Gut microbesGillian N F Larik, Emanuel E Canfora, Evert M van Schothorst, Ellen E Blaak
The gut microbiota‒host metabolism axis is a critical determinant of metabolic health, yet its functional activity remains difficult to monitor in vivo. The gut microbiota ferments undigested food components such as dietary fibers and proteins, yielding various important metabolites and gases that impact human metabolism. This review synthesizes current evidence on intestinal gases, primarily hydrogen (H2), methane (CH4) and hydrogen sulfide (H2S), as non-invasive markers of the trade-off between saccharolytic and proteolytic fermentation. Within the current review, we evaluate the concentrations of important gut metabolites and gases and techniques to measure intestinal gases, including stable isotope breath tests, volatile organic compound (VOC) profiling, and respiration chambers. Crucially, we highlight that these gases may function not only as metabolic byproducts and biomarkers of microbial activity but as active signaling molecules influencing gastrointestinal transit, satiety, and systemic inflammation. This review concludes that real-time gas monitoring provides a unique opportunity to study real-time gut microbial fermentation. We propose a framework for phenotyping individual or subgroup-based fermentation patterns to guide personalized nutritional interventions for obesity and type 2 diabetes.
Life science allianceOmar Flores-Sandoval, Skarleth Cárdenas-Romero, Adrián Báez-Ruiz, Roberto C Salgado-Delgado, Nadia Saderi
Increased sympathetic tone and hypertension are hallmarks of metabolic syndrome and contribute to chronic kidney disease. Although renal sympathetic denervation transiently lowers blood pressure, its role in the development of metabolic and renal alterations remains unclear. Here, we evaluated the contribution of renal sympathetic input to the onset and progression of high-fat diet-induced alterations. Male Wistar rats underwent bilateral renal denervation before metabolic challenge and were fed a standard or high-fat diet for 8 or 12 wk. High-fat feeding induced hypertension, proteinuria, increased angiotensin II, and reduced creatinine clearance, urinary flow, and potassium excretion, independently of denervation. Renal norepinephrine content confirmed effective denervation and was not affected by diet. Denervation attenuated ketonuria in high-fat diet-fed rats. The phosphorylation of AKT, PI3K, and ERK1/2 in the kidney was modulated by interactions among diet, renal sympathetic input, and time. These findings indicate that renal sympathetic nerves contribute to early stages of metabolic dysregulation, whereas prolonged hypercaloric exposure overrides autonomic control and promotes cardiovascular and renal complications.
Gut microbesBerengère Benoit, Pierre Letourneau, Vincent Verdier, Angélique Viney, Cécile Barnel, Karim Chikh, Oriane Vitalis, Audrey Jalabert, Sandra Wagner, Manolo Laiol…
Low-protein diets (LPD) are recommended in chronic kidney disease (CKD) to reduce disease progression. However, their clinical efficacy and safety are debated due to the risk of protein-energy wasting. A deeper mechanistic understanding is therefore required. Herein, the metabolic effects of LPD in both murine models and a randomized controlled trial in nondiabetic CKD patients were investigated, focusing on glucose homeostasis, plasmatic uremic toxin (UTs) levels, gut microbiota remodeling, and endocrine adaptations. In both experimental and clinical settings, LPD improved glucose tolerance and significantly decreased circulating levels of gut-derived UTs while reducing body weight (-33% weight gain in mice and a decrease in body mass index of ~-0.5 kg/m2 in humans). These metabolic improvements were associated with alterations in gut microbiota composition and function, including the downregulation of microbial pathways involved in aromatic amino acid biosynthesis. In both mice and patients, LPD triggered a significant hepatic induction of fibroblast growth factor 21 (FGF21), an endocrine regulator of amino acid deficiency (+2.9-fold in human and 28-fold in mice) FGF21 levels correlated negatively with lean mass and positively with fat mass and glycemic control, supporting a dual role in metabolic adaptation and catabolic signaling. To mitigate the adverse nutritional effects of LPD, we administered Lactiplantibacillus plantarum WJL (LpWJL), a probiotic previously found to enhance growth of under nutritional stress in CKD mice. LpWJL restored circulating amino acid levels, suppressed FGF21 induction (-26%) and stress-related biosynthetic responses, and preserved body weight (+247% weight gain) and composition, without impairing the benefits of LPD on kidney and metabolic parameters. The present findings identify UTs and FGF21 as crucial factors of the metabolic response to LPD, and support microbiota-targeted strategies, such as LpWJL supplementation, to enhance LPD efficacy. Clinical trials are, however, required to confirm their relevance in CKD management.
