Although the role of myo-inositol (MYO) in promoting the oocyte quality of PCOS patients has been documented in human studies; the cellular effects of this supplement on oocytes have not been directly examined due to ethical limitations. In the first phase of this study, MYO dosimetry was carried out simultaneously with the PCOS model development. An effective dose was obtained following the assessment of fasting insulin and testosterone levels using ELISA and ovarian morphology appraisal by histopathology. In the second phase, following the continuous administration of the effective dose of MYO and dehydroepiandrosterone (DHEA), cellular evaluation was performed. The quality of oocytes from superovulation was analyzed by examining maturity and normal morphology percentage using a stereomicroscope, intracellular reactive oxygen species (ROS) and glutathione (GSH) levels using fluorometry, and ATP count evaluation using ELISA. The results revealed that, among the four different MYO concentrations, the 0.36 mg/g dose compared with the DHEA group reduced testosterone levels and large atretic antral follicles (LAtAnF) diameter. This dose also increased the corpus luteum count and the granulosa:theca (G/T)layer thickness ratio in antral follicles. Furthermore, this dose increased mature oocytes and normal morphology percentage, ATP count, and GSH levels; however, it decreased ROS levels in mature oocytes. Our findings provide the grounds for further cellular and molecular studies on the PCOS mouse model, suggesting that the improvement in mitochondrial function and its antioxidant properties is probably one of the mechanisms by which MYO increases oocyte quality.

The incidence of preterm birth (PTB), delivery before 37 completed weeks of gestation, is rising in most countries. Several recent small clinical trials of myo-inositol supplementation in pregnancy, which were primarily aimed at preventing gestational diabetes, have suggested an effect on reducing the incidence of PTB as a secondary outcome, highlighting the potential role of myo-inositol as a preventive agent. However, the underlying molecular mechanisms by which myo-inositol might be able to do so remain unknown; these may occur through directly influencing the onset and progress of labour, or by suppressing stimuli that trigger or promote labour. This paper presents hypotheses outlining the potential role of uteroplacental myo-inositol in human parturition and explains possible underlying molecular mechanisms by which myo-inositol might modulate the uteroplacental environment and inhibit preterm labour onset. We suggest that a physiological decline in uteroplacental inositol levels to a critical threshold with advancing gestation, in concert with an increasingly pro-inflammatory uteroplacental environment, permits spontaneous membrane rupture and labour onset. A higher uteroplacental inositol level, potentially promoted by maternal myo-inositol supplementation, might affect lipid metabolism, eicosanoid production and secretion of pro-inflammatory chemocytokines that overall dampen the pro-labour uteroplacental environment responsible for labour onset and progress, thus reducing the risk of PTB. Understanding how and when inositol may act to reduce PTB risk would facilitate the design of future clinical trials of maternal myo-inositol supplementation and definitively address the efficacy of myo-inositol prophylaxis against PTB.

This study evaluated the effects of dietary myo-inositol (MI) on growth performance, antioxidant status and lipid metabolism of juvenile Chinese mitten crab (Eriocheir sinensis) fed different percentage of lipid. Crabs (4·58 (sem 0·05) g) were fed four diets including a normal lipid diet (N, containing 7 % lipid and 0 mg/kg MI), N with MI supplementation (N + MI, containing 7 % lipid and 1600 mg/kg MI), a high lipid diet (H, containing 13 % lipid and 0 mg/kg MI) and H with MI supplementation (H + MI, containing 13 % lipid and 1600 mg/kg MI) for 8 weeks. The H + MI group showed higher weight gain and specific growth rate than those in the H group. The dietary MI could improve the lipid accumulations in the whole body, hepatopancreas and muscle as a result of feeding on the high dietary lipid (13 %) in crabs. Besides, the crabs fed the H + MI diets increased the activities of antioxidant enzymes but reduced the malondialdehyde content in hepatopancreas compared with those fed the H diets. Moreover, dietary MI enhanced the expression of genes involved in lipid oxidation and exportation, yet reduced lipid absorption and synthesis genes expression in the hepatopancreas of crabs fed the H diet, which might be related to the activation of inositol 1,4,5-trisphosphate receptor (IP3R)/calmodulin-dependent protein kinase kinase-β (CaMKKβ)/adenosine 5’-monophosphate-activated protein kinase (AMPK) signalling pathway. This study demonstrates that MI could increase lipid utilisation and reduce lipid deposition in the hepatopancreas of E. sinensis fed a high lipid diet through IP3R/CaMKKβ/AMPK activation. This work provides new insights into the function of MI in the diet of crustaceans.

