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Interactions between the gut, adipose, and liver tissues play important roles in metabolic endotoxemia and gut dysbiosis. This study explored the effectiveness of Curcuma longa rhizome extract (CRE) in improving high-fat diet (HFD)-induced metabolic disorders and modulating gut environments. CRE treatment inhibited lipid accumulation in 3T3-L1 white adipocytes and activated thermogenesis-related genes in T37i brown adipocytes. CRE was administered to HFD-fed mice for 8 weeks, and serum, feces, colon, white adipose, and liver tissue were analyzed. CRE ameliorated the symptoms of metabolic disorders in mice with HFD-induced obesity by suppressing body weight and fat mass gain, adipocyte size, insulin resistance, and hepatic steatosis. CRE regulated gut axis-based mechanisms by inhibiting gut permeability, metabolic endotoxemia, and de novo lipogenesis, and promoting gut barrier integrity. Serum metabolites were negatively correlated with most biomarkers for metabolic disorders. Therefore, CRE could alleviate metabolic disorders by improving the intestinal environment and modulating the gut axis.

Abstract Unbalanced carbohydrate diets are linked to metabolic disorders; however, there is limited information on the role of gut microbiota. We explored differences in mice gut microbiota and metabolic phenotypes resulting from diets with different carbohydrate sources. To investigate the metabolic dysfunction and mechanism of the wheat flour and starch on metabolic disorders, we analyzed the changes of phenotype and biomarkers in rice and wheat flour diet in C57BL/6 mice (specific pathogen‐free) and fecal transplantation from antibiotic‐treated or germ‐free (GF) mice model. Rice‐fed mice presented normal metabolic reactions, whereas wheat‐fed mice exhibited increased body weight, insulin resistance, serum triglycerides, and fasting glucose levels. Wheat starch‐fed mice displayed lower fecal microbiota alpha diversity, with a reduced abundance of Bacteroidetes, than high‐fat diet (HFD)‐fed and chow‐fed mice. Fecal transplantation from antibiotic‐treated or GF mice revealed that metabolic disruption induced by wheat diet feeding was mediated through gut microbiota and stearoyl‐CoA desaturase 1 (SCD1) signaling in the colon. Taken together, wheat‐based diets induce gut microbiota alterations, causing obesity and metabolic diseases through molecular activity linked to colonic SCD1. Therefore, colonic SCD1 could be a therapeutic target for patients with metabolic diseases who consume high‐carbohydrate diets.

Obesity is caused by excessive adipogenesis and leads to metabolic diseases such as diabetes, hypertension, and degenerative arthritis. Therefore, there is an ever-increasing need to identify new anti-obesity compounds. In this study, the anti-obesity effects of (E)-3-(4-(tert-butyl)phenyl)-N-isobutyl-2-methylacrylamide (BPIMA) were evaluated using pre-adipocytes and a high-fat-fed C57BL/6J mouse model. As the results, BPIMA effectively inhibited adipocyte differentiation (64.3% at 40 μM) without exhibiting any cytotoxicity. Additionally, BPIMA decreased the protein levels of PPARγ, FAS, C/EBP, and SREBP in 3T3-L1 cells in a concentration-dependent manner. In C57BL/6J mice, a significant decrease in body weight, adipose tissue, and fatty liver was observed in the BPIMA-treated high-fat group compared to that observed in the vehicle-treated high-fat group; the serum levels of total cholesterol and glucose also significantly decreased in the BPIMA-treated high-fat group. Moreover, the weight and fat level of liver and serum AST, ALT activity in the BPIMA-treated high-fat group were similar to low fat diet-control group. These findings show that BPIMA may be a potential anti-obesity compound.

Osteoarthritis is one of the leading conditions that promote the consumption of these dietary supplements. Chondroitin sulfate, glucosamine, and methylsulfonylmethane are among the prominent alternative treatments for osteoarthritis. In this study, these dietary supplements were incubated with cytochrome P450 isozyme-specific substrates in human liver microsomes, and the formation of marker metabolites was measured to investigate their inhibitory potential on cytochrome P450 enzyme activities. The results revealed no significant inhibitory effects on seven CYPs, consistent with established related research data. Therefore, these substances are anticipated to have a low potential for cytochrome P450-mediated drug interactions with osteoarthritis medications that are likely to be co-administered. However, given the previous reports of interaction cases involving glucosamine, caution is advised regarding dietary supplement–drug interactions.