Gut microbesMengXuan Du, Wenzhao Wang, Min-Zhi Jiang, Xin-Wei Sun, Lei Sun, Chang Liu, Shuang-Jiang Liu
Next-generation probiotics derived from gut commensals show promise for metabolic disease intervention, yet effective anti-obesity strains remain limited. Here, we demonstrate that oral administration of Christensenella massiliensis markedly alleviates obesity and metabolic dysfunction in high-fat diet-induced obese mice. Treatment reduced food intake, improved glucose tolerance and insulin sensitivity, lowered blood glucose and lipid levels, and attenuated hepatic steatosis and adipose accumulation. C. massiliensis increased the levels of plasma GLP-1 and ileal GLP-1 receptor expression while decreasing ghrelin level, suggesting modulation of gut hormone regulation. C. massiliensis also suppressed systemic and colonic inflammation, accompanied by upregulation of metabolic homeostasis-related genes (ppara, pparg, ucp2). Targeted and quantitative metabolomics identified altered gut metabolic profiles, particularly reduced kynurenine levels. In vitro assays further showed that C. massiliensis converted kynurenine into kynurenic acid, and its lysate reversed kynurenine-induced lipid accumulation, inflammation, and PPARγ suppression in hepatocytes, providing mechanistic support for the observed in vivo metabolic benefits. These findings support C. massiliensis as a promising next-generation probiotic for obesity management.
Gut microbesEmily R Ebel, Abhijit Sanjiv Kulkarni, Dattatray S Mongad, Matthew R Olm, Sarangthem Indira Devi, Bilal Ahmad Mir, Shantanu Ozarkar, Erica D Sonnenburg, Yogesh…
Highly diverse gut microbiomes of non-industrialized populations share similarities with ancestral states of symbiosis and are linked to low rates of chronic inflammatory diseases. Yet there is still limited understanding of the diverse array of non-industrialized gut microbiomes throughout the world, including among the tribal populations of India. In this study, we surveyed dietary and fecal microbiome variation among 76 adults from eight tribal communities in four biogeographic regions of India, including Warli on the western coast, Gond and Madia in the northeast Deccan Plateau, Kabui (or Rongmei Naga) in the northeast hills of the Himalayas, and Balti, Boto, Brokpa, and Purigpa in the northwest Trans-Himalayas. Metagenomic and 16S sequencing of fecal samples identified Segatella, Agathobacter, and Faecalibacterium as core members of the gut microbiome of all populations, with Segatella copri (formerly Prevotella copri) dominant at mean 25%-47% relative abundance. Four Trans-Himalayan populations with diets uniquely defined by dairy and diverse cereals had elevated gut alpha diversity and distinct beta diversity, driven by prevalent and abundant Bifidobacterium as well as taxa shared with the ruminant microbiome. Strains of B. adolescentis present in the dairy-consuming populations were genetically distinct from industrialized strains around the world and encoded CAZymes consistent with selection by dairy and grain consumption. The gut microbiomes of a minority of subjects shared taxonomic and functional features with a previously described sample of Californians, suggesting that the pressures posed by globalization could be impacting the microbiomes of tribal populations. These results highlight the nutritional and microbiological contribution of dairy livestock in shaping gut communities and emphasize the large effect that lifestyle can have on the diversity and function of non-industrialized gut microbiomes.
