bims-kimdis 2025-01-12 papers

bims-kimdis

Biomed News

on Ketones, inflammation and mitochondria in disease

Issue of 2025–01–12
seventeen papers selected by
Matías Javier Monsalves Álvarez, Universidad Andrés Bello

Effect of ketosis induced by on delayed-onset muscle soreness, inflammation and redox status: a randomized, open-label, crossover pilot study.
Effects of the Ketogenic Diet on Microbiota Composition and Short-Chain Fatty Acids in Women with Overweight/Obesity.
Cannabis (THC) Aggravates the Deleterious Effects of Alcohol (EtOH) on Skeletal Muscles' Mitochondrial Respiration: Modulation by Age and Metabolic Phenotypes.
The ketone body β-Hydroxybutyrate mediated epigenetic chromatin β-hydroxybutyrylation protects kidneys.
The role of skeletal muscle respiratory capacity in exercise performance.
Beta-hydroxybutyrate.
BNIP3 Downregulation Ameliorates Muscle Atrophy in Cancer Cachexia.
Inhibition of Mitochondrial Fission Protein Drp1 Ameliorates Myopathy in the D2-mdx Model of Duchenne Muscular Dystrophy.
Dietary Restriction and Lipid Metabolism: Unveiling Pathways to Extended Healthspan.
Are Animal Models Necessary? Exploring (Dis)advantages and Alternatives.
Muscle-specific miRNAs in plasma and skeletal muscle of patients with idiopathic inflammatory myopathy are modulated by disease and training.
The effect of exercise and physical activity on skeletal muscle epigenetics and metabolic adaptations.
Epigenetic Mechanisms in Aging: Extrinsic Factors and Gut Microbiome.
Effects of moderate beer consumption on immunity and the gut microbiome in immunosuppressed mice.
Impact of resistance training on cardiometabolic health-related indices in patients with type 2 diabetes and overweight/obesity: a systematic review and meta-analysis of randomised controlled trials.
Fibre: The Forgotten Carbohydrate in Sports Nutrition Recommendations.
Exploring the health benefits of food bioactive compounds from a perspective of NLRP3 inflammasome activation: an insight review.

J Sports Med Phys Fitness. 2025 Jan 09.

Effect of ketosis induced by on delayed-onset muscle soreness, inflammation and redox status: a randomized, open-label, crossover pilot study.

Yoshihiko Mano, Nobuo Fukuda.

BACKGROUND: Previous studies show that ketosis caused by the consumption of low-carbohydrate diets improves cognitive functions and that ketogenic diets can be used to treat epilepsy. In vivo and in vitro experiments have shown that ketosis regulates pain, inflammation, and oxidative stress. Thus, we investigated the effects of ketosis induced by a low-carbohydrate diet on muscle soreness, inflammation, and redox status in human subjects.
METHODS: The research method was an open-label, crossover, pilot study. The study included eight men with no exercise habits associated with muscle soreness and consumed a low-carbohydrate and a normal diet for 6 days. Each dietary intake was for 3 days, and the participants performed the isotonic exercise on the fourth day. Before and after the exercise (immediately after, 24 h later, and 48 h later), the subjective value of muscle soreness, interleukin-6 level, tumor necrosis factor-alpha level, total ketone bodies, and redox status biomarkers were measured.
RESULTS: The results revealed that the low-carbohydrate-diet group showed no significant difference in the subjective value of muscle soreness, whereas the normal diet group showed a significant increase in the subjective muscle soreness scale after 24 h. There were no significant changes in biomarkers of inflammation and redox status in either group.
CONCLUSIONS: This result suggests that ketosis caused by consuming a low-carbohydrate diet suppresses delayed-onset muscle soreness. However, the ketosis state did not suppress inflammation or oxidative stress markers.

DOI: https://doi.org/10.23736/S0022-4707.24.16137-3
Nutrients. 2024 Dec 19. pii: 4374. [Epub ahead of print]16(24):

Effects of the Ketogenic Diet on Microbiota Composition and Short-Chain Fatty Acids in Women with Overweight/Obesity.