Prolonged intake of a high-fat diet (HFD) disturbs the composition of gut microbiota, contributing to the development of metabolic diseases, notably obesity and increased intestinal permeability. Thyme (Thymus vulgaris L.), an aromatic plant, is known for its several therapeutic properties. In this study, we explored the potential of thyme extract (TLE) to mitigate HFD-induced metabolic derangements and improve the gut environment. Eight-week-old C57BL/6 mice were administered 50 or 100 mg/kg TLE for eight weeks. Administration of 100 mg/kg TLE resulted in decreased weight gain and body fat percentage, alongside the regulation of serum biomarkers linked to obesity induced by a HFD. Moreover, TLE enhanced intestinal barrier function by increasing the expression of tight junction proteins and ameliorated colon shortening. TLE also altered the levels of various metabolites. Especially, when compared with a HFD, it was confirmed that 2-hydroxypalmitic acid and 3-indoleacrylic acid returned to normal levels after TLE treatment. Additionally, we investigated the correlation between fecal metabolites and metabolic parameters; deoxycholic acid displayed a positive correlation with most parameters, except for colon length. In contrast, hypoxanthine was negatively correlated with most parameters. These results suggest a promising role for thyme in ameliorating obesity and related gut conditions associated with a HFD.

The SARS-CoV-2 coronavirus, which causes a respiratory disease called COVID-19, has been declared a pandemic by the World Health Organization (WHO) and is still ongoing. Vaccination is the most important strategy to end the pandemic. Several vaccines have been approved, as evidenced by the ongoing global pandemic, but the pandemic is far from over and no fully effective vaccine is yet available. One of the most critical steps in vaccine development is the selection of appropriate antigens and their proper introduction into the immune system. Therefore, in this study, we developed and evaluated two proposed vaccines composed of single and multiple SARS-CoV-2 polypeptides derived from the spike protein, namely, vaccine A and vaccine B, respectively. The polypeptides were validated by the sera of COVID-19-vaccinated individuals and/or naturally infected COVID-19 patients to shortlist the starting pool of antigens followed by in vivo vaccination to hACE2 transgenic mice. The spike multiple polypeptide vaccine (vaccine B) was more potent to reduce the pathogenesis of organs, resulting in higher protection against the SARS-CoV-2 infection.

Abstract Background Chronic fatigue syndrome (CFS) is a long-term disabling illness accompanied by medically unexplained fatigue. This study aimed to explore the epidemiological characteristics of CFS in South Korea. Methods Using the nationwide medical records provided by the Korean Health Insurance Review & Assessment Service (HIRA), we analyzed the entire dataset for CFS patients diagnosed by physicians in South Korea from January 2010 to December 2020. Results The annual mean incidence of CFS was estimated to be 44.71 ± 6.10 cases per 100,000 individuals [95% CI: 40.57, 48.76], and the prevalence rate was 57.70 ± 12.20 cases per 100,000 individuals [95% CI: 49.40, 65.79]. These two rates increased by 1.53- and 1.94-fold from 2010 to 2020, respectively, and showed an increasing trend with aging and an approximately 1.5-fold female predominance. Conclusions This study is the first to report the nationwide epidemiological features of CFS, which reflects the clinical reality of CFS diagnosis and care in South Korea. This study will be a valuable reference for studies of CFS in the future.

Radish (Raphanus sativus L.) greens are consumed as a source of nutrition, and their polysaccharides such as rhamnogalacturonan-I possess certain beneficial properties. This study investigated the prebiotic effects of a radish green polysaccharide (RGP) on gut health and obesity. The prebiotic activity of RGP was evaluated based on the pH changes and short-chain fatty acids (SCFAs) concentration. The results showed that 0.5% RGP had a higher prebiotic activity score than inulin and increased SCFAs production in all five prebiotic strains. Moreover, RGP inhibited fat accumulation in 3T3-L1 adipocytes, indicating its potential to reduce obesity. Overall, these findings suggested that the polysaccharide of radish greens has prebiotic effects and may serve as a beneficial prebiotic for gut health and obesity.

