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In this study, ferulic acid was investigated for its potential in suppressing TNF-α-treated inflammation and insulin resistance in adipocytes. Ferulic acid suppressed TNF-α, IL-6, IL-1β, and MCP-1. TNF-α increased p-JNK and ERK1/2, but treatment with ferulic acid (1, 10, and 50 μM) decreased p-JNK and ERK1/2. TNF-α induced the activation of IKK, IκBα, and NF-κB p65 compared to the control, but ferulic acid inhibited the activation of IKK, IκBα, and NF-κB p65. Following treatment with TNF-α, pIRS-1ser307 increased and pIRS-1tyr612 decreased compared to the control. Conversely, as a result of treatment with 1, 10, and 50 μM ferulic acid, pIRS-1ser307 was suppressed, and pIRS-1tyr612 was increased. Therefore, ferulic acid reduced inflammatory cytokine secretion by regulating JNK, ERK, and NF-κB and improved insulin resistance by suppressing pIRS-1ser. These findings indicate that ferulic acid can improve inflammation and insulin resistance in adipocytes.

Background: (E)-5-hydroxy-7-methoxy-3-(2-hydroxybenzyl)-4-chromanone (HMC), a homoisoflavonoid isolated from Portulaca oleracea, has significant anti-adipogenesis potential; it regulates adipogenic transcription factors. However, whether HMC improves hepatic steatosis in hepatocytes remains vague. This study investigated whether HMC ameliorates hepatic steatosis in free fatty acid-treated human hepatocellular carcinoma (HepG2) cells, and if so, its mechanism of action was analyzed. Methods: Hepatic steatosis was induced by a free fatty acid mixture in HepG2 cells. Thereafter, different HMC concentrations (10, 30, and 50 µM) or fenofibrate (10 µM, a PPARα agonist, positive control) was treated in HepG2 cells.Results: HMC markedly decreased lipid accumulation and triglyceride content in free fatty acid-treated HepG2 cell; it (10 and 50 μM) markedly upregulated protein expressions of pAMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. HMC (10 and 50 μM) markedly inhibited the expression of sterol regulatory element-binding protein-1c, fatty acid synthase, and stearoyl-coA desaturase 1, which are the enzymes involved in lipid synthesis. Furthermore, HMC (10 and 50 μM) markedly upregulated the protein expression of peroxisome proliferator-activated receptor alpha (PPARα) and enhanced the protein expressions of carnitine palmitoyl transferase 1 and acyl-CoA oxidase 1. Conclusion: HMC inhibits lipid accumulation and promotes fatty acid oxidation by AMPK and PPARα pathways in free fatty acid-treated HepG2 cells, thereby attenuating hepatic steatosis.

Objectives: We investigated potential antihyperglycemic effects of HM-chromanone (HMC), a homoisoflavonoid isolated from Portulaca oleracea, in mice fed a high-fat diet (HFD). Methods: Five-week-old male C57BL/6J mice (n = 24) were divided into three groups: controls, mice fed an HFD (11 weeks), and HFD-fed mice receiving HMC supplementation (8 weeks). Various analyses assessed liver and skeletal muscle proteins, pancreatic β-cell histology, blood glucose and HbA1c levels, and homeostatic index of insulin resistance (HOMA-IR). Results: HMC supplementation significantly reduced fasting blood glucose and postprandial blood glucose levels in HFD-fed mice. HbA1c and serum insulin levels reduced significantly, and HOMA-IR improved. Compensatory β-cell hyperplasia was reduced, and pancreatic β-cell function improved. AMP-activated protein kinase (AMPK) was significantly activated in skeletal muscle and liver tissues. IRS-1tyr612 expression increased significantly. PI3K activation and Akt phosphorylation in skeletal muscles improved insulin signaling. Forkhead box protein O1 phosphorylation increased through hepatic AMPK activation. Phosphoenolpyruvate carboxykinase and glucose-6-phosphatase expression was inhibited. Glycogen synthase kinase 3β phosphorylation increased. Conclusions: HMC supplementation alleviated hyperglycemia by activating the AMPK and PI3K/Akt pathways in skeletal muscles and the AMPK pathway in the liver of HFD-fed mice.

This study investigated the effect of (E)-5-hydroxy-7-methoxy-3-(2-hydroxybenzyl)-4-chromanone (HM-chromanone) on palmitate-induced insulin resistance and elucidated the underlying mechanism in L6 skeletal muscle cells. Glucose uptake was markedly decreased due to palmitate-induced insulin resistance in these cells; however, 10, 25, and 50 µM HM-chromanone remarkably improved glucose uptake in a concentration-dependent manner. HM-chromanone treatment downregulated protein tyrosine phosphatase 1B (PTP1B) and phosphorylation of c-Jun N-terminal kinase (JNK) and inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ), which increased because of palmitate mediating the insulin-resistance status in cells. HM-chromanone promoted insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation and suppressed palmitate-induced phosphorylation of IRS-1 serine. This activated phosphoinositide 3-kinase (PI3K) and stimulated protein kinase B (AKT) phosphorylation. Phosphorylated AKT promoted the translocation of Glucose transporter type 4 to the plasma membrane and significantly enhanced glucose uptake into muscle cells. Additionally, HM-chromanone increased glycogen synthesis through phosphorylating glycogen synthase kinase 3 alpha/beta (GSK3 α/β) via AKT. Consequently, HM-chromanone may improve insulin resistance by downregulating the phosphorylation of IRS-1 serine through inhibition of negative regulators of insulin signaling and inflammation-activated protein kinases in L6 skeletal muscle cells.