Müge Güzey Akansel, Murat Baş, Cansu Gençalp, Meryem Kahrıman, Eray Şahin, Hakan Öztürk, Gürsel Gür, Ceren Gür.

  Background/Objectives: The ketogenic diet (KD) is a dietary model that can impact metabolic health and microbiota and has been widely discussed in recent years. This study aimed to evaluate the effects of a 6-week KD on biochemical parameters, gut microbiota, and fecal short-chain fatty acids (SCFAs) in women with overweight/obesity. Methods: Overall, 15 women aged 26-46 years were included in this study. Blood samples, fecal samples, and anthropometric measurements were evaluated at the beginning and end of this study. Results: After KD, the mean body mass index decreased from 29.81 ± 4.74 to 27.12 ± 4.23 kg/m2, and all decreases in anthropometric measurements were significant (p < 0.05). Fasting glucose, insulin, homeostasis model assessment of insulin resistance, hemoglobin A1C, urea, and creatinine levels decreased, whereas uric acid levels increased (p < 0.05). Furthermore, increased serum zonulin levels were noted (p = 0.001), whereas fecal butyrate, propionate, acetate, and total SCFA levels decreased (p < 0.05). When the changes in microbiota composition were examined, a decrease in beta diversity (p = 0.001) was observed. After the intervention, a statistically significant increase was noted in the Firmicutes/Bacteroidetes ratio (p = 0.001). Although Oscilibacter, Blautia, and Akkermensia relative abundances increased, Prevotella relative abundance and Bifidobacter abundance, which were the dominant genera before the KD, decreased. Moreover, the abundance of some pathogenic genera, including Escherichia, Klebsilella, and Listeria, increased. Conclusions: In healthy individuals, KD may cause significant changes in microbial composition, leading to dysbiosis and long-term adverse outcomes with changes in serum zonulin and fecal SCFA levels.

Keywords:  cardiometabolic risk; dietary intervention; gut microbiota; ketogenic diet; short-chain fatty acids

DOI:  https://doi.org/10.3390/nu16244374
Biology (Basel). 2024 Dec 21. pii: 1080. [Epub ahead of print]13(12):

Cannabis (THC) Aggravates the Deleterious Effects of Alcohol (EtOH) on Skeletal Muscles' Mitochondrial Respiration: Modulation by Age and Metabolic Phenotypes.

Anne-Laure Charles, Margherita Giannini, Alain Meyer, Anne Charloux, Samy Talha, Thomas Vogel, Jean-Sébastien Raul, Valérie Wolff, Bernard Geny.

  The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We therefore determined whether EtOH, alone and associated with THC, impairs skeletal muscle mitochondrial respiration. Further, we investigated potential modulation by metabolic phenotype and age by analyzing predominantly glycolytic gastrocnemius and oxidative soleus muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (-34.97 ± 2.97% vs. -37.50 ± 6.03% at 2.1 × 10-5 M; p < 0.05). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius (-49.92 ± 1.69%, vs. -34.97 ± 2.97 p < 0.05). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (-42.39 ± 2.42% vs. -17.09 ± 7.61% at 2.1 × 10-5 M, p < 0.001, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius (-49.92 ±1.69 vs. -27.22 ± 8.96% in gastrocnemius and soleus, respectively, p < 0.05). In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced effects on young glycolytic muscle. Age and metabolic phenotypes modulate these deleterious effects, with the glycolytic muscles of young rats being more prone to impairments than oxidative muscles.

Keywords:  EtOH; THC; aging; alcohol; cannabis; ethanol; glycolytic; marijuana; metabolic phenotype; mitochondria; oxidative; skeletal muscle; tetrahydrocannabinoid

DOI:  https://doi.org/10.3390/biology13121080
bioRxiv. 2024 Dec 21. pii: 2024.12.18.628574. [Epub ahead of print]

The ketone body β-Hydroxybutyrate mediated epigenetic chromatin β-hydroxybutyrylation protects kidneys.

