The study, led by Nuttapong Yawoot and corresponding author Sakara Tunsophon of Naresuan University, in collaboration with researchers at the Thailand Institute of Scientific and Technological Research, focused on muscle atrophy induced by dexamethasone, a synthetic glucocorticoid widely used as an anti-inflammatory and immunosuppressive drug. Dexamethasone is a mainstay of modern medicine, prescribed for conditions ranging from autoimmune disorders to severe respiratory infections, but one of its well-known side effects is the progressive loss of skeletal muscle mass. Patients on prolonged steroid therapy often experience weakness, frailty, and impaired physical function, a burden that currently has few targeted interventions. The Thai team set out to determine whether mung bean protein, enzymatically broken down into smaller, bioavailable peptides, could blunt this process.

The investigation was conducted at two levels, beginning with cell culture experiments. The researchers used C2C12 myotubes, a widely employed laboratory model derived from mouse skeletal muscle that allows investigators to study muscle differentiation and metabolism in a controlled environment. These myotubes were treated with graded concentrations of mung bean hydrolysates for periods of 24 and 48 hours. The team then measured a comprehensive panel of parameters: cell viability, proliferation, membrane toxicity, lactate dehydrogenase activity, intracellular ATP concentration, glucose consumption, and the expression of key genes governing muscle identity and growth.

The cellular results were encouraging. Myotubes exposed to mung bean hydrolysates showed increased expression of myosin heavy chain 1, or Myh1, a structural protein gene whose expression reflects mature muscle fiber function and myogenic activity. At the same time, ATP concentrations inside the cells rose, indicating enhanced energy generation within the muscle cells. Notably, the hydrolysates did not impair membrane integrity or reduce cell viability, which the researchers confirmed by assessing lactate dehydrogenase leakage, a standard marker of cytotoxicity. Together, these data suggested that the mung bean peptides were not merely benign but actively supportive of muscle cell metabolism and maturation.

Encouraged by these in vitro findings, the team moved to an animal model. Sprague Dawley rats were divided into five experimental groups: a healthy control group, a group receiving dexamethasone alone, two groups receiving dexamethasone together with mung bean protein hydrolysates at doses of either 250 or 500 milligrams per kilogram per day, and a comparison group receiving dexamethasone with branched-chain amino acids, or BCAAs, at 600 milligrams per kilogram per day. BCAAs, comprising leucine, isoleucine, and valine, are among the most heavily marketed muscle-preserving supplements, making them a meaningful benchmark against which to judge the mung bean extract. After ten days of dexamethasone administration, the researchers assessed body weight, muscle mass, and muscle strength, and collected muscle tissue for molecular and biochemical analysis.

The results were striking. Rats treated with dexamethasone and mung bean hydrolysates showed significantly improved muscle strength and tension compared with animals receiving the steroid alone. The researchers also observed improvements in insulin sensitivity, a finding linked to the muscle’s ability to take up glucose from the blood and store it as glycogen. This metabolic benefit is significant because skeletal muscle is the body’s largest site of glucose disposal, and steroid-induced atrophy frequently coexists with impaired glucose handling. By improving both glucose uptake and glycogen storage, the mung bean hydrolysates appeared to support the muscle’s energetic foundations even while the drug was still being administered.

At the molecular level, the hydrolysates shifted the delicate balance between protein synthesis and protein degradation that determines whether muscle grows or shrinks. Skeletal muscle mass is governed by a continuous turnover process: proteins are constantly being built up through synthesis pathways, including the mammalian target of rapamycin, or mTOR, signaling axis, and broken down through degradation systems such as the ubiquitin-proteasome pathway, in which markers like TRIM63, also known as muscle RING-finger protein 1, play a central role. The study documented a significant increase in protein synthesis markers alongside a decrease in protein degradation markers in the treated animals, effectively tilting the scales back toward muscle preservation. In the cell culture experiments, the hydrolysates also influenced myostatin, or Mstn, a powerful negative regulator of muscle growth whose suppression is a recognized strategy for combating wasting conditions.