A high-fat diet (HFD) has been associated with dysregulated immunity both at the systemic and mucosal levels in mouse models. The underlying mechanisms are partially known. We analysed the effect of diet on immunity in HLA-DQ8 (DQ8) transgenic mice, a specific model of gluten sensitivity, and investigated a possible interplay between gluten and an HFD. Our aim was to further dissect the impact of a long-term HFD regimen on both systemic and intestinal immunity. Adult DQ8 mice (n = 6/group) were fed a gluten-free diet (GFD), an HFD, or an HFD containing 8% gluten (HFD+G) for 23 weeks. We assessed clinical parameters, the phenotype and function of splenic and lamina propria (LP) T cells by flow cytometry, and multiparametric quantitation of cytokines induced in vitro. An HFD for 23 weeks increased body weight as expected, paralleled by a significant shortening of the caecum (P < 0.001). FACS analysis revealed that an HFD drastically increased the number of potentially cytotoxic (CD8+) T cells in the LP but not in the spleen. An HFD+G significantly reduced, but did not abolish, the percentage of these cells (p < 0.01). Induction of cytokine secretion in vitro showed that LP cells from both HFD- and HFD+G-fed mice did not secrete any cytokines, whereas both innate (TNF-α) and adaptive immunity (IL-4, IFN-γ and IL-17) cytokines were induced in the LP of GFD-fed mice. In conclusion, we found that a long-term HFD regimen impaired the phenotype of immune cells and their effector functions distinctly in the small intestine of gluten-sensitive DQ8 mice. The presence of gluten in the diet changed the phenotype but did not abolish the block of effector activity. Our findings could help further elucidate the functional status of the immune system under the HFD regimen.
Peritoneal dialysis (PD) disrupts glucose metabolism due to repeated exposure to glucose-based dialysate. This prospective cohort study evaluates whether impaired fasting glucose (IFG) confers cardiovascular and mortality risks comparable to those of diabetes mellitus (DM) and to analyze the contributions of β-cell dysfunction and insulin resistance (IR) in patients undergoing PD. 216 patients receiving PD in Taiwan were stratified by baseline glycemic status into normal fasting glucose (n = 71), IFG (n = 58), and DM (n = 87). β-cell function was assessed using the Homeostasis Model Assessment of β-cell Function (HOMA-β), while IR was evaluated using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and the triglyceride-glucose (TyG) index. The primary outcomes were all-cause mortality and 3-point major adverse cardiovascular events (3 P-MACE). Over a median follow-up of 41 months, 69 deaths (32%) occurred; 42% and 38% were attributed to cardiovascular and infectious causes, respectively. Survival curves for IFG and DM were nearly superimposable, and both were worse than that for normal glucose. In fully adjusted models, IFG independently predicted 3 P-MACE (sHR, 4.00; 95% CI, 1.50-10.66; p = 0.006) and all-cause mortality (HR, 2.48; 95% CI, 1.16-5.32; p = 0.02), with risks comparable to those observed in DM. The TyG index independently predicted both outcomes, whereas greater β-cell function was associated with a reduced risk of both endpoints. These findings suggest that cardiovascular and mortality risks in IFG are comparable to those in DM among PD patients, potentially mediated by β-cell dysfunction and increased IR.
Gut microbesGeorgios Marinos, Karlis Arturs Moors, Kristina Schlicht, Malte Rühlemann, Silvio Waschina, Wolfgang Lieb, Andre Franke, Matthias Laudes, Mathieu Groussin, Mat…
Microbiomes and their host environments form complex, interconnected ecosystems. The microbial species within a microbiome, on the one hand, compete for resources, while on the other hand, they exchange vital metabolites to support their survival. These interactions are influenced by the microbial genetic repertoire, environmental conditions, and availability of nutrients. We developed EcoGS (http://www.github.com/KaletaLab/EcoGS), a metabolic modeling tool designed to predict the ecological interactions between pairs of microbes. Applying EcoGS to the microbiomes of two distinct human cohorts revealed a shift from collaborative to exploitative ecological interactions associated with increased dietary intake of simple sugars (glucose and fructose) in diabetic individuals and those living industrialized lifestyles. On the other hand, the consumption of cobalamin (vitamin B12), phylloquinone (vitamin K1), and biotin (vitamin B7), among other compounds, was associated with increased collaboration in the gut microbiome. We conclude that the abundance of simple sugars as an energy source reduces the necessity for microbes to cooperate, thereby increasing competition and hostility among microbiome members. Moreover, our study proposes multiple compounds, such as urate, deoxyadenosine, deoxyguanosine, and hypoxanthine, for in vitro validation tests as dietary interventions that have the potential to restore the ecological balance within the community. EcoGS serves as a valuable tool for exploring microbiome dynamics and their connections to environmental changes and disease.