Juthika Mandal, Sachin Aryal, Ishan Manandhar, Saroj Chakraborty, Xue Mei, Beng San Yeoh, Blair Mell, Andrew Kleinhenz, Ramakumar Tummala, Tao Yang, Piu Saha, William T Gunning, Matam Vijay-Kumar, Venkatesha Basrur, Ivana de la Serna, Bina Joe.

Starvation, intermittent fasting and exercise, all of which are recommended lifestyle modifiers share a common metabolic signature, ketogenesis to generate the ketone bodies, predominantly β-hydroxybutyrate. β-hydroxybutyrate exerts beneficial effects across various contexts, preventing or mitigating disease. We hypothesized that these dynamic health benefits of β-hydroxybutyrate might stem from its ability to regulate genome architecture through chromatin remodeling via histone β-hydroxybutyrylation, thereby influencing the transcriptome. Focusing on the kidney, which is an end organ protected by β-hydroxybutyrate, we examined histone β-hydroxybutyrylation-mediated chromatin remodeling. Notably, regions of the genome associated with lipid catabolism were predominantly in an open chromatin configuration, leading to active transcription and translation. Significant β-hydroxybutyrylation was observed in the kidneys and the most highly upregulated gene actively transcribed and translated was 3-hydroxy-3-methyglutaryl CoA Synthase 2 ( Hmgcs2 ), a gene responsible for the biosynthesis of β-hydroxybutyrate in mitochondria. In contrast, regions with more compact chromatin structures were enriched with genes related to immune function such as protein tyrosine phosphatase receptor type C ( Ptprc ) and lymphocyte cytosolic protein 1 ( Lcp1 ), which exhibited reduced transcription and translation. These results reveal that renal epigenetic histone β-hydroxybutyrylation, which concurrently modulates both energy metabolism and immune function is a mechanism underlying the dynamic health effects of β-hydroxybutyrate to protect kidneys and lower hypertension.

DOI: https://doi.org/10.1101/2024.12.18.628574
Free Radic Biol Med. 2025 Jan 02. pii: S0891-5849(24)01169-9. [Epub ahead of print]

The role of skeletal muscle respiratory capacity in exercise performance.

Pablo M Garcia-Roves, Jorge Alvarez-Luis, Sandra Cutanda-Tesouro.

  The connection between the respiratory capacity of skeletal muscle mitochondria and athletic performance is widely acknowledged in contemporary research. Building on a solid foundation of prior studies, current research has fostered an environment where scientists can effectively demonstrate how a tailored regimen of exercise intensity, duration, and frequency significantly boosts mitochondrial function within skeletal muscles. The range of exercise modalities is broad, spanning from endurance and high-intensity interval training to resistance-based exercises, allowing for an in-depth exploration of effective strategies to enhance mitochondrial respiratory capacity-a key factor in improving exercise performance, in other words offering a better skeletal muscle capacity to cope with exercise demands. By identifying optimal training strategies, individuals can significantly improve their performance, leading to better outcomes in their fitness and athletic endeavours. This review provides the prevailing insights on skeletal muscle mitochondrial respiratory capacity and its role in exercise performance, covering essential instrumental and methodological aspects, findings from animal studies, potential sex differences, a review of existing human studies, and considerations for future research directions.

Keywords:  Exercise; athletic performance; mitochondrial respiratory capacity; skeletal muscle

DOI:  https://doi.org/10.1016/j.freeradbiomed.2024.12.060
Trends Endocrinol Metab. 2025 Jan;pii: S1043-2760(24)00165-6. [Epub ahead of print]36(1): 96-97

Beta-hydroxybutyrate.

Sidharth S Madhavan, Brianna J Stubbs.

DOI: https://doi.org/10.1016/j.tem.2024.06.005
Cancers (Basel). 2024 Dec 11. pii: 4133. [Epub ahead of print]16(24):

BNIP3 Downregulation Ameliorates Muscle Atrophy in Cancer Cachexia.

Claudia Fornelli, Marc Beltrà, Antonio Zorzano, Paola Costelli, David Sebastian, Fabio Penna.

