Once regarded merely as a metabolic waste product generated during anaerobic glycolysis, lactate has emerged as a pivotal metabolic and signaling molecule integral to diverse physiological and pathological processes. Traditionally associated with muscle fatigue during intense exercise, lactate’s role extends far beyond a simple byproduct; it serves as an essential energy substrate, a regulator of cellular metabolism, and a mediator of intercellular communication (Vavřička et al., 2024).

In cancer biology, lactate’s significance is profound. Tumors commonly exhibit a metabolic shift known as aerobic glycolysis or the “Warburg effect,” where glucose is preferentially converted to lactate despite sufficient oxygen availability (Zhong et al., 2022). This metabolic reprogramming leads to lactate accumulation within the tumor microenvironment, which promotes cancer cell proliferation, angiogenesis, and metastasis (de la Cruz-López et al., 2019). Elevated lactate also contributes to immune evasion by creating an acidic microenvironment that suppresses cytotoxic T cell and natural killer cell activity, facilitating tumor progression (Gu et al., 2025). Research has demonstrated that lactate acts through signaling pathways such as HIF-1α stabilization and GPR81 activation, further reinforcing cancer cell survival and immune modulation (Chen et al., 2025). Beyond oncology, lactate is implicated in several chronic inflammatory and metabolic diseases (Lee, 2021). For instance, in pulmonary hypertension and pulmonary fibrosis, elevated lactate levels correlate with vascular remodeling and fibrotic processes (Peng et al., 2025). Studies indicate that lactate stimulates fibroblast activation and extracellular matrix deposition, contributing to disease progression (Caslin et al., 2021). In heart failure and atherosclerosis, abnormal lactate metabolism is associated with impaired mitochondrial function and chronic inflammation. Elevated circulating lactate in these conditions reflects underlying tissue hypoxia and metabolic stress, exacerbating cardiac dysfunction and vascular pathology (Zymliński et al., 2018; Zhu et al., 2024). Polycystic kidney disease (PKD) also features altered lactate metabolism. Experimental models show that lactate accumulation in cystic epithelial cells supports their proliferation and survival, contributing to cyst growth (Ghazi et al., 2019; Pagliarini and Podrini, 2021). Similarly, metabolic disorders such as type 2 diabetes exhibit dysregulated lactate production, linking it to insulin resistance and chronic low-grade inflammation (Nareika et al., 2005; Wu et al., 2016). Lactate involvement extends to acute stress responses, including trauma, infection, myocardial infarction, and ischemia-reperfusion injury (Wang et al., 2025). Here, lactate serves as both a metabolic fuel for damaged tissues and a signaling molecule triggering adaptive responses. Elevated lactate levels in sepsis, for example, are a prognostic marker reflecting tissue hypoperfusion and metabolic derangement (Liu et al., 2024).

A groundbreaking discovery expanding lactate role in disease is its function in epigenetic regulation through histone lactylation. This recently identified posttranslational modification involves the addition of lactate-derived groups to histone lysine residues, altering chromatin structure and gene expression. Histone lactylation has been shown to modulate inflammatory gene expression in macrophages, promoting resolution of inflammation, while also contributing to oncogenic gene programs in cancer cells. This epigenetic mechanism underscores lactate’s capacity to link metabolic states with long-term changes in cellular phenotype and disease outcomes (Zhang et al., 2019).

Collectively, lactate acts as a critical mediator of metabolic adaptation, immune regulation, and pathophysiological remodeling across a spectrum of diseases. Its dual roles as an energy substrate and signaling molecule highlight the intricate connections between metabolism and cellular function. Ongoing research aims to eKMCTlucidate therapeutic strategies targeting lactate metabolism and signaling, offering promising avenues for treating cancer, inflammatory disorders, cardiovascular diseases, and metabolic syndromes. Understanding lactate’s diverse physiological and pathological functions is essential for developing novel interventions to modulate disease progression and improve patient outcomes (Li et al., 2022).

During vigorous exercise, skeletal muscles rely on anaerobic glycolysis, resulting in substantial lactate accumulation. Once thought to be simply a product of glycolysis, lactate is now recognized as a vital signaling molecule and energy source. It can be shuttled to the liver for gluconeogenesis or oxidized in oxidative muscle fibers and the heart. Lactate also modulates gene expression related to mitochondrial biogenesis and angiogenesis, supporting muscle adaptation during endurance training (Mandadzhiev, 2025).

