We previously proposed that oil heated with gluten was suitable for use as a safe oil for weightloss dieting. In the present paper, the properties of the oil were improved, and the weight-loss effect was compared with that of heated oil. Fresh oil was heated for 10 h at 180 with or without gluten and filtered using filter paper. A powdered diet (AIN93G; no fat) was mixed with 7 wt% of fresh oil (control) or filtrates of the heated oils described above, and the mixture was fed to male Wistar rats for 12 weeks. The gluten and heated oil groups showed no gross symptoms attributable to the experimental oils but had a slowed body weight increase; a significant difference was found in weight on and after 21 weeks of age as compared to rats consuming the control diet, and fecal excretion was increased as compared to the control group. Serum levels of triacylglycerol, phospholipids, cholesterol, and glucose of the gluten and heated oil groups were significantly lower than those of the control group. High aspartate aminotransferase (AST) levels occurred more frequently in the heated oil group than the gluten group. The number of rats with dark red patches on the surface of the liver, which are indicative of liver damage, was higher in the heated oil group. In conclusion, the weight-reducing effect of the oil heated with gluten was confirmed and improved by removing traces of heated gluten from the oil.

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Heated frying oils with different chemical properties in terms of AV (acid value), POV (peroxide value), COV (carbonyl value), and contents of polar compounds (PC) and triacylglycerol (TG), as well as color and odor, were obtained. Male Wistar rats were fed ad libitum for 12 weeks a powdered diet (AIN93G; no fat) containing 7 wt% of fresh oil (control) or one of the frying oils described above. The rats were subjected to anthropometric measurements, hematological analyses, and observations of the liver and kidneys. All of the rats grew well, and no gross symptoms attributable to the experimental oils were observed. However, the rats fed a diet containing the heated oil developed apparent liver damage to different degrees regardless of the chemical properties of the ingested oils. Thus, it was suggested that the chemical properties evaluated here had little to do with the cytotoxicity of heated oil, although the properties express quality of oil. Volatile compounds seem to be major candidates for the toxic agents in heated oil because oils with rancid and deteriorated odor show strong toxicity.

The insulinogenic index was investigated as a possible means for distinguishing between prirnary and secondary diabetes. This index is defined as the ratio.1 IRI/.1 glucose, where IRI is the plasma immunoreactive insulin level determined after the administration of a prescribed oral glucose load. The insulinogenic index values as measured 30 minutes after a 50 grn glucose load were as follows in normal subjects and those with primary diabetes: normal, 1.43 ± 0.17 (Mean ± SEM); mild diabetes, 0.39 ± 0.08; and moderate diabetes, 0.08 ± 0.02. In certain diseases associated with abnormal glucose tolerance, the values were as folIows; pheochromocytoma, 0.18 ± 0.12, acromegaly associated with severe glucose intolerance, 0.16 ± 0.08; acromegaly associated with mild glucose intolerance, 0.54 ± 0.20; and liver cirrhosis, 0.59 ± 0.10. These va lues were not significantly different from those in primary diabetes. On the other hand, in other diseases associated with abnormal glucose tolerance a marked difference was noted as folIows: hyperthyroidism, 1.01 ± 0.20; Cushing's syndrome, 1.37 ± 0.42; steroid diabetes, 1.22 ± 0.32; acute hepatitis, 1.16 ± 0.31; and chronic hepatitis, 1.48 ± 0.34. It was concluded, therefore, that in the latter cases, the insulinogenie index is a supplementary tool for distinguishing between primary and secondary diabetes.

Frying oil in use of cooking may contain acrylamide formed from frying foodstuffs. We have reported that administration of a diet containing 7% practically used frying oil for 12 weeks damaged liver and kidneys severely in Wistar rats. Then, male Wistar rats were fed ad libitum for 12 weeks a powdered diet (AIN93G; no fat) containing 7 wt% of fresh oil (control group) or frying oil heated with Asn + glucose for 20 h at 180 under a nitrogen flow in order to form acrylamide under the least thermal deterioration (experimental group). The rats were subjected to anthropometric measurements, hematological analyses, and observations of the liver and kidneys. All of the rats grew well, and no gross symptoms attributable to the experimental oil were observed. But the experimental rats had significantly low insulin and triacylglycerol levels. The liver and kidneys from the experimental rats had damages, but the degree of the histological changes looked lighter than that of the rats fed practically used frying oil described above. The serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were also not much increased. Thus, it was suggested that continuous intake of trace acrylamide induced characteristically low serum insulin level and that the effects of the used frying oil on the liver and kidneys were hardly attributable to acrylamide possibly contained therein.