Nocturnal eating disturbs phosphorus excretion in young subjects: a randomized crossover trial

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Abstract

Background

Nocturnal eating have recently increased. Serum phosphorus levels and regulators of phosphorus have circadian variations, so it is suggested that the timing of eating may be important in controlling serum phosphorus levels. However, there have been no reports on the effects of nocturnal eating on phosphorus metabolism.

The objective was to evaluate the effects of nocturnal eating on phosphorus metabolism.

Methods

Fourteen healthy men participated in two experimental protocols with differing dinner times. The design of this study was a crossover study. The subjects were served test meals three times (breakfast; 07:30 h, lunch; 12:30 h, dinner; 17:30 or 22:30 h) a day. Blood and urine samples were collected to assess diurnal variation until the following morning.

Results

The following morning, fasting serum phosphorus levels in the late dinner group were markedly higher than those in the early dinner group ( p < 0.001), although serum calcium levels were maintained at approximately constant levels throughout the day in both groups. Fluctuations in urinary calcium excretion were synchronized with the timing of dinner eating, however, fluctuations in urinary phosphorus excretion were not synchronized. Urinary phosphorus excretions at night were inhibited in the late dinner group. In the late dinner group, intact parathyroid hormone levels didn’t decrease, and they were significantly higher in this group compared with the early dinner group at 20:00 h ( p = 0.004). The following morning, fasting serum fibroblast growth factor 23 levels in the late dinner group had not changed, but those in the early dinner group were significantly increased ( p = 0.003). Serum free fatty acid levels before dinner were significantly higher in the late dinner group compared with the early dinner group.

Conclusions

Our results indicate that nocturnal eating inhibits phosphorus excretion. It is suggested that nocturnal eating should be abstained from to manage serum phosphorus levels to within an adequate range.

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Most cited references 39

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Relation between serum phosphate level and cardiovascular event rate in people with coronary disease.

Marcello Tonelli, Frank Sacks, Marc Pfeffer … (2005)

Higher levels of serum phosphate are associated with adverse cardiovascular outcomes, especially in the setting of overt hyperphosphatemia. Given the biological importance of phosphorus, it is plausible that higher levels of serum phosphate within the normal range may also be associated with adverse outcomes. We performed a post hoc analysis of data from the Cholesterol And Recurrent Events (CARE) study. Baseline serum phosphate levels were measured in 4127 fasting participants who were randomized to receive pravastatin 40 mg daily or placebo and followed up for a median of 59.7 months. We used Cox proportional-hazards models to examine the association between serum phosphate and adverse clinical outcomes after adjustment for potential confounders. During nearly 60 months of follow-up, 375 participants died. A significant association was noted between baseline serum phosphate level and the age-, race-, and sex-adjusted risk of all-cause death (hazard ratio per 1 mg/dL, 1.27; 95% confidence interval, 1.02 to 1.58). After categorization based on baseline phosphate level ( or =4 mg/dL) and further adjustment, a graded independent relation between phosphate and death was observed (P for trend=0.03). For instance, participants with serum phosphate > or =3.5 mg/dL had an adjusted hazard ratio for death of 1.27 (95% confidence interval, 1.02 to 1.59) compared with those with serum phosphate of <3.5 mg/dL. Higher levels of serum phosphate were also associated with increased risk of new heart failure, myocardial infarction, and the composite of coronary death or nonfatal myocardial infarction, but not the risk of stroke. We found a graded independent relation between higher levels of serum phosphate and the risk of death and cardiovascular events in people with prior myocardial infarction, most of whom had serum phosphate levels within the normal range. Given the ready availability and low cost of serum phosphate assays, this finding may prove clinically useful.

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Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism

Takashi Shimada, Makoto Kakitani, Yuji Yamazaki … (2004)

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Extracellular calcium sensing and extracellular calcium signaling.

Stephen B. R. E. Brown, Malcolm Macleod (2000)

The cloning of a G protein-coupled extracellular Ca(2+) (Ca(o)(2+))-sensing receptor (CaR) has elucidated the molecular basis for many of the previously recognized effects of Ca(o)(2+) on tissues that maintain systemic Ca(o)(2+) homeostasis, especially parathyroid chief cells and several cells in the kidney. The availability of the cloned CaR enabled the development of DNA and antibody probes for identifying the CaR's mRNA and protein, respectively, within these and other tissues. It also permitted the identification of human diseases resulting from inactivating or activating mutations of the CaR gene and the subsequent generation of mice with targeted disruption of the CaR gene. The characteristic alterations in parathyroid and renal function in these patients and in the mice with "knockout" of the CaR gene have provided valuable information on the CaR's physiological roles in these tissues participating in mineral ion homeostasis. Nevertheless, relatively little is known about how the CaR regulates other tissues involved in systemic Ca(o)(2+) homeostasis, particularly bone and intestine. Moreover, there is evidence that additional Ca(o)(2+) sensors may exist in bone cells that mediate some or even all of the known effects of Ca(o)(2+) on these cells. Even more remains to be learned about the CaR's function in the rapidly growing list of cells that express it but are uninvolved in systemic Ca(o)(2+) metabolism. Available data suggest that the receptor serves numerous roles outside of systemic mineral ion homeostasis, ranging from the regulation of hormonal secretion and the activities of various ion channels to the longer term control of gene expression, programmed cell death (apoptosis), and cellular proliferation. In some cases, the CaR on these "nonhomeostatic" cells responds to local changes in Ca(o)(2+) taking place within compartments of the extracellular fluid (ECF) that communicate with the outside environment (e.g., the gastrointestinal tract). In others, localized changes in Ca(o)(2+) within the ECF can originate from several mechanisms, including fluxes of calcium ions into or out of cellular or extracellular stores or across epithelium that absorb or secrete Ca(2+). In any event, the CaR and other receptors/sensors for Ca(o)(2+) and probably for other extracellular ions represent versatile regulators of numerous cellular functions and may serve as important therapeutic targets.

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Author and article information

Contributors

Masae Sakuma: 81-54-264-5596 , sakuma@u-shizuoka-ken.ac.jp

Journal

Journal ID (nlm-ta): Nutr J

Journal ID (iso-abbrev): Nutr J

Title: Nutrition Journal

Publisher: BioMed Central (London )

ISSN (Electronic): 1475-2891

Publication date (Electronic): 8 October 2015

Publication date PMC-release: 8 October 2015

Publication date Collection: 2015

Volume: 14

Electronic Location Identifier: 106

Affiliations

[ ]Laboratory of Clinical Nutrition and Management, Graduate School of Nutritional and Environmental Sciences, The University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka, 422-8526 Japan

[ ]School of Nursing Sciences, The University of Shizuoka, Shizuoka, Japan

Article

Publisher ID: 96

DOI: 10.1186/s12937-015-0096-y

PMC ID: 4599584

SO-VID: e97df577-da01-4adf-8041-11586325651e

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 9 March 2015

Date accepted : 30 September 2015

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ScienceOpen disciplines: Nutrition & Dietetics

Keywords: hyperphosphatemia,nocturnal eating,parathyroid hormone,fibroblast growth factor 23,free fatty acid

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ScienceOpen disciplines: Nutrition & Dietetics

Keywords: hyperphosphatemia, nocturnal eating, parathyroid hormone, fibroblast growth factor 23, free fatty acid

Nocturnal eating disturbs phosphorus excretion in young subjects: a randomized crossover trial

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Karger: Nutrition and Dietetics

Most cited references 39

Relation between serum phosphate level and cardiovascular event rate in people with coronary disease.

Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism

Extracellular calcium sensing and extracellular calcium signaling.

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