Erythrocytes, which lack mitochondria, depend entirely on anaerobic glycolysis for ATP production and continuously produce lactate. Recent studies highlight the role of MCTs in lactate transport, essential for maintaining acid-base balance. Erythrocyte-derived lactate significantly influences systemic metabolism, particularly in the heart and brain, and emerging evidence suggests its levels may serve as biomarkers for metabolic disorders such as diabetes and sepsis (Zhang T. et al., 2024).

In the brain, lactate plays a vital role through the astrocyte-neuron lactate shuttle. Astrocytes convert glucose into lactate, which neurons utilize during heightened activity. Lactate supports synaptic plasticity, learning, and memory by enhancing brain-derived neurotrophic factor (BDNF) signaling. Impaired lactate metabolism is linked to neurodegenerative diseases like Alzheimer’s and Parkinson’s, highlighting its therapeutic potential in cognitive disorders (Beard et al., 2022).

Cancer cells exhibit the Warburg effect, favoring glycolysis even in oxygen-rich environments, leading to lactate accumulation. This promotes immune evasion, angiogenesis, metastasis, and epigenetic changes that drive tumor aggressiveness. Lactate transporters such as MCT1 and MCT4 are emerging targets, with their inhibition shown to reduce tumor progression in breast cancer models. Modulating lactate metabolism offers a promising strategy for cancer therapy (Zhong et al., 2022).

Lactate is transported to the liver, heart, and oxidative muscle fibers, where it converts to pyruvate and enters the TCA cycle for ATP production (Wang et al., 2018). The lactate shuttle hypothesis, first introduced by Brooks (1985), describes lactate’s movement between glycolytic and oxidative tissues as a fuel source. The heart preferentially utilizes lactate as an energy substrate, with lactate oxidation playing a substantial role in myocardial energy production during both resting and stressed states (Brooks, 2021; Zhang H. et al., 2024) (Table 1). Through the Cori cycle, lactate is transported to the liver for gluconeogenesis (Figure 2), forming glucose that is released into the bloodstream (Melkonian et al., 2023). Lactate homeostasis is maintained through MCTs 1–4, enabling rapid cellular exchange (Figure 2). Elevated lactate levels (lactic acidosis) signal metabolic dysregulation. Lactate’s clearance mechanisms include oxidation via the TCA cycle, renal excretion through sodium/lactate transporters (Slc5a12 and Slc5a8), and microbiome incorporation (Lee, 2021). In a study, it has been demonstrated that hepatic gluconeogenesis is essential for glucose homeostasis during exercise and fasting (Meyer et al., 2002). The kidneys also contribute significantly, accounting for approximately 40% of systemic glucose production during prolonged fasting. Recent research challenges the traditional view of lactate as a glycolytic byproduct, showing that it directly fuels mitochondrial oxidative phosphorylation. Lactate enters mitochondria via the mitochondrial lactate oxidation complex (mLOC) and converts into pyruvate for ATP generation (Brooks et al., 2022). Hashimoto et al. (2008) provided compelling evidence that lactate oxidation occurs within mitochondria, highlighting its role in both normal and pathological states such as cancer and neurodegeneration (Hashimoto et al., 2008).