   BACKGROUND AND AIMS: Cancer cachexia is a complex syndrome affecting most cancer patients and is directly responsible for about 20% of cancer-related deaths. Previous studies showed muscle proteolysis hyper-activation and mitophagy induction in tumor-bearing animals. While basal mitophagy is required for maintaining muscle mass and quality, excessive mitophagy promotes uncontrolled protein degradation, muscle loss and impaired function. BNIP3, a key mitophagy-related protein, is significantly increased in the muscles of both mice and human cancer hosts. This study aimed to define the potential of mitigating mitophagy via BNIP3 downregulation in preserving mitochondrial integrity, counteracting skeletal muscle loss in experimental cancer cachexia.
METHODS: Two in vivo gene delivery methods were performed to knock down muscle BNIP3: electroporation of a BNIP3-specific shRNA expression vector or adenovirus injection.
RESULTS: The electroporation effectively reduced muscle BNIP3 in healthy mice but was ineffective in C26 tumor-bearing mice. In contrast, adenovirus-mediated BNIP3 knockdown successfully decreased BNIP3 levels also in tumor hosts. Although BNIP3 knockdown did not impact overall on body or muscle mass, it improved muscle fiber size in C26-bearing miceh2, suggesting partial prevention of muscle atrophy. Mitochondrial respiratory chain complexes (OxPhos) and TOM20 protein levels were consistently rescued, indicating improvements in mitochondrial mass, while H2O2 levels were unchanged among the groups, suggesting that BNIP3 downregulation does not impair the endogenous control of oxidative balance.
CONCLUSIONS: These findings suggest that a fine balance between mitochondrial disposal and biogenesis is fundamental for preserving muscle homeostasis and highlight a potential role for BNIP3 modulation against cancer-induced muscle wasting.

Keywords:  BNIP3; cancer cachexia; mitochondria; mitophagy; muscle wasting

DOI:  https://doi.org/10.3390/cancers16244133
bioRxiv. 2024 Dec 26. pii: 2024.12.26.628172. [Epub ahead of print]

Inhibition of Mitochondrial Fission Protein Drp1 Ameliorates Myopathy in the D2-mdx Model of Duchenne Muscular Dystrophy.

H Grace Rosen, Nicolas J Berger, Shantel N Hodge, Atsutaro Fujishiro, Jared Lourie, Vrusti Kapadia, Melissa A Linden, Eunbin Jee, Jonghan Kim, Yuho Kim, Kai Zou.

Although current treatments for Duchenne Muscular Dystrophy (DMD) have proven to be effective in delaying myopathy, there remains a strong need to identify novel targets to develop additional therapies. Mitochondrial dysfunction is an early pathological feature of DMD. A fine balance of mitochondrial dynamics (fission and fusion) is crucial to maintain mitochondrial function and skeletal muscle health. Excessive activation of Dynamin-Related Protein 1 (Drp1)-mediated mitochondrial fission was reported in animal models of DMD. However, whether Drp1-mediated mitochondrial fission is a viable target for treating myopathy in DMD remains unknown. Here, we treated a D2-mdx model of DMD (9-10 weeks old) with Mdivi-1, a selective Drp1 inhibitor, every other day (i.p. injection) for 5 weeks. We demonstrated that Mdivi-1 effectively improved skeletal muscle strength and reduced serum creatine kinase concentration. Mdivi-1 treatment also effectively inhibited mitochondrial fission regulatory protein markers, Drp1(Ser616) phosphorylation and Fis1 in skeletal muscles from D2-mdx mice, which resulted in reduced content of damaged and fragmented mitochondria. Furthermore, Mdivi-1 treatment attenuated lipid peroxidation product, 4-HNE, in skeletal muscle from D2-mdx mice, which was inversely correlated with muscle grip strength. Finally, we revealed that Mdivi-1 treatment downregulated Alpha 1 Type I Collagen (Col1a1) protein expression, a marker of fibrosis, and Interleukin-6 (IL-6) mRNA expression, a marker of inflammation. In summary, these results demonstrate that inhibition of Drp1-mediated mitochondrial fission by Mdivi-1 is effective in improving muscle strength and alleviating muscle damage in D2-mdx mice. These improvements are associated with improved skeletal muscle mitochondrial integrity, leading to attenuated lipid peroxidation.