Background and AimsExcessive intake of advanced glycation end products (AGEs), which are formed in foods cooked at high temperatures for long periods of time, has negative health effects, such as inflammatory responses and oxidative stress. Nε-(Carboxymethyl)lysine (CML) is one of the major dietary AGEs. Given their generally recognized as safe status and probiotic functionalities, lactic acid bacteria may be ideal supplements for blocking intestinal absorption of food toxicants. However, the protective effects of lactic acid bacteria against dietary AGEs have not been fully elucidated.Materials and MethodsWe investigated the effect of treatment with Lactococcus lactis KF140 (LL-KF140), which was isolated from kimchi, on the levels and toxicokinetics of CML. The CML reduction efficacies of the Lactococcus lactis KF140 (LL-KF140), which was isolated from kimchi, were conducted by in vitro test for reducing CML concentration of the casein-lactose reaction product (CLRP) and in vivo test for reducing serum CML level of LL-KF140 administered rats at 2.0 × 108 CFU/kg for14 days. In addition, 12 volunteers consuming LL-KF140 at 2.0 × 109 CFU/1.5 g for 26 days were determined blood CML concentration and compared with that before intake a Parmesan cheese.ResultsAdministration of LL-KF140 reduced serum CML levels and hepatic CML absorption in rats that were fed a CML-enriched product. In a human trial, the intake of LL-KF140 prevented increases in the serum levels of CML and alanine aminotransferase after consumption of a CML-rich cheese. LL-KF140 was determined to presence in feces through metagenome analysis. Furthermore, β-galactosidase, one of the L. lactis-produced enzymes, inhibited the absorption of CML and reduced the levels of this AGE, which suggests an indirect inhibitory effect of LL-KF140. This study is the first to demonstrate that an L. lactis strain and its related enzyme contribute to the reduction of dietary absorption of CML.

IL-32 plays a contradictory role such as tumor proliferation or suppressor in cancer development depending on the cancer type. In most cancers, it was found that the high expression of IL-32 was associated with more proliferative and progression of cancer. However, studying the isoforms of IL-32 cytokine has placed its paradoxical role into a wide range of functions based on its dominant isoform and surrounding environment. IL-32β, for example, was found mostly in different types of cancer and associated with cancer expansion. This observation is legitimate since cancer exhibits some hypoxic environment and IL-32β was known to be induced under hypoxic conditions. However, IL-32θ interacts directly with protein kinase C-δ reducing NF-κB and STAT3 levels to inhibit epithelial-mesenchymal transition (EMT). This effect could explain the different functions of IL-32 isoforms in cancer. However, pro- or antitumor activity which is dependant on obesity, gender, and age as it relates to IL-32 has yet to be studied. Obesity-related IL-32 regulation indicated the role of IL-32 in cancer metabolism and inflammation. IL-32-specific direction in cancer therapy is difficult to conclude. In this review, we address that the paradoxical effect of IL-32 on cancer is attributed to the dominant isoform, cancer type, tumor microenvironment, and genetic background. IL-32 seems to have a contradictory role in cancer. However, investigating multiple IL-32 isoforms could explain this doubt and bring us closer to using them in therapy.

Cytokines are significantly associated with the homeostasis of immune responses in health and disease. Interleukin-32 (IL-32) is a cytokine originally discovered in natural killer cell transcript 4. IL-32 with different disorders has been described in terms of pathogenesis and the progression of diseases. Clinical studies have investigated IL-32 under various conditions, such as viral infection, autoimmune diseases, inflammatory diseases, certain types of cancer, vascular disease, and pulmonary diseases. The high expression of IL-32 was identified in different tissues with various diseases and found to have multiple transcripts of up to seven isoforms. However, the purification and biological activities of these isoforms have not been investigated yet. Therefore, in this study, we purified and compared the biological activity of recombinant IL-32 (rIL-32) isoforms. This is the first time for seven rIL-32 isoforms (α, β, δ, γ, ϵ, ζ, and θ) to be cloned and purified using an Escherichia coli expression system. Next, we evaluate the biological activities of these seven rIL-32 isoforms, which were used to treat different types of cells by assessing the levels of inflammatory cytokine production. The results revealed that rIL-32θ possessed the most dominant biological activity in both immune and non-immune cells.