Glucose intolerance during pregnancy – a major driver of gestational diabetes mellitus (GDM) – has significant short- and long-term health consequences for both the mother and child. As GDM prevalence continues to escalate, there is growing need for preventative strategies. There is limited but suggestive evidence that myo-inositol (MI) and probiotics (PB) could improve glucose tolerance during pregnancy. The present study tested the hypothesis that MI and/or PB supplementation would reduce the risk of glucose intolerance during pregnancy. Female C57BL/6 mice were randomised to receive either no treatment, MI, PB (Lactobacillus rhamnosus and Bifidobacterium lactis) or both (MIPB) for 5 weeks. They were then provided with a high-fat diet for 1 week before mating commenced and throughout mating/gestation, while remaining on their respective treatments. An oral glucose tolerance test occurred at gestational day (GD) 16·5 and tissue collection at GD 18·5. Neither MI nor PB, separately or combined, improved glucose tolerance. However, MI and PB both independently increased adipose tissue expression of Ir, Irs1, Akt2 and Pck1, and PB also increased Pparγ. MI was associated with reduced gestational weight gain, whilst PB was associated with increased maternal fasting glucose, total cholesterol and pancreas weight. These results suggest that MI and PB may improve insulin intracellular signalling in adipose tissue but this did not translate to meaningful differences in glucose tolerance. The absence of fasting hyperglycaemia or insulin resistance suggests this is a very mild model of GDM, which may have affected our ability to assess the impact of these nutrients.

The effect of the ingestion of diets containing either myo-inositol or exogenous phytase on plasma metabolites was examined using 29 kg barrows. The diets were: control (maize, soya, rapeseed, rice bran), control plus 2 g/kg myo-inositol, control plus 1000 phytase units (FYT)/kg or 3000 FYT/kg exogenous phytase. Pigs were housed in a PigTurn device and blood was collected, from jugular catheters, via an automated system at −30, (30 min before feeding), 0, 15, 30, 45, 60, 90, 120, 150, 180, 240, 300 and 360 min post-feeding. The addition of 2 g/kg myo-inositol to the basal diet resulted in an increase in plasma myo-inositol concentration that was evident 45–60 min after diet introduction and persisted to 360 min post-feeding. Similarly, supplementation of the basal diet with either 1000 or 3000 FYT/kg exogenous phytase resulted in an increase in plasma myo-inositol concentration that was still rising 360 min post-feeding. Plasma P concentration was increased over time by the addition of 1000 and 3000 FYT/kg phytase, but not by the addition of myo-inositol. Other plasma metabolites examined were not affected by dietary treatment. It can be concluded that oral delivery of myo-inositol results in rapid increase in plasma myo-inositol concentrations that peak approximately 45–60 min after feeding. Use of supplemental phytase achieves similar increases in myo-inositol concentration in plasma but the appearance is more gradual. Furthermore, supplementation of pig diets with exogenous phytase results in rapid appearance of P in plasma that may be sustained over time relative to diets with no added phytase.

We previously reported that a chronic supplementation with myo-inositol (MI) improved insulin sensitivity and reduced fat accretion in mice. We then tested the potency of such dietary intervention in the prevention of insulin resistance in C57BL/6 male mouse fed a high-fat diet (HFD). In addition, some abnormalities in inositol metabolism were reported to be associated with insulin resistance in several animal and human studies. We then investigated the presence of such anomalies (i.e. inosituria and an inositol intra-tissue depletion) in this diet-induced obesity (DIO) mouse model, as well as the potential benefit of a MI supplementation for inositol intra-tissue deficiency correction. HFD (60 % energy from fat) feeding was associated with inosituria and inositol intra-tissue depletion in the liver and kidneys. MI supplementation (0·58 mg/g per d) restored inositol pools in kidneys (partially) and liver (fully). HFD feeding for 4 months induced ectopic lipid redistribution to liver and muscles, fasting hyperglycaemia and hyperinsulinaemia, insulin resistance and obesity that were not prevented by MI supplementation, despite a significant improvement in insulin sensitivity parameter Kinsulin tolerance test and a reduction in white adipose tissue (WAT) mass ( − 17 %, P< 0·05). MI supplementation significantly reduced fatty acid synthase activity in epididymal WAT, which might explain its beneficial, but modest, effect on WAT accretion in HFD-fed mice. Finally, we found some abnormalities in inositol metabolism in association with a diabetic phenotype (i.e. insulin resistance and fasting hyperglycaemia) in a DIO mouse model. Dietary MI supplementation was efficient in the prevention of inositol intra-tissue depletion, but did not prevent insulin resistance or obesity efficiently in this mouse model.

