Research to date has provided novel insights into lactate's positive role in multiple brain functions and several brain diseases. Although notable controversies and discrepancies remain, the neurobiological role and the metabolic mechanisms of brain lactate have now been described. A theoretical framework on the relevance between lactate and brain function and brain diseases is presented. This review begins with the source and route of lactate formation in the brain and food; goes on to uncover the regulatory effect of lactate on brain function; and progresses to gathering the application and concentration variation of lactate in several brain diseases (diabetic encephalopathy, Alzheimer's disease, stroke, traumatic brain injury, and epilepsy) treatment. Finally, the dual role of lactate in the brain is discussed. This review highlights the biological effect of lactate, especially L-lactate, in brain function and disease studies and amplifies our understanding of past research.

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Lactate Is Answerable for Brain Function and Treating Brain Diseases: Energy Substrates and Signal Molecule

It is well known that oxidative stress induces muscle atrophy, which decreases with the activation of Nrf2/HO-1. Fermented oyster extracts (FO), rich in γ-aminobutyric acid (GABA) and lactate, have shown antioxidative effects. We evaluated whether FO decreased oxidative stress by upregulating Nrf2/HO-1 and whether it decreased NF-κB, leading to decreased IL-6 and TNF-α. Decreased oxidative stress led to the downregulation of Cbl-b ubiquitin ligase, which increased IGF-1 and decreased FoxO3, atrogin1, and Murf1, and eventually decreased muscle atrophy in dexamethasone (Dexa)-induced muscle atrophy animal model. For four weeks, mice were orally administered with FO, GABA, lactate, or GABA+Lactate, and then Dexa was subcutaneously injected for ten days. During Dexa injection period, FO, GABA, lactate, or GABA+Lactate were also administered, and grip strength test and muscle harvesting were performed on the day of the last Dexa injection. We compared the attenuation effect of FO with GABA, lactate, and GABA+lactate treatment. Nrf2 and HO-1 expressions were increased by Dexa but decreased by FO; SOD activity and glutathione levels were decreased by Dexa but increased by FO; NADPH oxidase activity was increased by Dexa but decreased by FO; NF-κB, IL-6, and TNF-α activities were increased by Dexa were decreased by FO; Cbl-b expression was increased by Dexa but restored by FO; IGF-1 expression was decreased by Dexa but increased by FO; FoxO3, Atrogin-1, and MuRF1 expressions were increased by Dexa but decreased by FO. The gastrocnemius thickness and weight were decreased by Dexa but increased by FO. The cross-sectional area of muscle fiber and grip strength were decreased by Dexa but increased by FO. In conclusion, FO decreased Dexa-induced oxidative stress through the upregulation of Nrf2/HO-1. Decreased oxidative stress led to decreased Cbl-b, FoxO3, atrogin1, and MuRF1, which attenuated muscle atrophy.

Fermented Oyster Extract Attenuated Dexamethasone-Induced Muscle Atrophy by Decreasing Oxidative Stress

Introduction Oysters possess an excellent nutritional profile containing γ-aminobutyric acid (GABA). Previous data suggest that GABA is a potent bioactive compound for improving muscle health. Lactic acid fermentation is thought to increase GABA content. However, the effect of oral supplementation of fermented oyster extracts (FO) on human muscle strength and mass is unclear. Therefore, we tested the effects and safety of consumption of FO combined with regular walking for 12 weeks on muscle strength and mass in older adults with relatively low muscle mass. Materials and methods A randomized controlled trial was conducted on 54 adults between 50 and 78 years of age. Participants were randomized to receive either placebo or 1,200 mg FO daily for 12 weeks. By fermentation with Lactobacillus brevis BJ20, FO was prepared from Crassostrea gigas. At baseline and at 12 weeks after treatment, the following parameters of the participants were examined: knee strengths, handgrip strengths, body composition, blood tests, and 24-h dietary recall. All participants were required to walk for 30–60 min/day for >3 days/week during the trial period. Physical activity was assessed using an exercise log during the study. Results Of the 54 participants, 49 completed the trial without reporting adverse effects. FO supplementation over 12 weeks did not cause any increase in knee or grip strength compared to the control group. Also, no differences were observed in the muscle mass, growth hormone, muscle biomarkers, anti-inflammatory markers, and antioxidative markers between the two groups. None of the participants experienced adverse events. Application of FO was well tolerated, and no notable adverse effect was reported in both groups. Discussion FO supplementation with regular walking did not improve remarkably muscle function compared to regular walking alone in adults with relatively low muscle mass. Clinical Trial Registration [www.ClinicalTrials.gov], identifier [NCT04109911].

/pdf/effect-of-fermented-oyster-crassostrea-gigas-extracts-and-27101l1m.pdf

Effect of fermented oyster (Crassostrea gigas) extracts and regular walking on muscle strength and mass in older adults with relatively low muscle mass: A randomized controlled trial