Lactate serves as an efficient energy source, particularly in oxidative tissues like the heart and brain. The heart preferentially oxidizes lactate over glucose, emphasizing its role in cardiac metabolism (Lee, 2021). Schurr et al. (1999) demonstrated that lactate is a primary energy source for neurons, reinforcing its significance beyond glycolysis (Schurr et al., 1999). Lactate regulates gene expression, angiogenesis, and immune responses (Figure 2). Lactate promotes the stabilization of HIF-1α by inhibiting prolyl hydroxylase activity. This stabilization enhances HIF-1-mediated transcription of glycolytic enzymes and VEGF, supporting metabolic adaptation and angiogenesis under hypoxic or pseudohypoxic conditions (Li et al., 2022). A study demonstrated that lactate accumulation under hypoxic conditions enhances VEGF expression, facilitating angiogenesis and tissue survival. Lactate accumulation during high-intensity exercise leads to metabolic acidosis but is rapidly cleared and utilized as an energy source. It aids recovery by replenishing glycogen stores and supporting mitochondrial respiration (Mandadzhiev, 2025). Gladden and Hogan (2006) showed that lactate metabolism during and after exercise is crucial for sustaining muscle function and preventing fatigue (Gladden and Hogan, 2006). Lactate is essential for brain metabolism. The astrocyte-neuron lactate shuttle theory suggests that astrocytes produce lactate, which neurons use as an energy source. Lactate enhances synaptic plasticity and memory formation (Hu et al., 2021). Pellerin et al. (1994) identified lactate as a key neuronal energy substrate, while another study showed that lactate enhances long-term memory formation in animal models (Pellerin et al., 1994). Lactate influences immune cell metabolism and function, regulating macrophage polarization. It promotes anti-inflammatory M2 macrophages while inhibiting pro-inflammatory M1 macrophages. This is particularly relevant in cancer metabolism and immune evasion (Zhang T. et al., 2024). In research study showed that lactate accumulation in tumors promotes M2 macrophage polarization, contributing to immune suppression and tumor progression (Zhong et al., 2022). Cancer cells convert glucose to lactate even in oxygen-rich conditions, a phenomenon known as the Warburg effect. Lactate accumulation in the tumor microenvironment promotes angiogenesis, immune evasion, and metastasis. Warburg first described this metabolic shift, and more recent studies highlighted how lactate metabolism supports tumor growth and resistance to therapy. Lactate is a vital metabolic intermediate with diverse roles beyond glycolysis. Its involvement in energy production, signaling, neuroprotection, and immune modulation underscores its physiological significance. The traditional perception of lactate as a waste product has evolved into its recognition as a key player in metabolic homeostasis (Nath and Balling, 2024).

In summary (Table 1), Lactate, an energy substrate, efficiently fuels muscles, the heart, and the brain, especially under high-demand conditions (Hashimoto et al., 2008). In skeletal muscle, lactate promotes adaptation by enhancing mitochondrial biogenesis and oxidative capacity, thereby improving endurance and performance (Nalbandian et al., 2017). In the brain, it supports neuronal metabolism, prevents excitotoxicity, and enhances synaptic plasticity, contributing to neuroprotection (Suzuki et al., 2011). Lactate also plays a crucial role in immune modulation by regulating macrophage polarization, suppressing inflammation, and supporting regulatory T cell function (Zhang T. et al., 2024). Furthermore, it stimulates angiogenesis and wound healing by promoting vascular endothelial growth factor (VEGF) production in endothelial cells and skin (Hunt et al., 2007). In the liver, lactate serves as a precursor for gluconeogenesis via the Cori cycle, helping to maintain blood glucose levels (Rogatzki et al., 2015). Its influence extends to lipid metabolism, where it modulates free fatty acid oxidation and storage in adipose tissue (Bergman et al., 1999). During exercise recovery, lactate helps reduce muscle fatigue, maintain pH balance, and facilitate lactate shuttling between tissues (Gladden, 2004). Interestingly, in the tumor microenvironment, lactate supports cancer cell survival and immune evasion (Fischer et al., 2007). Lastly, in the heart, lactate serves as a preferred substrate over glucose during ischemic conditions, offering cardioprotection by reducing oxidative stress (Chatham, 2002). Collectively, these findings highlight lactate’s multifaceted and beneficial roles across various organs and systems, challenging its outdated reputation as merely a metabolic waste product. In the following section, we provide a detailed explanation of key aspects highlighted in (Table 1).

Glycolysis, a key metabolic pathway, processes glucose to generate ATP and essential precursors for cellular functions. While glycolysis contributes only ∼6% of cellular ATP via substrate-level phosphorylation, its regulation by enzymes such as hexokinase (HEX), phosphofructokinase (PFK), and pyruvate kinase (PK) is crucial. Pyruvate dehydrogenase (PDH) and pyruvate carboxylase (PC) further link glycolysis to mitochondrial metabolism. Traditionally considered a waste product of anaerobic metabolism, lactate is now recognized as a critical energy source. It is converted to pyruvate by lactate dehydrogenase (LDH) and utilized by muscles, the heart, and the brain for oxidative phosphorylation, particularly during exercise or metabolic stress (Chaudhry and Varacallo, 2023).

Lactate, first identified in sour milk through microbial fermentation, becomes the predominant metabolite in mammals when oxygen and ATP demands surpass supply. Contrary to its reputation as a metabolic waste product, lactate is now understood as a key circulating carbohydrate fuel. By balancing the NADH/NAD+ ratio, lactate serves as both an energy substrate and a redox buffer, facilitating metabolic flexibility. This shift in perspective redefines lactate’s role in energy metabolism (Li et al., 2022).