Gut microbial dysbiosis, induced by alcohol consumption, disrupts the gut-liver axis, leading to the development and progression of alcoholic liver disease. In this study, we investigated the protective effects of the water-soluble extract from molokhia (Corchorus olitorius L.) leaves (WM) on the alcohol-induced disruption of the gut-liver axis in mice. The administration of 50 and 100 mg/kg WM reduced the levels of serum biomarkers for liver injury. Moreover, WM treatment ameliorated the alcohol-induced increase in hepatic inflammation and lipogenic protein levels. WM improved the gut microbial composition disrupted by alcohol, which suggests the effects of WM in mediating the gut-liver axis. WM also improved gut barrier function via the regulation of gut permeability and tight junction protein expression. These results indicate that WM can be used as a food supplement to improve alcohol-induced liver damage by regulating the gut-liver axis.

Although the prevalence of metabolic disorders has progressively increased over the past few decades, metabolic disorders can only be effectively treated with calorie restriction and improved physical activity. Recent research has focused on altering the gut microbiome using prebiotics, probiotics, and postbiotics because various metabolic syndromes are caused by gut microbial dysbiosis. Postbiotics, substances produced or released by microorganism metabolic activities, play an important role in maintaining and restoring host health. Because postbiotics have a small amount of literature on their consumption, there is a need for more experiments on short- and long-term intake. This review discusses current postbiotic research, categories of postbiotics, positive roles in metabolic syndromes, and potential therapeutic applications. It covers postbiotic pleiotropic benefits, such as anti-obesity, anti-diabetic, and anti-hypertensive qualities, that could aid in the management of metabolic disorders. Postbiotics are promising tools for developing health benefits and therapeutic goals owing to their clinical, technical, and economic properties. Postbiotic use is attractive for altering the microbiota; however, further studies are needed to determine efficacy and safety.

Diet-induced obesity is one of the major causes of the development of metabolic disorders such as insulin resistance and nonalcoholic fatty liver disease (NAFLD). Recently, specific probiotic strains have been found to improve the symptoms of NAFLD. We examined the effects of Bifidobacterium animalis ssp. lactis MG741 (MG741) on NAFLD and weight gain, using a mouse model of high-fat-diet (HFD)-induced obesity. HFD-fed mice were supplemented daily with MG741. After 12 weeks, MG741-administered mice exhibited reduced fat deposition, and serum metabolic alterations, including fasting hyperinsulinemia, were modulated. In addition, MG741 regulated Acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), sterol regulatory element-binding protein 1 (SREBP-1), and carbohydrate-responsive element-binding protein (ChREBP) expression and lipid accumulation in the liver, thereby reducing the hepatic steatosis score. To determine whether the effects of MG741 were related to improvements in gut health, MG741 improved the HFD-induced deterioration in gut permeability by reducing toxic substances and inflammatory cytokine expression, and upregulating tight junctions. These results collectively demonstrate that the oral administration of MG741 could prevent NAFLD and obesity, thereby improving metabolic health.

This study was aimed at investigating the immunomodulating activities of molokhia leaf extract. To examine the immunomodulatory activities of a water-soluble molokhia (Corchorus olitorius) leaf extract (WME), nitric oxide (NO) and cytokine levels in relation to macrophage activation were estimated in a cyclophosphamide-induced murine model of immunosuppression, and a natural killer (NK) cell cytotoxicity assay was conducted. Administration of WME significantly augmented NK cell cytotoxicity against YAC-1 cells by inducing the release of granzyme B. In addition, murine peritoneal macrophages stimulated by WME produced various cytokines, including tumor necrosis factor (TNF)-α and interleukin (IL)-6. The results of this study showed that WME administration (50 and 100 mg/kg) increased thymus and spleen indices, and the leukocyte count in the blood of immunosuppressed mice. These results demonstrated that WME possesses immunomodulatory activity and may represent a potential immunostimulant for enhancing human immunity.

Retrogradation is the principal cause for bread staling and, therefore, it has attracted a lot of interest from the food industry. In this study, the inhibitory effect of citrus peel hydrolysates (CPH) on retrogradation of wheat starch (WS) in the presence of sucrose was investigated. The pasting properties showed that further addition of CPH caused a lower setback value than the addition of sucrose alone. Hardness of the gel, retrograded at 4 °C for five days, showed a similar tendency, which was reduced more in CPH addition than WS itself or sucrose addition alone. The low retrogradation enthalpy of the CPH including starch gel also indicated the positive effect of CPH on retarding retrogradation. These results suggested that incorporation of CPH in starch-based foods would be effective for inhibiting retrogradation, preventing the deterioration of the quality of food products.

