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Logical design of oral glucose ingestion pattern minimizing blood glucose in humans.

ABSTRACT: Excessive increase in blood glucose level after eating increases the risk of macroangiopathy, and a method for not increasing the postprandial blood glucose level is desired. However, a logical design method of the dietary ingestion pattern controlling the postprandial blood glucose level has not yet been established. We constructed a mathematical model of blood glucose control by oral glucose ingestion in three healthy human subjects, and predicted that intermittent ingestion 30?min apart was the optimal glucose ingestion patterns that minimized the peak value of blood glucose level. We confirmed with subjects that this intermittent pattern consistently decreased the peak value of blood glucose level. We also predicted insulin minimization pattern, and found that the intermittent ingestion 30?min apart was optimal, which is similar to that of glucose minimization pattern. Taken together, these results suggest that the glucose minimization is achieved by suppressing the peak value of insulin concentration, rather than by enhancing insulin concentration. This approach could be applied to design optimal dietary ingestion patterns.

SUBMITTER: Fujii M

PROVIDER: S-EPMC6718521 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Logical design of oral glucose ingestion pattern minimizing blood glucose in humans.

Fujii Masashi M Murakami Yohei Y Karasawa Yasuaki Y Sumitomo Yohei Y Fujita Suguru S Koyama Masanori M Uda Shinsuke S Kubota Hiroyuki H Inoue Hiroshi H Konishi Katsumi K Oba Shigeyuki S Ishii Shin S Kuroda Shinya S

NPJ systems biology and applications 20190902

Excessive increase in blood glucose level after eating increases the risk of macroangiopathy, and a method for not increasing the postprandial blood glucose level is desired. However, a logical design method of the dietary ingestion pattern controlling the postprandial blood glucose level has not yet been established. We constructed a mathematical model of blood glucose control by oral glucose ingestion in three healthy human subjects, and predicted that intermittent ingestion 30 min apart was t ...[more]

PMID: 31508240

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Project description:A central debate in the exercise sciences is the cause of the fatigue that develops especially during high intensity exercise of short duration. The most popular theory holds that this form of exercise is limited by a peripherally based, metabolite induced failure of skeletal muscle contractile function, independent of reduced muscle activation by the central nervous system; so-called peripheral fatigue. This theory arose originally from studies undertaken by Nobel Laureate Sir Archibald Vivian Hill and colleagues in Manchester, UK in the 1920s. In turn, their interpretations were crucially influenced by the earlier 1907 findings of Sir Frederick Gowland Hopkins, Nobel Laureate for his discovery of the vitamins, and Walter Morley Fletcher. The original model of Hill and his colleagues proposed that performance during exercise of high intensity was limited by skeletal muscle anaerobiosis that developed as the result of a limiting skeletal muscle blood flow, following the onset of myocardial ischaemia. Such skeletal muscle anaerobiosis ultimately prevented the neutralization of the lactic acid that, Hill believed, initiated muscle contraction. The resulting lactic acid accumulation impaired skeletal muscle relaxation, causing the (involuntary) termination of exercise. The evolutionary progression of this model led to the "catastrophe theory" of Richard Edwards, which posits that exercise terminates when the physiological and biochemical limits of the body are exceeded, causing a catastrophic failure of intracellular homeostasis. This paper addresses six hallmark physiological requirements that must be correct if Hill's cardiovascular/ anaerobic/catastrophic model is the exclusive explanation for the fatigue that develops during maximum exercise to exhaustion. This leads to a review of the evidence supporting other, related "catastrophe" models that have been developed to explain fatigue during exercise of lower intensities and longer durations. It is concluded that there is little published evidence supporting the theory that fatigue occurs only after physiological homeostasis fails according to the prediction of these catastrophe models. Rather, it is proposed that fatigue in any form of exercise may form part of a regulated, anticipatory response co-ordinated in the subconscious brain. The ultimate goal of this regulation is to preserve homeostasis in all physiological systems during exercise, regardless of intensity or duration or the environmental conditions in which it is undertaken.

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Logical design of oral glucose ingestion pattern minimizing blood glucose in humans.

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Logical design of oral glucose ingestion pattern minimizing blood glucose in humans.

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