Biochimica et biophysica acta. Molecular basis of diseaseWenqing Huang, Meng Ding, Qin Yi, Yuepeng Li, Wenzhi Gu, Ping Zhang, Rui Tian, Zhilong Zhang, Lan Zheng
Metabolic disorders leading to cardiac dysfunction have become a global health challenge, and the cardioprotective mechanisms of regular exercise remain unclear. This study focused on the small GTPase RalA and revealed its critical role in exercise-mediated improvement of high-fat-induced cardiac dysfunction. Using a high-fat-fed drosophila heart model, combined with genetic manipulation and exercise intervention, it was demonstrated that a high-fat diet upregulates RalA expression in the myocardium, accompanied by excessive mitochondrial fission and impaired cardiac function. Regular exercise not only effectively reversed these pathological phenotypes but also exerted its protective effects in a RalA -dependent manner within the myocardium. Mechanistically, RalA appeared to exert its effects not through traditional energy metabolism pathways, but rather through the regulation of Drp1-mediated mitochondrial fission, thereby preserving mitochondrial network homeostasis and energy supply in cardiomyocytes. This study is the first to propose a novel "exercise-RalA-mitochondrial dynamics" signaling axis, providing new mechanistic insight into the cardioprotective effects of exercise and suggesting that targeting the RalA pathway may represent a promising therapeutic strategy for metabolic heart disease.
Molecular and cellular endocrinologyFlorencia Heinecke, Jeremías Pablo Flores Quiroga, Marina Labiano, Rocío Galarza, Alicia Graciela Faletti, Alicia Jawerbaum, Verónica White
Obesity negatively impacts maternal and fetal metabolism, leading to the programming of metabolic disturbances in the offspring. We have previously reported numerous maternal, fetal and offspring alterations in a rat model of obesity. In this study, we administered butyrate-a short-chain fatty acid derived from gut microbiota metabolism-to obese mother rats during pregnancy and lactation in an attempt to improve maternal health and prevent the fetal features associated with the programming of fatty liver disease. The initial experimental study design comprised female Albino-Wistar rats assigned to either a control diet (C group) or a high-fat diet (FD group) to induce obesity, before being paired with control males. Pregnant rats received either butyrate (CB or FDB) or water as a vehicle (C or FD) during gestation and were euthanized at day 21 of pregnancy. The second experimental design comprised C, FD, and FDB rats that gave birth and breastfed their pups, with mothers being euthanized at the conclusion of the lactation period. At term gestation, rats with obesity exhibited increased adiposity, hepatic lipid accumulation, triglyceridemia, and circulating IL-1β. Their fetuses displayed increased body weight, liver lipid over-accumulation, and altered mRNA levels of genes involved in liver damage. Notably, butyrate administration decreased maternal circulating levels of triglycerides and IL-1β, and prevented fetal overweight status and hepatic lipid accumulation at term gestation. Importantly, butyrate exerted no effect on control rats or their fetuses. Moreover, butyrate administration ameliorated features of fatty liver disease in overweight rats at the end of lactation, further demonstrating its beneficial effects on both mothers and fetuses in this rat model of obesity.
