Abstract
BackgroundFasting serum phosphorus (P) was reported to be inversely related to serum glucose and insulin, while the impact of P ingestion is not well documented. The effect of P intake with or before glucose ingestion on postprandial glucose and insulin statuses was investigated.MethodTwo cross over experiments using healthy male subjects were conducted. Experiment 1: Overnight fasted subjects (n = 7) randomly received: 500 mg of P tablets, glucose (75 g) solution with placebo or 500 mg of P tablets. Experiment 2: Overnight fasted subjects (n = 8) underwent similar procedures to those of experiment 1, except that placebo or 500 mg P tablets were given 60 min prior to glucose ingestion.ResultsIn both experiments, serum P decreased following glucose ingestion. Co-ingestion of P with glucose improved, at time 60 min, postprandial glucose (P < 0.05), insulin (P < 0.05), and insulin sensitivity index (p < 0.006), while P pre-ingestion failed to exert similar effect.ConclusionThis study suggests that postprandial glucose and insulin are affected by exogenous P supply, especially when co-ingested with glucose.
Highlights
Over the past few decades, the high prevalence of metabolic syndrome has become a worldwide phenomenon, associated with an increased risk and prevalence of type 2 diabetes mellitus [1]
The aim of this study was to investigate the effect of exogenous P on postprandial glucose and insulin status in healthy subjects
Experiment 1: the effect of phosphorus ingestion on oral glucose tolerance test [OGTT] Seven overnight fasted subjects (age: 23.2 ± 1.83 years; BMI: 22.65 ± 0.82 kg/m2) (Table 1: Experiment 1) were asked to attend 3 experimental sessions that were separated by a minimum of 3 days
Summary
Over the past few decades, the high prevalence of metabolic syndrome has become a worldwide phenomenon, associated with an increased risk and prevalence of type 2 diabetes mellitus [1]. This increasing phenomenon has been found to be associated with dietary and lifestyle changes, which favor the consumption of phosphorus (P)-deficient food items [2]. Overweight and/or obesity, a known risk factor for type 2 diabetes mellitus, is reported to be inversely related to plasma P [2, 3].
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