Our findings suggest that prebiotics affect the intestinal microbiota and might maintain the antibody titers in elderly individuals.
In Japan, the incidence of heat illness in older people has rapidly increased during midsummer in the last decade, and we suggested that whey-protein+carbohydrate supplementation during aerobic training would increased plasma volume (PV) to enhance thermoregulatory adaptation in older men ( J Appl Physiol 107: 725-733, 2009); however, >60% of people age 65 and older suffer from hypertension, and the symptoms may be worsened by hypervolemia. To examine this, we randomly divided 21 older men (∼69 yr) with ∼160 mmHg for systolic and ∼90 mmHg for diastolic blood pressure at rest into two groups: Glc ( n = 11) consuming glucose alone (25 g) and Pro-Glc ( n = 10) consuming whey protein (10 g) + glucose (15 g), immediately after cycling exercise at 60–75% of peak aerobic capacity (V̇o2 peak) for 60 min/day, 3 days/wk, for 8 wk. Before and after training, we measured PV (dye dilution), baroreflex sensitivity (BRS) of heart rate (Valsalva maneuver), and carotid arterial compliance (CAC) from carotid arterial diameter (ultrasound imaging) responses to pulsatile arterial pressure change (photoplethysmography) at rest. Additionally, we measured esophageal temperature (Tes) and forearm skin blood flow (plethysmography) during exercise at 60% pretraining V̇o2 peak for 20 min in a warm environment. We found that the forearm skin vascular conductance response to increased Tes was enhanced in Pro-Glc with increased PV, but this was not found in Glc; however, despite the increased PV, arterial blood pressures rather decreased with increased CAC and BRS in Pro-Glc. Thus, the prescription was applicable to older men with hypertension to prevent heat illness during exercise.
This study aimed to investigate the effects of a combination of a dairy product fermented by lactobacilli (DFL) and galactooligosaccharides (GOS) on mineral balances in growing rats with hypochlorhydria induced by a proton pump inhibitor (PPI). Three-week-old male rats were assigned to receive one of six diets: a control diet, control diets containing 1.6 or 5.0 % GOS, a DFL diet and DFL diets containing 1.6 or 5.0 % GOS for 9 days. From day 5 of the feeding period, half of the rats fed with control diets were subcutaneously administered with saline, whereas the remaining rats were administered with PPI for 5 days. Calcium (Ca), phosphorus (P), magnesium (Mg), iron (Fe) and zinc (Zn) balances were determined from days 6 to 9. PPI administration significantly decreased the apparent absorption of Ca and Fe and increased urinary P excretion, resulting in decreased Ca, Fe and P retention. GOS dose-dependently increased the apparent absorption of Ca, Mg and Fe and urinary Mg excretion and decreased urinary P excretion. DFL significantly increased the apparent absorption of Ca and Mg and urinary Mg excretion. The combination of DFL and GOS additively affected these parameters, resulting in increased Ca, P and Fe retention, and it further increased the apparent absorption and retention of Zn at 5.0 % GOS. In conclusion, the combination of DFL and GOS improves Ca, P and Fe retention in an additive manner and increases the Zn retention in growing rats with hypochlorhydria induced by PPI.
The purpose of the present study is to investigate the effects of hypochlorhydria induced by proton pump inhibitor (PPI) administration and intake of a dairy product fermented by lactobacilli (DFL) on bone metabolism in growing rats. Male rats, aged 3 weeks, were divided into two groups: a control group fed a casein-based diet and a group fed a DFL-based diet. Each group was fed its respective experimental diets for 9 d. At day 5 of the feeding period, each group was divided into two subgroups: one that received a saline injection and one that received a PPI injection. Rats were subcutaneously administered saline or PPI for 5 d. Faecal Ca excretion was determined from day 6 to day 9. At the end of the experiment, plasma and femurs were collected. Administration of PPI significantly decreased bone mineral density (shown by X-ray computerised tomography) and bone strength (shown by a three-point bending test) in the control group. Plasma osteocalcin, type I collagen C-telopeptides, 1,25-dihydroxyvitamin D and parathyroid hormone concentrations were elevated by PPI administration in the control group. Faecal Ca excretion and urinary P excretion in the control group were remarkably increased by PPI administration. On the other hand, these adverse effects of PPI were not observed in the DFL group. These results suggest that hypochlorhydria-induced bone loss may result from high bone turnover induced by secondary hyperparathyroidism due to Ca malabsorption and that DFL intake cancels these adverse effects probably via improving Ca malabsorption in growing rats.Key words: Hypochlorhydria: Fermented milk: Bone: Calcium Most physiological functions decline progressively with age. Gastric acid secretion also decreases with advancing age in humans (1) and rats (2,3) . Recently, Aoki et al. reported that chronic atrophic gastritis, a factor of hypochlorhydria, is very common among the elderly (4) .There are some studies suggesting the association between hypochlorhydria and bone loss. Many researchers have reported that gastrectomy induces bone loss in rats (5 -8) and human subjects (9 -12) . However, gastrectomy in itself has multiple risk factors other than hypochlorhydria for bone loss. For example, the production of the stomach hormone ghrelin, which is involved in bone physiology, is suppressed by gastrectomy (13) . Some studies have shown that the use of proton pump inhibitors (PPI), the most potent acid-suppressing drugs, is associated with an increased risk of hip fracture (14,15) . However, there is limited research showing the effects of hypochlorhydria induced by PPI on bone metabolism in human subjects or animals.The absorbability of Ca is dependent on its solubility. The acidity in the stomach and resulting chyme increases Ca solubility (16) . Thus, hypochlorhydria is considered to have a potential adverse effect on bone metabolism via the inhibition of Ca absorption.The usefulness of cows' milk (17,18) or dairy products including cows' milk and yogurt (19) for the prevention of osteoporosis has been ...