During physical exertion, skeletal muscles and the heart preferentially utilize lactate over glucose and fatty acids. In the brain, the Astrocyte-Neuron Lactate Shuttle (ANLS) facilitates lactate transfer from astrocytes to neurons, promoting energy metabolism and neuroprotection (Cauli et al., 2023). Recent findings challenge the notion that lactate is merely converted to pyruvate in the cytosol; instead, it is processed in mitochondria via the Mitochondrial Lactate Oxidation Complex (mLOC), particularly in high-energy-demand tissues (Chen et al., 2016).

In resting humans, the lactate-to-pyruvate (L/P) ratio is ∼10, increasing to ∼500 during moderate exercise, underscoring lactate’s role in metabolic adaptation. Major lactate utilization pathways include intramuscular oxidation, cardiac uptake, and hepatic gluconeogenesis (Liu et al., 2025).

An inverse relationship exists between lactate and plasma free fatty acids (FFAs) during exercise. Lactate inhibits lipolysis in adipose tissue via Hydroxycarboxylic Acid Receptor 1 (HCAR1), modulating cAMP and CREB signaling pathways. Additionally, lactate impacts mitochondrial fatty acid oxidation by increasing acetyl-CoA and malonyl-CoA levels, inhibiting β-oxidation (Liu et al., 2009).

Lactate-induced secretion of Transforming Growth Factor Beta 2 (TGF-β2) from adipose tissue enhances glucose tolerance, highlighting its role in interorgan metabolic communication. These findings emphasize lactate’s dual role in acute metabolic regulation and long-term adaptation (Liu et al., 2025).

Neurons rely on astrocytes for metabolic support. While glucose remains the primary fuel, lactate serves as an essential alternative, particularly during hypoglycemia or ischemic stress. Lactate supplementation enhances recovery from traumatic brain injury (TBI) and supports memory formation by modulating epigenetic mechanisms and brain-derived neurotrophic factor (BDNF) expression. Lactate metabolism is altered in neurodegenerative diseases like Alzheimer’s and Parkinson’s, with reduced lactate transport linked to cognitive decline. Enhancing lactate availability may offer therapeutic benefits in restoring metabolic balance and neuroprotection (Beard et al., 2022).

Beyond metabolism, lactate functions as a signaling molecule influencing angiogenesis, tissue repair, and gene expression. It activates G-protein coupled receptors such as HCAR1, regulating neuroprotection and lipid metabolism. A novel post-translational modification, histone lactylation, links lactate to gene regulation (Figure 2). Increased lactate production under hypoxia or bacterial infections drives histone lactylation, influencing macrophage polarization, tumor progression, and inflammation resolution. These positions lactate as a crucial metabolic and epigenetic regulator with broad physiological and pathological implications (Zhang et al., 2019).

Lactate stabilizes HIF-1α, promoting angiogenesis and metabolic adaptation under low-oxygen conditions. Lactate signaling plays a central role in tumor metabolism and immune evasion; thus, its targeting represents an emerging avenue for cancer therapeutics (Gu et al., 2025).

Lactate modulates mitochondrial biogenesis and endurance adaptations through AMP-activated protein kinase (AMPK) and PGC-1α signaling. It also influences immune responses, shaping macrophage polarization and cytokine production, with implications for inflammation, metabolism, and disease progression (Takeda et al., 2022).

Lactic Acid Bacteria (LAB) have adapted to survive in different environments, including the human gut, by relying primarily on fermentation for energy production. Unlike many other bacteria, LAB cannot perform respiration because they lack functional cytochromes, which are essential for oxidative metabolism. Instead, they obtain energy by breaking down sugars into lactic acid, which acidifies their surroundings and helps them outcompete harmful bacteria (Wang et al., 2020).

LAB have evolved unique metabolic pathways that enable their survival in diverse environments, particularly within the human gut. Among these pathways, amino acid deamination serves as a crucial mechanism for energy production, allowing LAB to thrive in nutrient-poor conditions by converting amino acids into usable energy. Additionally, acid decarboxylation plays a fundamental role in maintaining pH balance, which is essential for LAB survival in acidic environments such as the gastrointestinal tract (Feng and Wang, 2020).