Perhaps the most novel aspect of the study concerns oxidative stress. Glucocorticoid-induced muscle wasting is associated with the excessive production of reactive oxygen species, which damage cellular components and trigger the breakdown of muscle proteins. The researchers measured malondialdehyde, or MDA, a well-established byproduct of lipid peroxidation that serves as a chemical fingerprint of oxidative damage. In atrophic muscles from the mung bean-treated rats, MDA levels were significantly reduced. Concurrently, the activity of endogenous antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, increased. These enzymes form the cell’s first line of defense against reactive oxygen species, and their induction suggests that the mung bean peptides activated the muscle’s own antioxidant machinery rather than simply acting as passive scavengers. The study also points to the involvement of nuclear factor erythroid 2-related factor 2, or Nrf2, the master transcription factor that orchestrates cellular antioxidant responses.

The authors conclude that mung bean hydrolysates effectively enhanced myogenesis and ATP generation while mitigating oxidative stress and muscle degradation, resulting in improved muscle function in the atrophy model. The dual action, simultaneously supporting protein synthesis and defending against oxidative damage, distinguishes the hydrolysates from interventions that target only one side of the atrophy equation. The fact that a modest daily dose of a plant-derived protein supplement produced measurable benefits in a matter of days adds to the translational appeal.

Several practical considerations follow from the work. Mung beans are inexpensive, widely cultivated across Asia, and already consumed as a protein source in many cultures, which could ease the path from laboratory to functional food or nutraceutical. The enzymatic hydrolysis process used to produce the peptides enhances their bioavailability by breaking intact proteins into shorter fragments that are more readily absorbed in the gut. The researchers used high-performance liquid chromatography to characterize the hydrolysates, ensuring the consistency of the material administered in their experiments. Still, important caveats remain. The study was conducted in rats over a relatively short ten-day treatment window, and dexamethasone-induced atrophy, while a clinically relevant model, does not capture every form of human muscle wasting. Whether comparable benefits can be achieved in humans, at what doses, and with what long-term safety profile, will require clinical trials that have not yet been performed.

The research also carries implications beyond steroid therapy. Muscle atrophy is a central feature of sarcopenia, the age-related loss of muscle mass and strength that affects hundreds of millions of older adults worldwide, as well as of cachexia in cancer and chronic disease. Interventions that safely promote muscle protein synthesis, improve glucose metabolism, and reduce oxidative stress are urgently sought across all of these fields. A dietary component as accessible as the humble mung bean, if validated in human studies, could become a low-cost tool in a much larger arsenal.

For now, the Thai team’s contribution lies in mapping the mechanisms: showing that plant-derived peptides can act on muscle cells in culture, strengthen atrophic muscle in living animals, rebalance protein turnover, and activate antioxidant defenses. The work was supported by the Thailand Institute of Scientific and Technological Research, the National Science, Research, and Innovation Fund, Naresuan University research funds, and the Center of Excellence for Innovation in Chemistry. The underlying data and methods are openly available under a Creative Commons license, allowing other laboratories to replicate and extend the findings. As interest in plant-based functional foods continues to accelerate, this study adds muscle health to the growing list of potential benefits attributed to one of the world’s oldest cultivated legumes.

FFAR4 is a membrane receptor that senses long-chain fatty acids, classically implicated in metabolic control. Here, the team shows that when FFAR4 signals through Gαq, downstream pathways change gene-expression programs tied to lipid handling and insulin sensitivity. Instead of merely adjusting energy balance, the mechanism interrupts a transcriptional network that normally supports metabolic imbalance.

A central finding is that FFAR4–Gαq activation perturbs Nr1h3 (also known as LXRα) signaling, thereby disturbing the downstream communication to PPARγ. PPARγ is a master regulator of adipocyte differentiation and lipid uptake, and it is frequently discussed in the context of insulin resistance and metabolic syndrome. By disrupting this axis, FFAR4 activation shifts metabolic behavior toward a more protected state.

Mechanistically, the authors connect receptor-level signaling to nuclear transcriptional outcomes. The study suggests that changes in Nr1h3 activity alter PPARγ-driven transcription, reducing the expression of gene programs that contribute to dysfunctional metabolic phenotypes. This provides a coherent pathway linking extracellular fatty acid detection to intracellular, genome-scale metabolic control.

The researchers also emphasize functional outcomes in metabolic systems, reporting improvements consistent with suppressed disease-associated dysfunction. While the specific experimental models span multiple layers of validation, the theme is consistent: FFAR4 engagement through Gαq produces protective metabolic effects.

Importantly for translational interest, the findings highlight a direction for therapeutic strategy: rather than broadly modulating fatty acid receptors, selectively steering FFAR4 signaling toward Gαq could achieve more targeted rewiring of transcriptional control.