DOI: https://doi.org/10.1101/2024.12.26.628172
Nutrients. 2024 Dec 23. pii: 4424. [Epub ahead of print]16(24):

Dietary Restriction and Lipid Metabolism: Unveiling Pathways to Extended Healthspan.

Hye-Yeon Lee, Kyung-Jin Min.

  Dietary restriction (DR) has been reported to be a significant intervention that influences lipid metabolism and potentially modulates the aging process in a wide range of organisms. Lipid metabolism plays a pivotal role in the regulation of aging and longevity. In this review, we summarize studies on the significant role of lipid metabolism in aging in relation to DR. As a potent intervention to slow down aging, DR has demonstrated promising effects on lipid metabolism, influencing the aging processes across various species. The current review focuses on the relationships among DR-related molecular signaling proteins such as the sirtuins, signaling pathways such as the target of rapamycin and the insulin/insulin-like growth factor (IGF)-1, lipid metabolism, and aging. Furthermore, the review presents research results on diet-associated changes in cell membrane lipids and alterations in lipid metabolism caused by commensal bacteria, highlighting the importance of lipid metabolism in aging. Overall, the review explores the interplay between diet, lipid metabolism, and aging, while presenting untapped areas for further understanding of the aging process.

Keywords:  Ins/IGF-1; cell membrane; commensal bacteria; dietary restriction; healthspan; lipid profile; sirtuin; target of rapamycin

DOI:  https://doi.org/10.3390/nu16244424
Eur J Neurosci. 2025 Jan;61(1): e16651

Are Animal Models Necessary? Exploring (Dis)advantages and Alternatives.

Ana Isabel Guimarães.

Animal models have been crucial for scientific development, allowing researchers to understand the underlying mechanisms of various human conditions, and are far from becoming obsolete in scientific research. However, the ethics of animal experimentation has been a prevalent question between both experts and nonexperts. This essay tackles the advantages and disadvantages of the usage of animal models while delving into new alternatives that have emerged in light of contemporary science.

DOI: https://doi.org/10.1111/ejn.16651
Rheumatology (Oxford). 2025 Jan 07. pii: keae704. [Epub ahead of print]

Muscle-specific miRNAs in plasma and skeletal muscle of patients with idiopathic inflammatory myopathy are modulated by disease and training.

Nikoleta Alchus Laiferová, Lucia Vernerová, Michal Nemec, Daria Barkova, Katarína Rerková, Karin Marček Malenovská, Martina Vokurková, Sabína Oreská, Martin Klein, Maja Špiritović, Michal Tomčík, Jozef Ukropec, Jiří Vencovský, Barbara Ukropcová.

   OBJECTIVES: Objective of this work was to examine myomiR levels in plasma, skeletal muscle, and skeletal muscle cells of patients with idiopathic inflammatory myopathy (IIM), their interrelations with the disease-related clinical phenotypes and with the effects of the disease-modifying 6-month training-intervention.
METHODS: Samples of vastus lateralis muscle (n = 12/13) and plasma (n = 20/21) were obtained from IIM patients and healthy controls, respectively. Muscle and plasma were obtained before and after a 6-month training-intervention in 7 patients. MyomiRs miR-1,-206,-133a,-133b were quantified by qPCR. Effects of pro-inflammatory (TNF), metabolic (glucose, insulin) systemic factors and the immunosuppressive therapy (dexamethasone) on the myomiRs were examined in muscle cells in vitro.
RESULTS: MiR-133b was lower in skeletal muscle of IIM patients compared with healthy controls (p= 0.03). Levels of miR-133a, miR-1, and miR-206 were not regulated. Moreover, plasma levels of miR-133b and miR-1 were reduced in IIM compared with healthy controls (p< 0.05). Exercise induced reciprocal regulation of specific myomiRs in muscle and plasma of IIM patients, it lowered miR-133b in muscle while increasing miR-133b and miR-206 in plasma. Treatment of myotubes with TNF, insulin, and glucose and dexamethasone induced distinct myomiRs down-regulation.
CONCLUSION: Lower myomiR levels in skeletal muscle of IIM patients might indicate reduced muscle regenerative potential in IIM, which could be linked to inflammation, metabolic dysfunction, and immunosuppressive therapy. Training-induced changes of muscle and plasma myomiRs indicate an increase in myomiRs release, which could contribute to the adaptive response underlying the positive systemic effects of exercise in IIM.