Experimental neurologyMaud Petrault, Patrick Gele, Vincent Berezowski, David Devos, Thavarak Ouk, Olivier Petrault, Michèle Bastide
Visceral fat gain and the progressive onset of metabolic disorders precipitate stroke risk and prompt the middle-aged population to cognitive decline. Preclinical research has recently focused on total apelin, a neuroprotective peptide whose cerebral action after release in plasma by adipose tissue remains elusive. The ratio between plasma apelin and lipids is suspected to influence prognosis in patients with cardiovascular diseases. This study challenged ratios of plasma apelin to cholesterol or glucose in reflecting post-stroke recovery of mature adult mice after a 6-month high-fat diet (HFD). Mice under HFD developed overweight (+10%, p < 0.001), hyperglycemia (21%, p < 0.001) and hypercholesterolemia (+68%, p < 0.001). Plasma apelin decreased with age in all mice (F2,360 = 35.94, p < 0.001), but a 30-min middle cerebral artery occlusion (MCAO) induced a 27% drop in plasma apelin (p < 0.01) in HFD-fed mice only, as well as a higher acute mortality (29%) than in normal diet (ND)-fed mice (19%). Ten days after MCAO, apelin levels normalized in HFD-fed mice, but were still decreasing in ND-fed mice (p < 0.01). However, high pre-stroke ratios revealed an upregulation of brain apelin receptor expression in these mice, that was lost in metabolically disturbed mice displaying lower ratios. This was functionally confirmed since mice with higher pre-stroke ratios displayed significantly better locomotor and cognitive performances, as validated by ROC analysis (AUC = 0.85). This study highlights pre-stroke ratios of plasma apelin to cholesterol or glucose as potential new biomarkers of post-stroke recovery.
Journal of the International Society of Sports NutritionBarbara Strasser, Johannes Burtscher, Jesus Álvarez-Herms, Martin Kopp, Benjamin Pageaux, Martin Burtscher
BACKGROUND: Exercise tolerance is a pivotal factor in determining athletic competitive success, as well as mobility and quality of life in elderly individuals and those afflicted by chronic ailments. Since tolerance to endurance exercise is closely related to the perception of effort, any measure that influences this perception may also impact endurance performance. METHODS: The aim of this brief review was to evaluate how dietary interventions can improve endurance performance by reducing perceived effort. We contextualize our review within theoretical frameworks that consider effort perception to be a key regulator of endurance performance. Next, we integrate evidence on the ergogenic effects of various dietary interventions with existing knowledge on the perception of effort. RESULTS: Dietary interventions may enhance endurance performance by improving motor command transmission, slowing fatigue development and related compensatory increase in motor command, and/or modifying the activity of brain networks involved in effort perception and fatigue. Beta-alanine, caffeine or carbohydrate mouth rinsing are examples of evidence-based ergogenic aids. The impact on endurance performance is achieved through their potential to overcome cardiorespiratory and metabolic limitations or through modulation of the central nervous system. Other dietary supplements, such as branched-chain amino acids, citrulline, taurine, and probiotics, may indirectly impact performance by influencing tolerance to physical exertion. CONCLUSION: While current evidence supports a key role for dietary interventions on endurance performance by influencing individuals' perceived effort, more research is needed to determine the optimal doses and precise formulations for different sports, in order to employ a personalized strategy.
Molecular and cellular endocrinologyMatheus Ajackson, Elisa Bernardes Monteiro, Fabiane Ferreira Martins, José Xavier do Nascimento Junior, Eduardo Soares Cavadas Neto, Maria do Socorro Medeiros …
Metabolic-associated steatotic liver disease (MASLD) is strongly associated with obesity and type 2 diabetes (T2D), emerging as a consequence of sustained disturbances in hepatocellular metabolic signaling, inflammatory regulation, and organelle homeostasis induced by nutritional overload. Sulforaphane (SFN), a dietary bioactive compound, has been associated with metabolic protection, yet its ability to preserve hepatic cellular regulation and ultrastructural integrity during MASLD development remains incompletely defined. In this study, C57BL/6 mice were exposed to a high-fat, high-sucrose diet for 14 weeks to induce MASLD, with concomitant SFN administration (2 mg/kg/day, intraperitoneally, 5 days/week). Hepatic and adipose tissue remodeling, insulin signaling, inflammatory pathways, and subcellular architecture were evaluated using biochemical analyses, histology, gene expression profiling, and transmission electron microscopy. SFN markedly attenuated hepatic steatosis, collagen deposition, and glycogen degeneration, while modulating insulin signaling pathway and shifting hepatic gene expression toward oxidative metabolic pathways. These effects were accompanied by suppression of inflammatory mediators, including Nlrp3, Tnfa, and Il1β. At the ultrastructural level, SFN preserved mitochondrial architecture and endoplasmic reticulum organization, preventing diet-induced organelle stress, lipid overload and energy imbalance. Collectively, these findings demonstrate that SFN protects against diet-induced MASLD by maintaining hepatocellular metabolic and inflammatory regulation and preserving organelle integrity, highlighting the relevance of cellular regulatory mechanisms in the control of hepatic intermediary metabolism.