Dietary habits and gut microbiota play an essential role in non-alcoholic fatty liver disease (NAFLD) and related factors such as insulin resistance and de novo lipogenesis. In this study, we investigated the protective effects of Bacteroides uniformis CBA7346, isolated from the gut of healthy Koreans, on mice with high-fat diet (HFD)-induced NAFLD. Administration of B. uniformis CBA7346 reduced body and liver weight gain, serum alanine aminotransferase and aspartate aminotransferase levels, liver steatosis, and liver triglyceride levels in mice on an HFD; the strain also decreased homeostatic model assessment for insulin resistance values, as well as serum cholesterol, triglyceride, lipopolysaccharide, leptin, and adiponectin levels in mice on an HFD. Moreover, B. uniformis CBA7346 controlled fatty liver disease by attenuating steatosis and inflammation and regulating de novo lipogenesis-related proteins in mice on an HFD. Taken together, these findings suggest that B. uniformis CBA7346 ameliorates HFD-induced NAFLD by reducing insulin resistance and regulating de novo lipogenesis in obese mice.

Diabetic nephropathy (DN) is one of the most significant microvascular complications in diabetic patients. DN is the leading cause of end-stage renal disease, accounting for approximately 50% of incident cases. The current treatment options, such as optimal control of hyperglycemia and elevated blood pressure, are insufficient to prevent its progression. DN has been considered as a nonimmune, metabolic, or hemodynamic glomerular disease initiated by hyperglycemia. However, recent studies suggest that DN is an inflammatory disease, and immune cells related with innate and adaptive immunity, such as macrophage and T cells, might be involved in its development and progression. Although it has been revealed that kidney dendritic cells (DCs) accumulation in the renal tissue of human and animal models of DN require activated T cells in the kidney disease, little is known about the function of DCs in DN. In this review, we describe kidney DCs and their subsets, and the role in the pathogenesis of DN. We also suggest how to improve the kidney outcomes by modulating kidney DCs optimally in the patients with DN.

Innate immune system might be a useful strategy for antimetastatic therapy. To examine the antitumor and immunomodulatory activities of a glycoprotein isolated from rice bran (GRB), we made an experiment on innate immune response against lung metastasis of colon 26-M3.1 carcinoma cells. To prove the effects of GRB, natural killer (NK) cytotoxicity assay and cytokine level estimation in relation to macrophage activation were performed. In experimental lung metastasis of colon 26-M3.1 cells, intravenous administration of GRB 2 days before tumor inoculation induced significant inhibition, by 77%. Intravenous GRB significantly augmented NK cell cytotoxicity against YAC-1 cells by releasing lymphocyte granule-mediated cytotoxic granzyme B. In addition, murine peritoneal macrophages stimulated by GRB produced various cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-12. The results suggest that GRB possesses an antitumor activity that prophylactically prevented tumor metastasis and may be associated with the activation of NK cells and macrophages.

6-paradol is a non-pungent and biotransformed metabolite of 6-shogaol. It has recently been shown to exhibit a variety of biological activities including anti-cancer, anti-inflammatory, and anti-oxidative activities. This study was designed to investigate biotransformation of 6-shogaol to 6-paradol from 6-shogaol-enriched ginger extracts (SGE) by Schizosaccharomyces pombe and evaluate the neuroprotective effect of fermented ginger extract (FGE). During fermentation of SGE by S. pombe, 6-gingerol content was maintained, whereas 6-shogaol was efficiently biotransformed to 6-paradol. FGE was evaluated for its neuroprotective effect against amyloid-beta (Aβ)-induced neurotoxicity in rat primary hippocampal cells. Cell viability was reduced to 68%, and to 65% when exposed to Aβ oligomer and Aβ plaque for 18 h, and 50 μg/mL of FGE increased cell viability (92% and 89.6%, respectively). These results indicate that fermentation of SGE can provide an efficient method of 6-pradol formation and that FGE has potential as a neuroprotective agent.

Methylglyoxal (MG) is known to form advanced glycation end products (AGEs) and has emerged as a leading cause of diabetes and the associated complications. We aimed to explore the therapeutic effects and action mechanism of Schizonepeta tenuifolia, by investigating its protective effect on MG-induced cytotoxicity in mouse mesangial cells. Schizonepeta tenuifolia exerted inhibitory effect on MG-mediated AGE formation and AGE–protein cross-linking. MG treatment also reduced cell viability and increased reactive oxygen species (ROS), but S. tenuifolia treatment reversed these phenomena. We also confirmed that S. tenuifolia can activate the Nrf2-ARE pathway. While MG treatment reduced the expression of Nrf2 and its downstream molecules, S. tenuifolia treatment upregulated these protein expression. In conclusion, S. tenuifolia ameliorates cytotoxicity and oxidative stress in mouse mesangial cells via inhibition of AGE formation and AGE–protein cross-linking. Thus, S. tenuifolia can serve as a health food and potential candidate for treating MG-induced glucotoxicity.