Keywords:  exercise; idiopathic inflammatory myopathy; microRNA; muscle cells; myomiR; plasma; skeletal muscle; training intervention

DOI:  https://doi.org/10.1093/rheumatology/keae704
Eur J Appl Physiol. 2025 Jan 08.

The effect of exercise and physical activity on skeletal muscle epigenetics and metabolic adaptations.

Gregg Mallett.

  Physical activity (PA) and exercise elicit adaptations and physiological responses in skeletal muscle, which are advantageous for preserving health and minimizing chronic illnesses. The complicated atmosphere of the exercise response can be attributed to hereditary and environmental variables. The primary cause of these adaptations and physiological responses is the transcriptional reactions that follow exercise, whether endurance- (ET) or resistance- training (RT). As a result, the essential metabolic and regulatory pathways and myogenic genes associated with skeletal muscle alter in response to acute and chronic exercise. Epigenetics is the study of the relationship between genetics and the environment. Exercise evokes signaling pathways that strongly alter myofiber metabolism and skeletal muscle physiological and contractile properties. Epigenetic modifications have recently come to light as essential regulators of exercise adaptations. Research has shown various epigenetic markers linked to PA and exercise. The most critical epigenetic alterations in gene transcription identified are DNA methylation and histone modifications, which are associated with the transcriptional response of skeletal muscle to exercise and facilitate the modification to exercise. Other changes in the epigenetic markers are starting to emerge as essential processes for gene transcription, including acetylation as a new epigenetic modification, mediated changes by methylation, phosphorylation, and micro-RNA (miRNA). This review briefly introduces PA and exercise and associated benefits, provides a summary of epigenetic modifications, and a fundamental review of skeletal muscle physiology. The objectives of this review are 1) to discuss exercise-induced adaptations related to epigenetics and 2) to examine the interaction between exercise metabolism and epigenetics.

Keywords:  Chronic disease; Endurance training; Metabolism; Resistance training; Skeletal muscle epigenetics

DOI:  https://doi.org/10.1007/s00421-025-05704-6
Genes (Basel). 2024 Dec 14. pii: 1599. [Epub ahead of print]15(12):

Epigenetic Mechanisms in Aging: Extrinsic Factors and Gut Microbiome.

Alejandro Borrego-Ruiz, Juan J Borrego.

   BACKGROUND/OBJECTIVES: Aging is a natural physiological process involving biological and genetic pathways. Growing evidence suggests that alterations in the epigenome during aging result in transcriptional changes, which play a significant role in the onset of age-related diseases, including cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. For this reason, the epigenetic alterations in aging and age-related diseases have been reviewed, and the major extrinsic factors influencing these epigenetic alterations have been identified. In addition, the role of the gut microbiome and its metabolites as epigenetic modifiers has been addressed.
RESULTS: Long-term exposure to extrinsic factors such as air pollution, diet, drug use, environmental chemicals, microbial infections, physical activity, radiation, and stress provoke epigenetic changes in the host through several endocrine and immune pathways, potentially accelerating the aging process. Diverse studies have reported that the gut microbiome plays a critical role in regulating brain cell functions through DNA methylation and histone modifications. The interaction between genes and the gut microbiome serves as a source of adaptive variation, contributing to phenotypic plasticity. However, the molecular mechanisms and signaling pathways driving this process are still not fully understood.
CONCLUSIONS: Extrinsic factors are potential inducers of epigenetic alterations, which may have important implications for longevity. The gut microbiome serves as an epigenetic effector influencing host gene expression through histone and DNA modifications, while bidirectional interactions with the host and the underexplored roles of microbial metabolites and non-bacterial microorganisms such as fungi and viruses highlight the need for further research.