Raffinose, stachyose and phytin are undesirable compounds for soybean food and animal feed products. In seeds, raffinose and stachyose are believed to contribute to desiccation and cold stress tolerance. Thus, removal of these compounds from soybean by genetic mutation has resulted in a more commercially desirable composition, but potentially less physiologically viable seeds. In an effort to develop a method to improve viability and seed storability in soybean, stem–leaf–pod explants of three low raffinose, low stachyose lines, two of which were also low in phytin, and a check line were fed solutions containing d-chiro-inositol, myo-inositol or d-pinitol, free cyclitols which unload through the seed coat to the developing embryo where they accumulate as fagopyritols, galactinol and galactopinitols, respectively, during seed maturation. Increased galactopinitol and fagopyritol accumulation may substitute for the roles of raffinose and stachyose in low raffinose, stachyose and phytin seeds. Explants of all lines unloaded d-chiro-inositol, myo-inositol and d-pinitol. Fed d-chiro-inositol accumulated in leaf tissues demonstrating uptake into explants. Fed d-chiro-inositol and myo-inositol accumulated in pod wall and seed coat tissues of one or more lines. The results indicate that d-chiro-inositol was unloaded from the seed coat to the embryo in increased amounts after feeding. The potential use of increased maternal d-chiro-inositol for synthesis of fagopyritols in embryos to improve seed performance in low-stachyose and low-phytin soybean seeds is supported. The seed coat cup unloading of fed free cyclitols may provide a model system to test effective unloading of upregulated maternally synthesized cyclitols.

Sucrose, raffinose and stachyose accumulate in soybean [Glycine max L. (Merrill)] embryos during seed maturation. To determine the relationship of plant maternal composition on seed composition, soluble carbohydrates in three 1-cm2 leaf punches at three plant growth stages (R2, R3, R6) and in seed coat cup exudates in planta were analysed at four 30-min intervals on soybean plants (R5) with low-raffinose, low-stachyose (LRS) seeds expressing the mutant stc1 phenotype; low-raffinose, low-stachyose and low-phytin (LRSP1, LRSP2) seeds expressing the mutant mips phenotype; or normal raffinose, stachyose and phytin (CHECK) seeds expressing the Stc1 and Mips phenotype. Leaf sucrose (23.6 μg cm− 2), myo-inositol (9.3 μg cm− 2), d-chiro-inositol (6.7 μg cm− 2), d-ononitol (0.76 μg cm− 2), d-pinitol (50.1 μg cm− 2) and total soluble carbohydrates (107.1 μg cm− 2) were not significantly different between phenotypes. d-chiro-Inositol, myo-inositol, d-pinitol and sucrose were unloaded from soybean seed coat cups in planta at decreasing rates over the four sequential periods of sampling. Unloading rates of sucrose and myo-inositol were highest for LRS, d-pinitol was highest for LRSP2, and d-chiro-inositol was not different between LRS, LRSP1, LRSP2 and CHECK. Free cyclitols were 60% of total soluble carbohydrates in leaves and 20% in seed coat cup exudates. Except for sucrose and d-pinitol, seed phenotype had little influence on the composition of compounds unloaded from seed coats to maturing embryos of low-raffinose, low-stachyose seeds. Maternally supplied cyclitols may contribute, in part, to changes in the composition of cyclitol galactosides stored in mature seeds.

The effects of lithium on vascular development were examined using the chick embryo area vasculosa in shell-less culture as an experimental model. Embryos were explanted after 48 h in ovo and LiCl (50, 100, 150 and 200 μg in 10 μl water) was applied to the centre of the blastodisc. Controls were untreated or given equimolar amounts of NaCl. At 24 h and 48 h after treatment, untreated and NaCl controls were identical, having well developed extraembryonic vessels. At doses of 100 μg and greater, LiCl significantly inhibited normal vascular development and expansion of the area vasculosa in the majority of explants. In many specimens blood islands continued to form but their assembly into primitive vessels was prevented, indicating that lithium affects the mechanism regulating the assembly of vascular endothelium. At the same time the embryos were alive but retarded in development compared with controls. When LiCl (150 μg) was applied to cultures explanted after 72 h in ovo (when the primary vascular network had already formed through vasculogenesis) no adverse effects were seen. This suggests that lithium affects vasculogenesis but not angiogenesis. Treatment with myo-inositol completely reversed the effects of lithium in a time dependent manner indicating that the phosphatidylinositol second messenger cycle may be involved in the cellular events of vasculogenesis. Finally the results of this study show that the yolk sac vasculature is particularly vulnerable to lithium and the consequent effects of this interference on embryonic development are discussed.