Obesity involves white adipose tissue (WAT) expansion via hyperplasia and hypertrophy. Impaired adipocyte proliferation leads to pathological hypertrophy, inflammation and metabolic dysfunction. Aberrant F‑actin turnover disrupts proliferation/differentiation. Twinfilin‑1 (Twf1) regulates actin dynamics and cell proliferation/differentiation, but its role in adipocytes is unknown. Obese mice were induced by high‑fat diet (HFD) and weight loss by calorie restriction. Inguinal, epididymal and scapular adipose tissues were collected. Proteomics used pressure cycling, DDA library building and DIA quantification. Twf1 expression was validated by RT‑qPCR and Western blot. In C3H10T1/2 preadipocytes, Twf1 knockdown and overexpression were established. Differentiation was induced with dexamethasone, rosiglitazone, insulin and IBMX. Adipogenesis and proliferation were assessed by RT‑qPCR, Western blot, Oil Red O and CCK8. Nuclear‑cytoplasmic fractionation evaluated Yap localization and HIPPO activity. HFD mice showed weight gain, dyslipidemia and adipocyte hypertrophy, reversed by weight loss. Proteomics identified 43 proteins intersecting obesity, weight loss, and actin‑related datasets; Twf1 was upregulated in obese epididymal/inguinal fat and downregulated after weight loss. In C3H10T1/2 cells, Twf1 knockdown enhanced white adipocyte differentiation (upregulated Pparg2, Fsp27, Fabp4) and proliferation (2.28‑fold vs. control), promoted Yap nuclear accumulation, and inhibited HIPPO signalling. Twf1 overexpression reduced differentiation, lipid droplets, and proliferation (to 44.7% of control). Twf1 is upregulated in white/beige adipose tissue of obese mice and downregulated after weight loss. Twf1 knockdown promotes Yap nuclear accumulation, inhibits HIPPO and enhances adipocyte proliferation and white adipocyte maturation, indicating a key role in obesity development.
Given the established positive role of Lipoxin A4 (LXA4) in adipose browning at the cellular level, this study investigated its possible effect on white fat browning and the underlying molecular mechanisms. The obese insulin resistance mouse model was established. The body weight, subcutaneous and visceral fat, and food intake of the mice were observed. Haematoxylin-eosin staining was used to determine the effects of LXA4 on the morphology of inguinal white adipose tissue and brown adipose tissue, and to analyse the changes in fat mass and serum insulin levels, lipid metabolism and other indexes. The cellular experiments included the induction of browning in 3T3-L1 precursor adipocytes, the screening of miRNAs related to adipose browning and their downstream target genes using TargetScan, qRT-PCR, RNA immunoprecipitation and dual luciferase reporter assay. LXA4 attenuated weight gain, inhibited fat accumulation, and improved hyperlipidaemia and insulin resistance in high-fat diet-treated mice. LXA4 also promoted browning of 3T3-L1 precursor adipocytes. Activation of miR-133a-3p partially abrogated LXA4-induced promotion of white adipose browning. The effects of LXA4 and miR-133a-3p could be reversed by SIRT1. Collectively, LXA4 alleviates obesity-related metabolic disorders by promoting inguinal white adipose browning and improving insulin resistance possibly through the miR-133a-3p/SIRT1 pathway.