Keywords:  aging; epigenetics; extrinsic factors; gut microbiome; microbial metabolites; neurodegenerative diseases

DOI:  https://doi.org/10.3390/genes15121599
Biosci Microbiota Food Health. 2025 ;44(1): 32-42

Effects of moderate beer consumption on immunity and the gut microbiome in immunosuppressed mice.

Shumin Hu, Hua Yin, Xiaxia Li, Minghao Fan, Huajun Li.

  Beer contains a variety of bioactive ingredients and trace elements that can regulate bodily functions, and moderate consumption of beer can enhance immune responses. This study aimed to investigate the potential benefits of moderate consumption of alcoholic or non-alcoholic beer on the gut microbiome, immunity, and intestinal barrier function in immunosuppressed BALB/c mice induced by cyclophosphamide (CTX). Model mice with CTX-induced immunosuppression were administered alcoholic or non-alcoholic beer or galacto-oligosaccharides (GOS) for 28 consecutive days. The GOS and beer intervention groups all showed alleviation of spleen tissue damage, an increased immune organ index, decreased gut inflammation, and reduced serum concentrations of D-lactic acid, lipopolysaccharide, and tumor necrosis factor α. High-throughput 16S rRNA gene sequencing revealed higher relative abundances of Firmicutes and Actinobacteriota, and lower relative abundances of Bacteroidota, Lactobacillus, and Bifidobacterium, in CTX mice than in normal control mice. In addition, Firmicutes showed lower abundance, while Desulfobacterota showed higher abundance in CTX mice with non-alcoholic beer intake than without it. Spearman correlation analysis indicated that Bacteroidota was negatively correlated with propionic acid and butyric acid, while Desulfobacterota was positively correlated with butyric acid. Proteobacteria was negatively correlated with acetic acid, propionic acid, isobutyric acid, and valeric acid. Helicobacter was positively correlated with valeric acid. In conclusion, this is one of the first studies to examine the modulatory effects of moderate alcohol consumption in immunocompromised mice. Our findings indicate that beer consumption can alter the gut microbiome and metabolites, enhancing immunity in mice.

Keywords:  alcoholic beer; cyclophosphamide; gut microbiome; immunosuppression; moderate drinking; non-alcoholic beer

DOI:  https://doi.org/10.12938/bmfh.2024-045
Br J Sports Med. 2025 Jan 07. pii: bjsports-2024-108947. [Epub ahead of print]

Impact of resistance training on cardiometabolic health-related indices in patients with type 2 diabetes and overweight/obesity: a systematic review and meta-analysis of randomised controlled trials.

Sameer Badri Al-Mhanna, Barry A Franklin, John M Jakicic, Emmanuel Stamatakis, Linda S Pescatello, Deborah Riebe, Walter R Thompson, James Skinner, Sheri R Colberg, Nouf H Alkhamees, Bodor Bin Sheeha, Mehmet Gülü, Abdullah F Alghannam, Alexios Batrakoulis.

   OBJECTIVE: To evaluate the effects of resistance training on cardiometabolic health-related outcomes in patients with type 2 diabetes mellitus (T2DM) and overweight/obesity.
DESIGN: Systematic review and meta-analysis of randomised controlled trials (RCTs).
DATA SOURCES: PubMed, Web of Science, Scopus, Science Direct, Cochrane Library and Google Scholar databases were searched from inception up to May 2024. The search strategy included the following keywords: diabetes, resistance exercise and strength training.
ELIGIBILITY CRITERIA FOR SELECTING STUDIES: RCTs published in English comparing resistance training alone with non-exercising standard treatment. Participants were adults diagnosed with T2DM and concurrent overweight/obesity (body mass index (BMI) ≥25 kg/m2).
RESULTS: A total of 18 RCTs qualified involving 1180 patients (48.6/51.4 female/male ratio; 63.3±7.0 years; 29.3±4.3 kg/m2). Waist circumference (standardised mean differences (SMD) -0.85 cm, 95% CI -1.66 to -0.04), waist-to-hip ratio (SMD -0.72, 95% CI -1.30 to -0.15), high-density lipoprotein cholesterol (SMD +0.40 mg/dL, 95% CI 0.07 to -0.72), triglycerides (SMD -0.54 mg/dL, 95% CI -1.06 to -0.02), fasting blood glucose (SMD -0.65 mmol/L, 95% CI -1.19 to -0.12), fasting insulin (SMD -0.74 uIU/mL, 95% CI -1.12 to -0.36) and glycated haemoglobin (SMD -0.32%, 95% CI -0.63 to -0.01) improved compared with standard treatment. The risk of bias was low to unclear, and the quality of evidence was very low to moderate.
CONCLUSIONS: Resistance training as a standalone exercise intervention in the management and treatment of T2DM with concurrent overweight/obesity is associated with many cardiometabolic benefits when compared with standard treatment without exercise.
PROSPERO REGISTRATION NUMBER: CRD42022355612.