BackgroundMuscle atrophy with aging is closely associated with chronic systemic inflammation and lifestyle-related diseases. In the present study, we assessed whether post-exercise milk product intake during 5-month interval walking training (IWT) enhanced the increase in thigh muscle strength and ameliorated susceptibility to inflammation in older women.MethodsSubjects [n = 37, 66±5 (standard deviation) yrs] who had been performing IWT for >6 months participated in this study. They were randomly divided into the following 3 groups: IWT alone (CNT, n = 12), IWT + low-dose post-exercise milk product intake (LD, n = 12; 4 g protein and 3 g carbohydrate) or IWT + a 3-times higher dose of milk product intake than the LD group (HD, n = 13). They were instructed to repeat ≥5 sets of fast and slow walking for 3 min each at ≥70% and 40% peak aerobic capacity for walking, respectively, per day for ≥4 days/week.ResultsAfter IWT, thigh muscle strength increased in the HD group (8±2%) more than in the CNT group (-2±3%, P = 0.022), despite similar IWT achievements between the groups (P>0.15). Pyrosequencing analysis using whole blood showed that methylation of NFKB1 and NFKB2, master genes of inflammation, was enhanced in the HD group (29±7% and 44±11%, respectively) more than in the CNT group (-20±6% and -10±6%, respectively; P<0.001). Moreover, the genome-wide DNA methylation analysis showed that several inflammation-related genes were hyper-methylated in the HD group compared with that in the CNT group, suggesting greater pro-inflammatory cytokine gene suppression in the HD group.ConclusionHD milk product intake after exercise produced a greater percent increase in thigh muscle strength and NFKB1 and NFKB2 gene methylation during IWT in physically active older women.Trial registrationUMIN-CTR No. UMIN000024544 and No. UMIN000024912
We examined zinc (Zn) metabolism in rats given diets containing excess calcium (Ca). Rats were given phytate-free diet containing 5 g Ca/kg (control), 12.5 g Ca/kg, or 25 g Ca/kg for 4 wk in Experiment 1. The dietary treatment did not affect Zn concentration in the plasma, testis, kidney, spleen and liver; however, Zn concentration in the femur and its cortex was significantly higher in rats given diet containing 25 g Ca/kg than in other rats. Rats were given phytate-free diet containing 5 g Ca /kg or 25 g Ca /kg for 4 wk in Experiment 2. After 12-h food deprivation, rats were given a diet extrinsically labeled by 67Zn with dysprosium as a fecal marker for 4 h. Feces were collected from 1 d before administration of the labeled diet to 5 d after administration. Excess Ca did not affect the true absorption of Zn and its endogenous excretion but increased femoral Zn. These results suggest that excess Ca improves Zn bioavailability without affecting Zn absorption when diets do not contain phytate.
Phosphorus is an essential nutrient for many biological functions, including cellular signal transduction, mineral metabolism, and energy exchange. On the other hand, a relatively high serum phosphorus level is reportedly a risk factor for cardiovascular disease (1, 2) because inorganic phosphates have been shown to stimulate differentiation of vascular smooth muscle cells into calcifying vascular cells (3). Therefore, serum phosphorus regulation may help to prevent cardiovascular diseases.Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that plays a regulatory role in phosphorus homeostasis. FGF23 has been shown to reduce serum phosphorus levels by inhibition of proximal tubular phosphorus reabsorption through decreased expression of types 2a and 2c sodium-phosphate cotransporters and by decreasing intestinal phosphorus absorption through inhibiting calcitriol synthesis in the kidney (4). Moreover, FGF23-null mice were shown to exhibit severe vascular calcification with concomitant hyperphosphatemia (5). These facts suggest that FGF23 may have a protective effect on vascular calcification by hyperphosphatemia suppression. In contrast, several hemodialysis studies reported that elevated FGF23 levels were associated with aortic calcification (6) and mortality (7, 8) independent of serum phosphorus levels. Elevated serum FGF23 levels, even within the normal range, are reportedly associated with increased left ventricular mass index and increased risk for the presence of left ventricular hypertrophy in elderly subjects (9). Furthermore, a recent study suggested that elevated FGF23 levels contributed directly to high rates of left ventricular hypertrophy and mortality in individuals with chronic kidney diseases (10). Thus, FGF23 regulation may also play a clinically significant role in the prevention of cardiovascular diseases.Oral phosphorus supplementation is known to stimulate FGF23 secretion, although the underlying mechanism has not been clarified. In our preliminary study, we found that plasma FGF23 levels in rats increased after oral phosphorus administration at a physiological dose; however, this increase slowly began around the time that plasma phosphorus levels had decreased (unpublished data). Based on these findings, we reasoned that oral phosphorus supplementation may secondarily increase FGF23 secretion. Parathyroid hormone (PTH) is also secreted in response to phosphorus administration (11) and subsequently increases urinary phosphorus excre- Note Oral Phosphorus Supplementation Secondarily Increases Circulating Fibroblast Growth Factor 23 Levels at Least Partially via Stimulation of Parathyroid Hormone SecretionSatoshi Takasugi, Miho Akutsu and Masashi Nagata Food Science Research Laboratories, Division of Research and Development, Meiji Co., Ltd., 540 Naruda, Odawara, Kanagawa 250-0862, Japan (Received August 20, 2013) Summary Oral phosphorus supplementation stimulates fibroblast growth factor 23 (FGF23) secretion; however, the underlying mechanism remains unclear. The aim of this ...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.