Curcuma longa L. (turmeric) has been used as a functional food material, but other parts of it such as leaves are wasted as a byproduct. This work concentrated on developing turmeric leaves as a functional food material by establishing its optimal extraction condition. Response surface methodology was applied to optimize turmeric leaf extraction conditions. Turmeric leaves were pulled out with water and ethanol (10, 30, and 50%). Then, total phenolic compound content, total flavonoid content, and radical-scavenging activity of each extract were quantified to confirm the optimal extracting solvent. According to the results, water was the most efficient solvent to extract antioxidant contents such as total phenolic compounds (3.65 ± 0.02 mg GAE/g) and flavonoids (4.99 ± 0.17 mg QCE/g) content. Radical-scavenging activity was also higher in water extract compared with others such as DPPH (51.10 ± 2.29%), H2O2 (25.39 ± 2.69%), and ABTS (91.08 ± 0.15%). Central composite design was applied to confirm the effect of independent variables such as temperature (X1) and time (X2) to the yield (Y1). After conducting experiments, the extraction condition was established as 150 min with 1 : 25 ratio at 85°C with a 15.58% yield. Proximate compositions of the extract were determined to suggest background data for further research. In conclusion, this study confirmed the antioxidant property of turmeric leaves and developed the optimal extraction condition of the leaves to promote its application in food industry as a new food source.

Inflammatory bowel disease is a chronic relapsing disease. Multiple factors can cause inflammatory bowel disease (IBD), including diet, imbalance of the immune system, and impaired intestinal barrier function. Type 2 diabetes mellitus is a complex and chronic metabolic disease caused by a combination of insulin resistance and an ineffective insulin secretory response. The co-occurrence of these two diseases, demonstrating interrelated effects within the gut microbiota, has been frequently reported. This study evaluated the effects of a fermented glycated conjugate of whey protein and galactose with Lactobacillus gasseri 4M13 (FMRP) to prevent type 2 diabetes mellitus with inflammatory bowel disease. C57BLKS/J- db/db mice were orally administered FMRP for 14 consecutive days and 2% dextran sulfate sodium (DSS) in water ad libitum for 5 days to induce colitis. FMRP-fed mice showed improved insulin secretion and symptoms of colitis. Compared to the DSS group, the FMRP group showed a decreased abundance of six bacterial genera and increased abundance of Alistipes and Hungateiclostridium. In cecal contents, the levels of short-chain fatty acids increased in the FMRP group compared to those in the DSS group. Continuous administration of FMRP thus may improve the homeostasis of not only insulin secretion and inflammation, but also the intestinal environment in inflammatory bowel disease and type 2 diabetes mellitus.

This study was designed to investigate the neuroprotective effect of fermented shogaol-enriched extract (FSE), which is converted to 6-paradol by Aspergillus niger. FSE was fermented for varying time points (FSE-0, FSE-30, and FSE-60). Optimal condition for 6-paradol produced by A. niger was determined as initial inoculated cell concentration (1.5 × 106 spores/mL) from shogaol-enriched extract (240 µg/mL) for 60 h. The ability of FSE to protect the rat primary hippocampal cells from beta-amyloid (Αβ) oligomer and Αβ plaque induced neurotoxicity and to inhibit acetylcholinesterase (AChE) activity was evaluated. Hippocampal cell viability was reduced to 70% when exposed to Αβ oligomer, and exposure to Αβ plaque for 18 h and 50 µg/mL of FSE-60 increased cell viability (92% and 95.3%, respectively). In addition AChE inhibitory activity of FSE-60 at 50 µg/mL was 53%, which was similar to 0.1 µM tacrine. Therefore, these results demonstrate that FSE-60 has potential as a neuroprotective agent.