Keywords:  Body composition; Exercise; Glucose metabolism; Lipids; Physical activity

DOI:  https://doi.org/10.1136/bjsports-2024-108947
Sports Med. 2025 Jan 08.

Fibre: The Forgotten Carbohydrate in Sports Nutrition Recommendations.

Laura Mancin, Louise M Burke, Ian Rollo.

Although dietary guidelines concerning carbohydrate intake for athletes are well established, these do not include recommendations for daily fibre intake. However, there are many scenarios in sports nutrition in which common practice involves the manipulation of fibre intake to address gastrointestinal comfort around exercise, or acute or chronic goals around the management of body mass or composition. The effect of fibre intake in overall health is also important, particularly in combination with other dietary considerations such as the elevated protein requirements in this population. An athlete's habitual intake of dietary fibre should be assessed. If less than 20 g a day, athletes may consider dietary interventions to gradually increase intake. It is proposed that a ramp phase is adopted to gradually increase fibre ingestion to ~ 30 g of fibre a day (which includes ~ 2 g of beta-glucan) over a duration of 6 weeks. The outcomes of achieving a daily fibre intake are to help preserve athlete gut microbiome diversity and stability, intestinal barrier function as well as the downstream effects of short-chain fatty acids produced following the fermentation of microbiome accessible carbohydrates. Nevertheless, there are scenarios in which daily manipulation of fibre intake, either to reduce or increase intake, may be valuable in assisting the athlete to maintain gastrointestinal comfort during exercise or to contribute to body mass/composition goals. Although further research is required, the aim of this current opinion paper is to ensure that fibre is not forgotten as a nutrient in the athlete's diet.

DOI: https://doi.org/10.1007/s40279-024-02167-1
Crit Rev Food Sci Nutr. 2025 Jan 06. 1-26

Exploring the health benefits of food bioactive compounds from a perspective of NLRP3 inflammasome activation: an insight review.

Yabo Li, Xinyi Wang, Ying Ren, Bei-Zhong Han, Yansong Xue.

  The food industry has been focusing on food bioactive compounds with multiple physiological and immunological properties that benefit human health. These bioactive compounds, including polyphenols, flavonoids, and terpenoids, have great potential to limit inflammatory responses especially NLRP3 inflammasome activation, which is a key innate immune platform for inflammation. Current studies have revealed numerous food bioactive compounds with promising activities for unraveling immune metabolic disorders and excessive inflammatory responses by directly and indirectly regulating the NLRP3 inflammasome activation. This review explores the food hazards, including microbial and abiotic factors, that may trigger NLRP3-mediated illnesses and inflammation. It also highlights bioactive compounds in food that can suppress NLRP3 inflammasome activation through various mechanisms, linking its activation and inhibition to different pathways. Especially, this review provided further insight into NLRP3-related targets where food bioactive compounds can interact to block the NLRP3 inflammasome activation process, as well as mechanisms on how these compounds facilitate inactivation processes.

Keywords:  Food bioactive compounds; functional food; immunity; inflammasome; nutrition

DOI:  https://doi.org/10.1080/10408398.2024.2448768