus examined by determining the plasma insulin responsiveness of normal weight and obese, nondiabetic and diabetic subject to oral glucose loading. These plasma insulin were measured by three methods : the value of the rat diaphragm assay = DILA, the value of the rat epididymal fat pad assay = FILA, and the value of the radio-immunoassay = IRI.
By comparison among these three assayed values, the investigation was undertaken to study about the effect of obesity on insulin activity.
In comparison with normal subjects, non-obese diabetics in fasting and after oral glucose loading, exhibited the low DILA, elevated FILA, slightly elevated IRI with delayed peak. It was considered that this pattern of assayed values by three methods resulted from diabetes mellitus and represented a diabetic changes. Obese diabetic subjects more definitely manifested these diabetic changes on the insulin responsiveness to glucose loading by three methods.
Despite the normal glucose tolerance, obese subjects had also diabetic changes on the insulin responsiveness by three methods.
This investigation had shown that the decrease in plasma NEFA following glucose administration was slower and smaller in obese and obese diabetic subjects than in normal subjects.
From these findings, it supposed that the high plasma NEFA levels following glucose loading gave the diabetic pattern on the insulin responsiveness by three methods.
Then for the purpose of observing what effects were made by the high plasma NEFA on the insulin activity by three methods, the rabbits fed high fat diet for fifty to seventy days. It noted that the high fat diet fed rabbit became obesity and had fasting high plasma NEFA concentration and disturbing the decrease of plasma NEFA following glucose loading.
The plasma of rabbit which had high NEFA concentration showed the same diabetic pattern of insulin activity by three assay methods as that of the obese human subjects.
To study the effect of NEFA on the biological insulin activity to muscle and adipose tissue in vitro, the elevated plasma NEFA were obtained from the obese rabbits following intravenous heparin injection after seventy days fed high fat diet. This elevated plasma NEFA exhibited the pattern of insulin activity that DILA was low, FILA was elevated and IRI was unchangeable.
From these findings, it became evident that the high NEFA concentration produced the diabetic insulin responsiveness (i.e. low DILA, elevated FILA and IRI) on plasma of the obese subjects.
Generally speaking, obesity had a normal glucose tolerance, however
1) obesity showed diabetic changes on the insulin responsiveness by three insulin assay methods,
2) obesity exhibited abnormal fat metabolism with fasting high NEFA levels and disturbing of decrease in plasma NEFA following glucose administration.
3) obesity had a insulin resistance to muscle glucose metabolism (DILA↓) 4) obesity demanded the increased insulin secretion from pancreatic β-cells (IRI↑).
From these points obesity might become the diabetic stress and might caused one who had a family history of diabetes mellitus and fragile pancreatic β-cell, diabetes mellitus.