Overall, the study presents FFAR4–Gαq as a lever that can disrupt the Nr1h3–PPARγ axis, offering a viral-sounding new angle on metabolic disease intervention. By connecting membrane sensing to nuclear metabolic regulation, it expands the repertoire of actionable nodes within the fatty acid signaling network.

Subject of Research: Metabolic dysfunction; fatty acid receptor signaling; transcriptional regulation (Nr1h3–PPARγ axis).

Article Title: Gα_q activation of free fatty acid receptor 4 suppresses metabolic dysfunction by disrupting Nr1h3-PPARγ axis.

Article References: Kong, Y., Wang, J., Wang, Z. et al. Gα_q activation of free fatty acid receptor 4 suppresses metabolic dysfunction by disrupting Nr1h3-PPARγ axis. Nat Commun (2026). https://doi.org/10.1038/s41467-026-75589-2

Image Credits: AI Generated

Type 1 diabetes is a chronic autoimmune condition characterized by the destruction of insulin-producing beta cells in the pancreas, necessitating lifelong exogenous insulin administration. Insulin’s pivotal role is to facilitate the transport of glucose from the bloodstream into muscle and liver tissue, where it is metabolized for energy. Absent adequate insulin, hyperglycemia ensues, predisposing individuals to a spectrum of acute and long-term complications. However, the degree of insulin required varies among patients, influenced not only by endogenous production capacity but also by insulin sensitivity—the efficiency by which cells respond to insulin’s signaling.

The phenomenon of insulin resistance, commonly associated with type 2 diabetes, is increasingly recognized in subsets of people with type 1 diabetes, complicating glycemic control. Dietary fat intake is known to exacerbate this resistance by impeding glucose uptake at the cellular level. Against this backdrop, the Physicians Committee’s investigation focused on how a low-fat vegan diet, which minimizes animal-derived fats and incorporates plentiful plant-based carbohydrates and fiber, impacts insulin sensitivity and overall insulin usage.

The study juxtaposed two dietary regimes over a 12-week period: a low-fat vegan diet without restrictions on caloric or carbohydrate intake, and a traditionally recommended portion-controlled diet. Remarkably, participants adhering to the vegan diet experienced a notable 28% reduction in their total daily insulin dose, equating to an average decrease of 12.1 units. Conversely, the portion-controlled group showed no meaningful change in insulin requirements during the trial period. This pronounced difference signals a substantial dietary influence on metabolic insulin demands intrinsic to type 1 diabetes management.

Importantly, the observed decrement in insulin dose within the vegan cohort implies enhanced insulin sensitivity. Improved sensitivity means cells respond more effectively to the insulin administered, facilitating glucose transport and utilization without necessitating higher doses. This metabolic improvement carries profound clinical significance, potentially translating into fewer hypoglycemic events, better glycemic control, and mitigation of insulin-induced side effects.

Economic implications accompany these physiological benefits. The research documented an average 27% reduction in insulin costs for participants following the vegan dietary regimen—a daily saving of approximately $1.08. While this amount may seem modest on a daily basis, extrapolated over a year and across the millions affected by type 1 diabetes, the cost-saving potential is enormous, particularly as insulin prices continue their steep ascent in the United States. Over the past decade, insulin spending has more than tripled, attributed partly to both increased demand and the skyrocketing unit price, with a 24% inflation-adjusted rise from 2017 to 2022 alone.

The comprehensive 2024 clinical trial underpinning this secondary analysis delineated additional metabolic and health benefits associated with the low-fat vegan diet. Participants not only improved insulin sensitivity but also attained an average weight loss of 11 pounds. Improvements in glycemic control parameters further confirmed the diet’s efficacy, while favorable shifts in cholesterol profiles and kidney function suggested broad-spectrum benefits, extending beyond glucose metabolism to cardiovascular and renal health—two domains frequently compromised in diabetes.

At the mechanistic level, the plant-based diet’s low fat content likely mitigates lipotoxic effects that impair insulin signaling pathways. Plant foods rich in fiber, antioxidants, and phytochemicals may further enhance endothelial function and reduce systemic inflammation, factors that synergistically augment insulin action. Moreover, the absence of animal fats decreases saturated fat intake—a known contributor to insulin resistance—fostering an environment conducive to improved glucose homeostasis.