To investigate the effect and regulatory mechanism of resveratrol supplementation on the mitochondrial energy metabolism of rats with exercise-induced fatigue.Forty-eight Sprague-Dawley male rats were divided randomly into a blank control group (C), resveratrol group (R), exercise group (E), and exercise and resveratrol group (ER), with 12 rats in each group. Group ER and group E performed 6-wk swimming training with 5% wt-bearing, 60 min each time, 6 days a wk. Group ER was given resveratrol 50 mg/kg by gavage one hour after exercise; group R was only given resveratrol 50 mg/kg by gavage; group C and group E were fed normally. The same volume of solvent was given by gavage every day.Resveratrol supplementation could reduce the plasma blood urea nitrogen content, creatine kinase activity, and malondialdehyde content in the skeletal muscle, increase the total superoxide dismutase activity in the skeletal muscle, and improve the fatigue state. Resveratrol supplementation could improve the activities of Ca2+-Mg2+-ATPase, Na+-K+-ATPase, succinate dehydrogenase, and citrate synthase in the skeletal muscle. Furthermore, resveratrol supplementation could up-regulate the sirtuin 1 (SIRT1)-proliferator-activated receptor gamma coactivator-1α (PGC-1α)-nuclear respiratory factor 1 pathway.Resveratrol supplementation could promote mitochondrial biosynthesis via the SIRT1/PGC-1α pathway, increase the activity of the mitochondrial energy metabolism-related enzymes, improve the antioxidant capacity of the body, and promote recovery from exercise-induced fatigue. 

Resveratrol promotes mitochondrial energy metabolism in exercise-induced fatigued rats

Recently, the role of the gut microbiota in metabolic health, immunity, behavioral balance, longevity, and intestine comfort has been the object of several studies from scientific communities. They were encouraged by a growing interest from food industries and consumers toward novel fermented ingredients and formulations with powerful biological effects, such as pre, pro, and postbiotic products. Depending on the selected strains, the operating conditions, the addition of suitable reagents or enzymes, the equipment, and the reactor configurations, functional compounds with high bioactivity, such as short-chain fatty acids, gamma-aminobutyric acid, bioactive peptides, and serotonin, can be enhanced and/or produced through fermentation of several vegetable matrices. Otherwise, their formation can also be promoted directly in the gut after the dietary intake of fermented foods: In this case, fermentation will aim to increase the content of precursor substances, such as indigestible fibers, polyphenols, some amino acids, and resistant starch, which can be potentially metabolized by endogenous gut microorganisms and converted in healthy molecules. This review provides an overview of the main functional components currently investigated in literature and the associated gut health benefits. The current state of the art about fermentation technology as a promising functionalization tool to promote the direct or indirect formation of gut-health-enhancing components was deepened, highlighting the importance of optimizing microorganism selection, system setups, and process conditions according to the target compound of interest. The collected data suggested the possibility of gaining novel functional food ingredients or products rich in functional molecules through fermentation without performing additional extraction and purification stages, which are needed when conventional culture broths are used.

Gut health benefits and associated systemic effects provided by functional components from the fermentation of natural matrices.

Exogenous lactate administration has more recently been investigated for its various prophylactic effects. Lactate derived from potential functional foods, such as fermented oyster extract (FO), may emerge as a practical and effective method of consuming exogenous lactate. The current study endeavored to ascertain whether the lactate derived from FO may act on muscle cell biology, and to what extent this may translate into physical fitness improvements. We examined the effects of FO in vitro and in vivo, on mouse C2C12 cells and exercise performance indicators in mice, respectively. In vitro, biochemical analysis was carried out to determine the effects of FO on lactate content and muscle cell energy metabolism, including adenosine triphosphate (ATP) activity. Western blot analysis was also utilized to measure the protein expression of total adenosine monophosphate-activated protein kinase (AMPK), p-AMPK (Thr172), lactate dehydrogenase (LDH), succinate dehydrogenase (SDHA) and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) in response to FO administration. Three experimental groups were formed: a positive control (PC) treated with 1% horse serum, FO10 treated with 10 μg/mL and FO50 treated with 50 μg/mL. In vivo, the effects of FO supplementation on exercise endurance were measured using the Rota-rod test, and Western blot analysis measured myosin heavy-chain 2 (MYH2) to assess skeletal muscle growth, alongside p-AMPK, total-AMPK, PGC-1α, cytochrome C and UCP3 protein expression. Biochemical analysis was also performed on muscle tissue to measure the changes in concentration of liver lactate, lactate dehydrogenase (LDH), glycogen and citrate. Five groups (n = 10/per group) consisted of a control group (CON), exercise group (Ex), positive control treated with Ex and 500 mg/kg Taurine (Ex-Tau), Ex and 100 mg/kg FO supplementation (Ex-FO100) and Ex and 200 mg/kg FO supplementation (Ex-FO200) orally administered over the 4-week experimental period.FO50 significantly increased PGC-1α expression (p < 0.001), whereas both FO10 and FO50 increased the expression of p-AMPK (p < 0.001), in C2C12 muscle cells, showing increased signaling important for mitochondrial metabolism and biogenesis. Muscle lactate levels were also significantly increased following FO10 (p < 0.05) and FO50 (p < 0.001). In vivo, muscle protein expression of p-AMPK (p < 0.05) and PGC-1α were increased, corroborating our in vitro results. Cytochrome C also significantly increased following FO200 intake. These results suggest that the effects of FO supplementation may manifest in a dose-response manner. FO administration, in vitro, and supplementation, in vivo, both demonstrate a potential for improvements in mitochondrial metabolism and biogenesis, and even for potentiating the adaptive effects of endurance exercise. Mechanistically, lactate may be an important molecule in explaining the aforementioned positive effects of FO.

In Vitro and In Vivo Effects of Fermented Oyster-Derived Lactate on Exercise Endurance Indicators in Mice.

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In Vitro and In Vivo Effects of Fermented Oyster-Derived Lactate on Exercise Endurance Indicators in Mice.