Basal and postprotein insulin and glucagon levels during a high and low carbohydrate intake and their relationships to plasma triglycerides > 1920-1999

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1920-1999

Basal and postprotein insulin and glucagon levels during a high and lo…

작성자 채식영양
작성일 75-01-01 00:00 | 조회 0 | 댓글 0

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Y. Fukita, AM. Gott o and RH. Unger (1975). Basal and postprotein insulin and glucagon levels during a high and low carbohydrate intake and their relationships to plasma triglycerides. Diabetes, 24(6), 552-8. https://doi.org/10.2337/diab.24.6.552

PubMed 1095439


[Abstract]
The effects of acute and chronic differences in the carbohydrate content of the diet on plasma insulin, glucagon, insulin-glucagon molar ratio (I/G), and triglycerides were studied. Acute effects were studied by varying the carbohydrate content of a single test meal, while chronic effects were determined by varying the carbohydrate content of the diet for a week. A test meal containing 0.6 gm of gelatin per kilogram plus 0.6 gm. per kilogram of glucose resulted in much higher levels of insulin and I/G (p smaller than 0.005), lower glucagon levels (p smaller than 0.05), and slightly higher triglycerides (N.S.) than did a meal of 1.2 gm, per kilogram of gelatin alone. One week of a 12 gm. carbohydrate, 2870-calorie diet lowered insulin (p smaller than 0.001), I/G (p smaller than 0.05), and triglycerides (p smaller than 0.001) and increased glucagon (N.S.), whereas a 390-gm. carbohydrate, 2784-calorie intake significantly increased insulin, I/G, and triglycerides (p smaller than 0.005) and lowered glucagon (p smaller than 0.02) within two days; even greater changes in hormones were observed on a 510-gm. carbohydrate intake. Of those patients in whom a high carbohydrate intake induced a triglyceride rise of at least 40 mg. per deciliter, a significant correlation between the change in I/G and the change in triglycerides was noted (r equals 0.85; p smaller than 0.01). The results are compatible with but do not prove the proposal that pancreatic alpha and beta cells play a mediating role in carbohydrate induction of hyperlipidemia.

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