This evidence emerges at a crucial juncture, given the escalating financial burden insulin imposes on patients and healthcare systems alike. The findings advocate for dietary modifications as a practical, non-pharmacologic avenue to optimize insulin therapy, potentially transforming standard care practices for type 1 diabetes. The clinical implications are vast: by embracing a low-fat vegan diet, patients could achieve better glycemic metrics, reduce insulin dosages, and consequently ease the economic stress of diabetes management.

Dr. Hana Kahleova, MD, PhD, lead author and director of clinical research at the Physicians Committee for Responsible Medicine, emphasizes the urgent need to disseminate knowledge about this dietary approach. She underscores that in light of rising insulin costs, the adoption of a low-fat vegan diet could be a strategic measure to improve patient outcomes and financial accessibility. Her assertion ignites renewed discourse on integrating nutritional science within therapeutic frameworks traditionally dominated by pharmacology.

The scientific community has increasingly recognized the profound impact of dietary patterns on chronic disease modulation. This study’s robust methodology—a randomized controlled trial—strengthens the validity of the findings, setting a precedent for further large-scale trials to refine dietary guidelines catering to type 1 diabetes specifically. Historically, dietary recommendations for type 1 diabetes have focused predominantly on carbohydrate counting and portion control; the inclusion of fat reduction and plant-based eating enriches this paradigm.

While the study represents significant progress, it invites exploration into the long-term sustainability of the vegan dietary approach and replicability across diverse patient populations with varying demographic and clinical profiles. Further research may unravel whether similar benefits extend to those with advanced diabetes complications or concomitant autoimmune disorders, potentially broadening the diet’s applicability.

In summary, this pioneering research illuminates the powerful intersection of diet and endocrinology, demonstrating that a low-fat vegan diet can be a pivotal adjunct in type 1 diabetes management. By improving insulin sensitivity, enabling insulin dose reduction, and delivering tangible cost savings, this nutritional strategy holds transformative potential for millions worldwide facing the daily challenges of insulin dependency. As the healthcare community confronts escalating insulin costs and the complexities of diabetes care, such innovative, evidence-based dietary interventions are poised to redefine paradigms and empower patients towards better health and economic outcomes.

Subject of Research: People

Article Title: Can a vegan diet help people with type 1 diabetes save on insulin? A secondary analysis of a 12-Week randomized clinical trial

News Publication Date: 14-Oct-2025

Web References:
– https://bmcnutr.biomedcentral.com/articles/10.1186/s40795-025-01175-2
– https://diabetesjournals.org/clinical/article/42/3/419/154329/Effect-of-a-Dietary-Intervention-on-Insulin

References:
– Physicians Committee for Responsible Medicine, 2024 Clinical Trial Data
– American Diabetes Association, Insulin Spending Statistics (2022)

Keywords: Type 1 diabetes, insulin sensitivity, low-fat vegan diet, insulin costs, randomized clinical trial, glycemic control

In the modern world, diabetes has emerged as one of the most pressing health concerns, with millions of individuals affected globally. The rise in insulin resistance, a hallmark of type 2 diabetes, underscores the necessity for innovative treatment modalities. Researchers have long been exploring natural compounds that could potentially mitigate these health issues. Ginsenoside Rf, a bioactive compound derived from ginseng, has attracted considerable attention for its promising pharmacological effects, particularly in metabolic regulation.

The novel research zeroes in on the role of Ginsenoside Rf in insulin-resistant AML12 cells, a common model used to study glucose metabolism and insulin actions. By employing advanced biochemical methodologies and in-depth analyses, the authors meticulously dissect the underlying mechanisms by which Ginsenoside Rf exhibits its beneficial effects on glucose metabolism and insulin sensitivity. This study significantly contributes to the existing literature on herbal medicine and its application in managing metabolic diseases.

One of the crucial findings of this study revolves around the signaling pathways involved in glucose metabolism. The researchers elucidated that Ginsenoside Rf activates the IRS/PI3K/Akt signaling pathway, which is vital for insulin signaling and mediating glucose uptake in cells. This activation leads to enhanced glucose uptake, providing a critical mechanism by which Ginsenoside Rf exerts its metabolic effects. The authors meticulously describe how this signaling cascade plays a role in promoting insulin sensitivity and improving glucose homeostasis in insulin-resistant settings.