Scandinavian journal of primary health careSanna Rotonen, Juha Auvinen, Aini Bloigu, Pirjo Härkönen, Jari Jokelainen, Markku Timonen, Sirkka Keinänen-Kiukaanniemi
BACKGROUND: Previous studies have shown an association between dementia and diabetes. This study focused on examining whether insulin resistance is a risk factor for mild cognitive impairment (MCI). We also evaluated whether common cardiovascular risk factors or depressive symptoms modify the risk of MCI along with insulin resistance and compared the health-related quality of life (HRQoL) with or without MCI. METHODS: The participants were followed from 57 to 69 years of age and divided into two groups, MCI and non-MCI, according to their Consortium to Establish a Registry for Alzheimer's Disease (CERAD) total score at the follow-up. The changes in Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and fasting insulin level during the follow-up were determined. Smoking, alcohol consumption, physical activity, depressive symptoms, and HRQoL were obtained by questionnaire. Body weight, height, blood pressure, and low-density lipoprotein (LDL) cholesterol were measured at baseline and follow-up. Adjustments were made for baseline cognitive performance, professional education and physical activity. RESULTS: Greater increases in HOMA-IR (OR 2.20, 95% CI 1.05-4.62) and fasting insulin (OR 3.49, 95% CI 1.48-8.23) increased the risk of MCI. Lower cognitive performance at baseline (OR 6.33; 95% CI 3.27-12.29), lower level of education (OR 3.94, 95% CI 1.76-8.81) and lower level of physical activity (OR 2.44, 95% CI 1.06-5.65) also increased the risk of MCI at follow-up. There was a greater decline in health-related quality of life among the MCI group. CONCLUSION: Insulin resistance is a risk factor for MCI and MCI causes worsening of HRQoL during aging.
Food research international (Ottawa, Ont.)Bingxin Huangfu, Teng Wang, Dongbao Cai, Jia Xu, Kunlun Huang, Zhihong Liang, Weibin Bai, Xiaoyun He
Zearalenone (ZEA) is a mycotoxin frequently detected in food. Cyanidin-3-glucoside (C3G), an anthocyanin abundant in food, exhibits regulatory effects on hepatic metabolism; however, its role in ZEA-induced hepatic lipotoxicity remains unclear. In this study, C57BL/6 J mice were exposed to low-dose ZEA (0.5 mg/kg·bw) combined with a combined with a high-fat diet (HFD) for 96 days, and HepG2 and HepaRG cells were treated with ZEA and oleic acid to investigate chronic ZEA-induced metabolic disturbances. C3G was administered to evaluate its protective effects. ZEA disrupted hepatic energy metabolism, promoted lipid accumulation, and induced more severe lipotoxicity. Mechanistically, ZEA activated the pregnane X receptor (PXR), upregulating fatty acid transporters CD36 and FABP4, thereby enhancing fatty acid uptake and lipid synthesis. C3G inhibits ZEA-induced PXR activation, thereby suppressing PXR signaling and alleviating ZEA-induced hepatic lipotoxicity under HFD conditions. Collectively, C3G mitigates ZEA-induced hepatic lipotoxicity by inhibiting PXR activation, highlighting anthocyanins as potential interventions against mycotoxin-associated metabolic injury.
