| Project/Area Number |
09470111
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Public health/Health science
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| Research Institution | Yamanashi Medical University |
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Principal Investigator |
SATO Akio Yamanashi Medical University, Department of Environmental Health, Professor, 医学部, 教授 (40020747)
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| Co-Investigator(Kenkyū-buntansha) |
WANG Pei-Yu Yamanashi Medical University, Department of Environmental Health, Assistant Professor, 医学部, 助手 (10283201)
KANEKO Takashi Yamanashi Medical University, Department of Environmental Health, Associate Professor, 医学部, 助教授 (10233876)
TAWATA Masto Yamanashi Medical University, Third Department of Internal Medicine, Associate Professor, 医学部, 助教授 (40109187)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥5,300,000 (Direct Cost: ¥5,300,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥3,900,000 (Direct Cost: ¥3,900,000)
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| Keywords | Diabetes mellitus / Low-carbohydrate diet / High-carbohydrate diet / Glucose tolerance / Insulin secretion / Insulin sensitivity / Free fatty acids / Randle effect / 高脂質食 / 75g oral glucose tolerance test / 糖質 |
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| Research Abstract |
1) Our research demonstrated that a high-fat/low-carbohydrate diet before an oral glucose diet impairs glucose tolerance both in humans and rats. In order to determine which nutrient is responsible for the glucose intolerance caused by a low-carbohydrate/low-fat diet, we assessed the effect of overnight fasting on glucose tolerance. The working hypothesis was that if fasting impairs glucose tolerance, the decreased component (carbohydrate) would be more responsible than the increased component (fat) for the impairment of glucose tolerance caused by a high-fat/low-carbohydrate diet. The degree of glucose tolerance impairment by a low-carbohydrate/high-fat diet was almost the same as that resulting from overnight fasting. This finding establishes that the decreased intake of carbohydrate is more responsible than the increased intake of fat for the impairment of glucose tolerance that is caused by a high-fat/low-carbohydrate diet.
2) The impairment of glucose tolerance after restricted car
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bohydrate intake was invariably accompanied by an increase in free fatty acid (FFA) level in the fasting plasma. With a perifusion system including pancreatic islets of Langerhans from rats, we demonstrated that a low-carbohydrate diet inhibits the secretion of insulin by β-cells in the islets in response to glucose and that FFA infusion inhibits the insulin secretion of Langerhans islets from normally fed rats. This suggests that the impairment is associated with the Randle effect, which is the activation of the glucose-free fatty acid cycle.
3) In an ongoing clinical trial, where 7 diabetic patients were placed on a high-carbohydrate diet (80% carbohydrate, 5% fat and 15% protein) or a control diet (60% carbohydrate, 25% fat and 15% protein) for one week each in a crossover design, we confirmed that the high-carbohydrate diet improves the glucose tolerance in mildly diabetic patients.
4. From these observations, we conclude that the long-term ingestion of a low-carbohydrate diet is the factor determining the onset of diabetes mellitus in individuals with a predisposition to the disease. Less
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