Recent studies report that microbiota in the human intestine play an important role in host health and that both long- and short-term diets influence gut microbiota. These findings have fueled interest in the potential of food to promote health by shaping the intestinal microbiota. Despite the fact that large populations in Asia consume high quantities of carbohydrates, such diets have been ignored in comparison to the attention received by Western diets containing high quantities of fat and animal protein. We gathered data that suggest an association between imbalanced high-carbohydrate intake and gut microbiota and host health. In this review, we identify not only the effect of total carbohydrates on the intestinal microbiota specifically and the health of their hosts in general, but also how specific types of carbohydrates influence both factors.

Diets high in gelatinized starch and high in gelatinized starch supplemented with salt-induced metabolic disorders and changes in gut microbiota have scarcely been studied. In this study, mice on wheat starch diets (WD) exhibited significantly higher body weight, white adipose tissue (WAT), and gut permeability compared to those on normal diet (ND). However, gelatinized wheat starch diet (GWD) and NaCl-supplemented gelatinized wheat starch diet (SGW) mice did not increase body and WAT weights or dyslipidemia, and maintained consistent colon pH at ND levels. WD mice showed higher levels of Desulfovibrio, Faecalibaculum, and Lactobacillus and lower levels of Muribaculum compared to ND mice. However, GWD and SGW mice showed a significantly different gut microbial composition, such as a lower proportion of Lactobacillus and Desulfovibrio, and higher proportion of Faecalibaculum and Muribaculum compared to WD mice. High starch diet-induced dysbiosis caused increase of lipid accumulation and inflammation-related proteins’ expression, thereby leading to non-alcoholic fatty liver disease. However, GWD and SGW showed lower levels than that, and it might be due to the difference in the gut microbial composition compared to WD. Taken together, diets high in gelatinized starch and high in gelatinized starch supplemented with salt induced mild metabolic disorders compared to native starch.

Spatholobus suberectus (SS) is a medicinal herb commonly used in Asia to treat anemia, menoxenia and rheumatism. However, its effect of diabetes-induced renal damage and mechanisms of action against advanced glycation end-products (AGEs) are unclear. In this study, we evaluated the effects of SS on diabetes-induced renal damage and explored the possible underlying mechanisms using db/db type 2 diabetes mice. db/db mice were administered SS extract (50 mg/kg) orally for 6 weeks. SS-treated group did not change body weight, blood glucose and glycated hemoglobin (HbA1c) levels. However, SS treatment reversed diabetes-induced dyslipidemia and urinary albumin/creatinine ratio in db/db mice. Moreover, SS administration showed significantly increased protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), which is a transcription factor for antioxidant enzyme. SS significantly upregulated glyoxalase 1 (Glo1) and NADPH quinine oxidoreductase 1 (NQO1) expression but reduced CML accumulation and downregulated receptor for AGEs (RAGE). Furthermore, SS showed significant decrease of periodic acid–Schiff (PAS)-positive staining and AGEs accumulation in histological and immunohistochemical analyses of kidney tissues. Taken together, we concluded that SS ameliorated the renal damage by inhibiting diabetes-induced glucotoxicity, dyslipidemia and oxidative stress, through the Nrf2/antioxidant responsive element (ARE) stress-response system.

High fat diet-induced changes in gut microbiota have been linked to intestinal permeability and metabolic endotoxemia, which is related to metabolic disorders. However, the influence of a high-glucose (HGD) or high-fructose (HFrD) diet on gut microbiota is largely unknown. We performed changes of gut microbiota in HGD- or HFrD-fed C57BL/6J mice by 16S rRNA analysis. Gut microbiota-derived endotoxin-induced metabolic disorders were evaluated by glucose and insulin tolerance test, gut permeability, Western blot and histological analysis. We found that the HGD and HFrD groups had comparatively higher blood glucose and endotoxin levels, fat mass, dyslipidemia, and glucose intolerance without changes in bodyweight. The HGD- and HFrD-fed mice lost gut microbial diversity, characterized by a lower proportion of Bacteroidetes and a markedly increased proportion of Proteobacteria. Moreover, the HGD and HFrD groups had increased gut permeability due to alterations to the tight junction proteins caused by gut inflammation. Hepatic inflammation and lipid accumulation were also markedly increased in the HGD and HFrD groups. High levels of glucose or fructose in the diet regulate the gut microbiota and increase intestinal permeability, which precedes the development of metabolic endotoxemia, inflammation, and lipid accumulation, ultimately leading to hepatic steatosis and normal-weight obesity.