Food research international (Ottawa, Ont.)Shuyi Zhou, Qunyan Fan, Yujie Fang, Yunxia Zhu, Xuncai Liu, Na Zhang, Guansheng Ma
Edible bird's nest (EBN) is a traditional functional food in Asia, with reported antioxidant and metabolic regulatory properties in preclinical studies, but evidence from controlled human studies describing its metabolic effects remains limited. This study aimed to characterize the serum metabolomic response to dietary EBN supplementation in healthy adults. In a 12-week randomized, double-blind, placebo-controlled trial, 109 healthy women were randomly assigned to placebo, low-dose EBN (3.5 g/day), or high-dose EBN (7.0 g/day). Untargeted serum metabolomics was conducted at baseline and during follow-up to assess metabolic changes associated with EBN intake. EBN intake was associated with time- and dose-dependent alterations in serum metabolomic profiles, with separation from the placebo group emerging by Week 4 and further separation observed at Week 8, followed by attenuation at Week 12. The metabolic response was primarily characterized by changes in amino acid- and lipid-related metabolites, including reduced circulating branched-chain amino acids and increased levels of phosphatidylcholine (PC 18:0) and nordihydroguaiaretic acid. Pathway analysis indicated coordinated modulation of branched-chain amino acid metabolism, glycerophospholipid metabolism, and pentose phosphate pathway-related redox processes, whereas pathway-level changes in the placebo group were limited. These findings provide human-based metabolomic evidence supporting EBN as a functional food with potential dose-dependent metabolic effects. Further studies are warranted to assess these responses across populations and intake durations, and to clarify optimal intake levels and their physiological relevance.
Food research international (Ottawa, Ont.)Wenyu Zhang, Mengxi Kang, Qiuhui Xu, Shasha Zhu, Guangyu Chen, Yihan Wang, Ruxun Zhao, Yihao Yuan, Yan Li, Wenhua Ling, Dongliang Wang
Epidemiological studies have shown that consumption of plant-based foods is associated with reduced risk of atherosclerotic cardiovascular disease. This protective effect is partially attributed to their unique phenolic acid compositions. However, previous studies have substantially underestimated the phenolic acid contents in plant foods, as conventional quantification methods primarily detect soluble free phenolic acids, while neglecting their soluble conjugated and insoluble-bound forms. This study investigated the profiles of eight phenolic acids in soluble free, soluble conjugated, and insoluble-bound forms across 322 plant foods, and further explored their associations with cardiovascular and all-cause mortality among 719 patients with coronary artery disease. The contents and ratios of phenolic acids in the three forms varied substantially across all tested food items. Salsify had the highest total phenolic acid content, 21818-fold higher than that of cucumber with the lowest level. Soluble conjugated and insoluble-bound forms predominated the phenolic acid profiles in cereals, whereas fruits were primarily rich in the soluble free form. Over a 9.33-year follow-up period, 105 cardiovascular deaths and 154 all-cause deaths were recorded. Cox proportional hazards regression analysis revealed that higher dietary intakes of total soluble free phenolic acids and gallic acid in soluble free or soluble conjugated forms were associated with increased risks of cardiovascular and all-cause mortality, whereas no significant associations were observed for total phenolic acids, or total soluble conjugated and total insoluble-bound phenolic acids. Collectively, this study provides a comprehensive food phenolic acid database, highlighting the value of distinguishing the effects of different phenolic acid forms on atherosclerotic cardiovascular disease.
Food research international (Ottawa, Ont.)Caoyu Li, Xinyi Zhao, Ran Zhang, Ruotong Bao, Qiuhui Hu, Yuxi Zhang, Gaoxing Ma, Rui Weng
3D printing can create visually appealing, personalized and nutritious foods, making it an ideal pathway for the development of dysphagia-friendly diets. Shiitake mushroom, characterized by its high protein and low fat, is particularly suitable for consumption by the elderly and can be used as a raw material for the development of 3D-printed dysphagia diet. However, there are significant quality differences between varieties, especially in nutrition, rheology and texture profile analysis, which decides deficiency of its development in the background of 3D printing. Therefore, this study tried to optimize printing ink based on varietal quality differences of five shiitake mushroom. Through investigating the nutritional quality differences among five shiitake mushroom varieties and the feasibility of 3D printing in different solid-liquid ratio(22%, 26%, 30%), it was found that the protein of Qingke212 was the most ideal among these five varieties. In addition, results also revealed all varieties performed well in ratio of 26%, particularly Qingke212 exhibited excellent in rheology and texture profile analysis and could be classified as Level 5-minced and moist dysphagia diets within IDDSI framework. This work provides valuable insights that advance the development of 3D-printed diets for individuals with dysphagia.