Additionally, the study highlights the involvement of the PPARα/PGC1α signaling pathway. Peroxisome proliferator-activated receptors (PPARs), particularly PPARα, are known for their roles in lipid metabolism and energy homeostasis. By engaging this pathway, Ginsenoside Rf not only enhances glucose metabolism but also facilitates the regulation of fatty acid oxidation. The combined activation of both IRS/PI3K/Akt and PPARα/PGC1α pathways suggests a multifaceted approach through which Ginsenoside Rf can combat insulin resistance and improve overall metabolic health.

The implications of these findings are profound. Understanding the dual action of Ginsenoside Rf on both glucose and lipid metabolism provides a holistic view of managing insulin resistance. This highlights the therapeutic potential of employing natural compounds in addressing complex metabolic conditions. The promising results from the in vitro model may warrant further exploration in vivo, leading researchers to consider clinical trials to substantiate these effects in human populations.

Moreover, the safety profile of Ginsenoside Rf further augments its appeal as a therapeutic candidate. Natural products historically have been associated with fewer side effects than synthetic compounds. This presents a significant advantage, especially for individuals who are sensitive to pharmaceuticals or are looking for adjunct therapies to enhance conventional treatments for diabetes.

The study also opens avenues for future research. Exploring the synergistic effects of Ginsenoside Rf with other therapeutic agents could amplify its benefits. Moreover, investigating the pharmacokinetics and optimal dosing regimens will be critical steps in translating these laboratory findings into clinical practice. The potential to incorporate Ginsenoside Rf into dietary recommendations or as a supplement could offer a revolutionary approach to managing insulin resistance.

Furthermore, the broader implications of this research extend beyond diabetes management. As the world grapples with increasing obesity rates and metabolic syndrome prevalence, Ginsenoside Rf could serve as a core component in preventive strategies. Public health interventions aimed at reducing the risk of metabolic diseases could benefit from including such natural agents in lifestyle recommendations.

It’s paramount to acknowledge that while the results are promising, additional research is necessary to fully comprehend the extent of Ginsenoside Rf’s effects and to clarify its mechanisms further. Long-term studies and clinical trials will be crucial in establishing not only efficacy but also safety in diverse populations.

In conclusion, the work spearheaded by Hong et al. represents a significant leap towards understanding the impact of Ginsenoside Rf on glucose metabolism in insulin-resistant settings. Their findings could herald a new chapter in the management of metabolic disorders, with the potential for Ginsenoside Rf to emerge as a vital ally in improving insulin sensitivity and overall health. The integration of such natural compounds into therapeutic regimes holds hope for a future where metabolic diseases can be more effectively managed through holistic and integrative approaches.

Ultimately, as the scientific community continues to unravel the complexities of metabolism and its disruptions, Ginsenoside Rf stands out as a beacon of hope—a testament to the potential of nature in combating the growing epidemic of diabetes and related conditions.

Subject of Research: Insulin resistance and glucose metabolism improvement via Ginsenoside Rf.

Article Title: Ginsenoside Rf improves glucose metabolism via the IRS/PI3K/Akt and PPARα/PGC1α signaling pathways in insulin-resistant AML12 cells.

Article References:

Hong, S., Lee, J., Choi, S.Y. et al. Ginsenoside Rf improves glucose metabolism via the IRS/PI3K/Akt and PPARα/PGC1α signaling pathways in insulin-resistant AML12 cells.
BMC Complement Med Ther 25, 340 (2025). https://doi.org/10.1186/s12906-025-05091-7

Image Credits: AI Generated

DOI: https://doi.org/10.1186/s12906-025-05091-7

Keywords: Ginsenoside Rf, insulin resistance, glucose metabolism, IRS/PI3K/Akt signaling, PPARα/PGC1α pathways, diabetes management.

Carnosine, a naturally occurring dipeptide composed of beta-alanine and histidine, has captured the interest of researchers due to its purported antioxidant properties and potential role in cellular aging. The exploration of carnosine supplementation offers a glimpse into its multifaceted effects on glucose metabolism and insulin sensitivity, particularly in the context of prediabetes and type 2 diabetes. These conditions are characterized by impaired insulin action and relative insulin deficiency, which can lead to significant complications if not managed effectively.

On the other hand, beta-alanine, another amino acid, is primarily known for its role as a precursor to carnosine and its established benefits in exercise performance and muscle endurance. However, emerging evidence suggests that beta-alanine may also enhance glucose uptake and improve metabolic parameters in individuals with insulin resistance. This dual action makes both supplements worthy of comprehensive examination, especially as demographic trends indicate rising rates of type 2 diabetes globally.