Beyond their metabolic adaptability, LAB engage in intricate interactions with host cells, significantly influencing gut health and immune function. Through cross-talk with the host, LAB can modulate intestinal gene expression, thereby impacting digestive processes and immune responses. Furthermore, LAB contributes to gut homeostasis by producing bioactive compounds, such as gamma-aminobutyric acid (GABA), which not only relaxes gut smooth muscles but also has broader implications for mood regulation. Another essential feature of LAB is their antimicrobial effect, primarily mediated by lactic acid production. It acidifies the gut environment and inhibits the growth of pathogenic bacteria, thereby fostering a balanced microbiome (Yu et al., 2024).

Lactate plays a dual role in gut health. On the one hand, it serves as an important metabolic intermediate, supporting the growth of lactate-consuming bacteria, which convert it into beneficial SCFAs (Table 4). On the other hand, excessive lactate accumulation can lead to acidosis, which disrupts microbial stability. This phenomenon is well-documented in ruminants, where diets rich in fermentable carbohydrates can promote the overgrowth of lactate-producing bacteria, causing a dangerous drop in pH and leading to metabolic disorders such as lactic acidosis. In the human gut, lactate metabolism is tightly regulated through cross-feeding interactions between different bacterial species (Yu et al., 2024).

Lactate plays a significant role in gut health, immunity, and disease prevention. If lactate-consuming bacteria are insufficient, lactate can accumulate, leading to a drop in pH and potential gut dysbiosis. Excess lactate has been linked to inflammatory bowel diseases (IBD), irritable bowel syndrome (IBS), and metabolic disorders (Wang et al., 2020). Colonocytes (intestinal cells) utilize lactate to produce butyrate through cross-feeding by bacteria such as Eubacterium and Anaerostipes, which strengthen the gut lining and support overall intestinal health. Lactate lowers the pH, inhibiting harmful bacteria (Escherichia coli, Salmonella) while promoting beneficial microbes (Bifidobacteria, Akkermansia) (Zhao et al., 2024). Additionally, lactate helps regulate immune responses by modulating immune cells and reducing inflammatory cytokines (TNF-α, IL-6), preventing excessive inflammation (Llibre et al., 2025).

Recent studies highlight the pivotal role of lactate and its receptor, GPR81, in regulating intestinal homeostasis and immune responses, particularly in inflammatory bowel diseases (IBD) (Ranganathan et al., 2018). Understanding these metabolic pathways and their microbial contributors provides valuable insight into potential probiotic interventions aimed at promoting gut health and preventing dysbiosis-associated diseases (Li et al., 2022).

In Plasmodium falciparum (the parasite responsible for malaria), the enzyme pfLDH is essential for energy production, as the parasite relies on anaerobic glycolysis due to the absence of a citric acid cycle. Inhibitors of pfLDH could potentially lead to the death of the malaria parasite (Penna-Coutinho et al., 2011). Similarly, in cancer, human LDH isoform-5 (hLDH-5 or LDH-A) is upregulated in tumor cells, supporting the Warburg effect, where tumors rely more on anaerobic glycolysis than oxidative phosphorylation for energy. Targeting hLDH-5 could disrupt tumor growth and invasiveness (Alam et al., 2014).

While lactate serves as a critical metabolic intermediate, excessive accumulation can lead to lactic acidosis, a pathological condition characterized by a decrease in blood pH. This occurs in cases of severe hypoxia, sepsis, or mitochondrial dysfunction, where lactate clearance is impaired. Studies have shown that elevated lactate levels in critically ill patients are associated with poor outcomes due to systemic metabolic disturbances (Table 3) (Li et al., 2022). Recently, research highlighted the role of excessive lactate in disrupting cellular homeostasis, leading to impaired enzyme function and metabolic stress (Cai et al., 2024).

Excessive lactate accumulation, as detailed in Table 3, has significant implications for human health by contributing to the progression of various diseases. In cancer, elevated lactate levels promote tumor growth through enhanced glycolysis and suppression of immune responses, affecting multiple organs (de la Cruz-López et al., 2019) (Table 3). Lactate buildup can also activate inflammatory pathways and cytokine release, leading to increased inflammation in the immune system and other tissues (Llibre et al., 2025) (Table 3). Metabolic disorders arise when high lactate concentrations disrupt glucose and lipid metabolism, particularly impacting the liver, muscles, and adipose tissue (Ishitobi et al., 2019). In skeletal muscles, lactate accumulation results in acidosis and impairs muscle contraction, contributing to muscle fatigue (Chen et al., 2025) (Table 3). The brain is also vulnerable, as lactate buildup may play a role in neurological diseases such as epilepsy and Alzheimer’s (Cai et al., 2022) (Table 3). Lastly, in the heart, elevated lactate can reduce oxygen availability and increase the risk of ischemia (Fang et al., 2024) (Table 3). This summary underscores the multifaceted and detrimental effects of excess lactate on various organ systems.