The systematic review of randomized controlled trials scrutinized diverse study designs, patient demographics, and intervention protocols to convey a thorough assessment of the impact of these supplements. The analysis included scrutinizing biochemical markers indicative of glycemic control, lipid profiles, and general metabolic health. Such markers are critical in determining the validity of carnosine and beta-alanine supplementation as effective therapeutic strategies.

Critically, different trials exhibited varying methodologies that could affect their outcomes. Several studies focused on short-term interventions, while others evaluated long-term supplementation, underscoring the necessity for standardized protocols in future research to ascertain definitive conclusions. Importantly, the review highlighted the need for recognizing individual variability in response to supplementation, which can be influenced by genetic, lifestyle, and dietary factors.

Among the compelling findings of this meta-analysis was the observation that participants receiving carnosine displayed improved glycemic control, demonstrated by reduced fasting blood glucose and HbA1c levels. These changes suggest a potential for carnosine to enhance pancreatic function or improve peripheral insulin sensitivity. Such insights are particularly relevant given the complex nature of diabetes management, which extends beyond medications to involve lifestyle interventions.

Conversely, the results pertaining to beta-alanine were equally promising, showing that its supplementation contributed to favorable changes in lipid profiles and enhanced insulin sensitivity. The molecular mechanisms underlying these effects are still being deciphered but could involve the modulation of key signaling pathways linked to glucose metabolism. Further research is needed to explore these pathways in greater detail, which may lead to significant therapeutic advancements.

Furthermore, the review incorporated an analysis of side effects and tolerability. Initial concerns regarding the safety of high-dose supplementation were alleviated as studies demonstrated that moderate doses of both carnosine and beta-alanine were generally well tolerated, with minimal adverse effects reported. This aspect is vital, especially when considering long-term administration as an adjunct therapy for chronic conditions such as diabetes.

The influence of diet and lifestyle on the effectiveness of these supplements cannot be understated. Efficacy may vary in the context of accompanying dietary intake, physical activity levels, and existing nutritional deficiencies. The complexities of individual metabolic responses highlight the importance of holistic approaches that consider environmental and behavioral factors alongside nutritional supplementation.

While the potential of carnosine and beta-alanine in diabetes management appears encouraging, the researchers emphasized that these supplements should not replace existing treatment modalities but rather act as complementary options. Future clinical guidelines may need to incorporate these findings as part of multi-faceted treatment plans to better address the intricacies of diabetes care.

In conclusion, the systematic review and meta-analysis underscore the therapeutic potential of carnosine and beta-alanine in improving health outcomes for individuals with prediabetes and type 2 diabetes. This innovative research adds weight to the growing body of evidence supporting the role of nutritional supplementation in metabolic disease management. The exploration of these supplements may not only enhance patient quality of life but could also offer new insights into preventive strategies against the broader epidemic of diabetes.

As we advance, it becomes essential for researchers, healthcare providers, and patients to remain informed about these developments. Continuous investigation into commonplace dietary substances opens up discussions around treatment methods that are not only effective but also align with patient preferences and lifestyles. The intersection of nutrition and diabetes management represents a fertile ground for future research, promising to enhance the quality of care that is both effective and sustainable.

Ultimately, with diabetes affecting vast segments of the global population, innovative approaches such as the investigation of carnosine and beta-alanine supplementation present an exciting frontier. Harnessing these findings could lead to not only improved glycemic control but may also inspire the development of integrative practices that embrace the holistic management of metabolic health.

Subject of Research:
The effects of carnosine and beta-alanine supplementation in managing prediabetes and type 2 diabetes mellitus.

Article Title:
Effect of carnosine or beta-alanine supplementation therapy for prediabetes or type 2 diabetes mellitus: a systematic review and meta-analysis of randomized controlled trials.

Article References:

Li, N., Yan, X., Lin, J. et al. Effect of carnosine or beta-alanine supplementation therapy for prediabetes or type 2 diabetes mellitus: a systematic review and meta-analysis of randomized controlled trials.
BMC Endocr Disord 25, 210 (2025). https://doi.org/10.1186/s12902-025-02016-w

Image Credits: AI Generated

DOI: 10.1186/s12902-025-02016-w

Keywords:
carnosine, beta-alanine, prediabetes, type 2 diabetes, supplementation, systematic review, meta-analysis, glycemic control, insulin sensitivity.