The Warburg effect, a hallmark of cancer metabolism, leads to high lactate production, which significantly alters the tumor microenvironment. Accumulated lactate promotes immune evasion, angiogenesis, and metastasis by modulating tumor-associated macrophages and regulatory T cells. Studies have shown that lactate enhances HIF-1α stabilization, upregulating VEGF expression and supporting tumor growth. In study showed that targeting lactate transporters, such as MCT1 and MCT4, can disrupt tumor metabolism and enhance the efficacy of cancer therapies (Zhong et al., 2022).

Elevated lactate levels are frequently observed in cardiovascular diseases, especially in conditions like heart failure and ischemic injury, where tissue hypoxia impairs oxidative metabolism. The heart preferentially oxidizes lactate as an energy source under normal conditions; however, in pathological states, excessive lactate accumulation can contribute to acidosis and impaired myocardial function (Ouyang et al., 2023). A study illustrated that heart failure patients exhibit altered lactate metabolism, leading to reduced cardiac efficiency (Revelly et al., 2005). Moreover, lactate-driven inflammation in vascular endothelial cells has been implicated in atherosclerosis progression, highlighting the need for therapeutic strategies targeting lactate balance in cardiovascular health (Dong et al., 2021).

Dysregulated lactate metabolism has been implicated in neurodegenerative diseases, including Alzheimer’s, Parkinson’s, and multiple sclerosis. While lactate plays a neuroprotective role under physiological conditions, impaired lactate transport and utilization can contribute to neuronal energy deficits and oxidative stress (Yang et al., 2024). A research study demonstrated that disruptions in the astrocyte-neuron lactate shuttle lead to cognitive impairment (Suzuki et al., 2011). Furthermore, excessive lactate accumulation in the brain has been associated with neuroinflammation and excitotoxicity, exacerbating disease progression in conditions such as epilepsy and traumatic brain injury (Roh et al., 2023).

In individuals with muscular dystrophy and metabolic myopathies, lactate metabolism is often impaired, leading to exercise intolerance and muscle fatigue. Mutations affecting glycolytic enzymes or lactate transporters result in an inability to efficiently clear lactate, leading to muscle damage and weakness (Jeppesen et al., 2013). A study highlighted the role of lactate accumulation in muscle dysfunction, emphasizing its contribution to oxidative stress and mitochondrial impairment. Therapeutic approaches aimed at optimizing lactate metabolism are being explored to improve muscle function in dystrophic conditions (Tarnopolsky, 2018; Wen et al., 2025).

While many lactate-producing bacteria play beneficial roles in maintaining gut homeostasis, certain species can contribute to dysbiosis and inflammation when their growth is dysregulated (Louis et al., 2022). For instance, an overgrowth of Lactobacillus or Enterococcus species can lead to excessive lactate accumulation, which may exacerbate gastrointestinal conditions such as IBS, IBD, and even metabolic diseases like obesity. In these cases, the excess lactate can lower gut pH, leading to an imbalance in the microbiota and promoting the growth of pathogenic bacteria (Figure 3; Table 4) (Portincasa et al., 2024).

The Table 4 highlights the beneficial roles of various gut bacteria in human health through their mechanisms of lactate production. Lactobacillus spp. (including L. acidophilus and L. casei) ferment carbohydrates to produce lactate, which helps maintain gut acidity, supports digestion, and prevents pathogenic overgrowth by enhancing immune function and barrier integrity. Bifidobacterium spp. generate lactate from dietary fibers and oligosaccharides, modulating the gut microbiota, improving gut health, and exerting anti-inflammatory effects by promoting the production of beneficial short-chain fatty acids. Faecalibacterium prausnitzii converts carbohydrates into lactate and butyrate, supporting a balanced microbiome and enhancing anti-inflammatory responses, thereby strengthening gut barrier function. Lactobacillus plantarum produces lactic acid under anaerobic conditions, promoting gut barrier integrity and potentially aiding in the management of irritable bowel syndrome (IBS) and other inflammatory conditions. Together, these bacteria contribute significantly to gut health by modulating inflammation, supporting digestion, and maintaining a balanced microbiome (Table 4).