Health-oriented tourism has emerged as one of the fastest-growing niche tourism fields worldwide. Although there have been studies on the relationship between health and travel behavior, most have been from the perspective of travel motivation and have rarely examined the impact of travel on health. This study explores those travel elements that have a positive influence on health in the domestic health tourism industry, with health being viewed across three domains: psychological, physical, and social. A total of 28 health-contributing travel items reported by 862 package tour participants were analyzed. On the psychological health dimension, experiencing good feelings and escaping bad ones is important. On the physical wellness dimension, natural patterns of food intake during the day is strongly recognized, including the results of increased appetite and improved digestion. On the social health dimension, relationship improvements were experienced, along with a greater understanding of partner(s). These findings add to our understanding of traveler wellness, a significant step towards having the right information to enhance the quality of travel services, especially in the domestic health tourism industry.

Context: 2,7″-Phloroglucinol-6,6′-bieckol is a type of phlorotannin isolated from brown algae, Ecklonia cava Kjellman (Phaeophyceae; Laminareaceae). 2,7″-Phloroglucinol-6,6′-bieckol mediates antioxidant activities. However, there has been no research on improving postprandial hyperglycaemia using 2,7″-phloroglucinol-6,6′-bieckol.Objective: This study investigated the inhibitory effects of 2,7″-phloroglucinol-6,6′-bieckol on activities of α-glucosidase and α-amylase as well as its alleviating effect on postprandial hyperglycaemia in streptozotocin-induced diabetic mice.Materials and methods: α-Glucosidase and α-amylase inhibitory assays were carried out. The effect of 2,7″-phloroglucinol-6,6′-bieckol on hyperglycaemia after a meal was measured by postprandial blood glucose in streptozotocin-induced diabetic and normal mice. The mice were treated orally with soluble starch (2 g/kg BW) alone (control) or with 2,7″-phloroglucinol-6,6′-bieckol (10 mg/kg bw) or acarbose (10 mg/kg BW) dissolved in 0.2 mL water. Blood samples were taken from tail veins at 0, 30, 60, and 120 min and blood glucose was measured by a glucometer.Results: 2,7″-Phloroglucinol-6,6′-bieckol showed higher inhibitory activities than acarbose, a positive control against α-glucosidase and α-amylase. The IC50 values of 2,7″-phloroglucinol-6,6′-bieckol against α-glucosidase and α-amylase were 23.35 and 6.94 μM, respectively, which was found more effective than observed with acarbose (α-glucosidase IC50 of 130.04 μM; α-amylase IC50 of 165.12 μM). In normal mice, 2,7″-phloroglucinol-6,6′-bieckol significantly suppressed the postprandial hyperglycaemia caused by starch. The 2,7″-phloroglucinol-6,6′-bieckol administration group (2349.3 mmol·min/L) had a lower area under the curve (AUC) glucose response than the control group (2690.83 mmol·min/L) in diabetic mice.Discussion and conclusion: 2,7″-Phloroglucinol-6,6′-bieckol might be used as an inhibitor of α-glucosidase and α-amylase as well as to delay absorption of dietary carbohydrates.

This study investigated the protective effects of Sargassum sagamianum extract (SSE) on INS-1 pancreatic β cells against high glucose-induced oxidative stress and apoptosis. Treatment with glucose at high concentrations (30 mM) caused β cell apoptosis, whereas treatment with SSE protected the β cells from high glucose-induced damage, by recovering the cell viability. Treatment with SSE at concentrations of 10–100 μg/mL decreased lipid peroxidation and intracellular reactive oxygen species and nitric oxide levels, and increased cell viability and insulin secretion in high glucose pretreated INS-1 cells in a dose-dependent manner. Moreover, SSE treatment significantly reduced the expression of pro-apoptotic Bax, cytochrome c , caspase-3, and caspase-9, while the expression of anti-apoptotic Bcl-2 increased. The type of cell death was examined by annexin V/propidium iodide staining, which revealed that SSE treatment markedly reduced high glucose-induced apoptosis. These findings suggest that SSE could be useful as a functional food, protecting pancreatic β cells against high glucose-induced oxidative stress and apoptosis.

The purpose of this study was to determine the anti-obesity effects of Gelidium amansii extract (GAE) in the C57BL/6J-ob/ob mice. The ob/ob mice were fed GAE at 0.5% for 4 weeks, after which body weight, epididymal adipose tissue weight, plasma triglycerides, and hepatic lipid accumulation were significantly reduced in GAE-fed mice compared with ob/ob control mice. Plasma adiponectin levels were significantly higher in GAE-fed mice than in ob/ob control mice. These findings were supported by the expression levels of enzymes and proteins related to lipid metabolism assessed by western blotting: protein expression levels of the peroxisome proliferator-activated receptor γ and CCATT/enhancer binding protein α decreased significantly, while hormone-sensitive lipase and phospho-AMP-activated protein kinase levels increased in the GAE-fed mice compared with ob/ob control mice. These findings demonstrate that GAE regulates plasma lipid profiles and increasing highdensity lipoprotein cholesterol levels as well as by regulating the expression levels of lipid metabolic factors, resulting in reduced weight gain in ob/ob mice.

Background Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with dysbiosis of the gut microbiota. We evaluated the effect of next generation probiotics ( Lactobacillus delbrueckii subsp. Lactis [LL001], L. helveticus [LH001], and Pediococcus pentosaceus KID7 [PPKID7]) on liver function parameters and stool microbiome in patients with MASLD. Methods We conducted a double-blind parallel trial of 110 patients diagnosed with MASLD. Participants were randomly assigned to four groups given three probiotics (3 capsules [9 × 10 9 CFU]/day, n  = 85) or placebo ( n  = 25) alongside sylimarin for 8 weeks. Clinical characteristics, serum samples, and stool samples for 16 S rRNA gene sequencing were collected at the start and end point of the study. The primary endpoint was improvement in liver function. Results In the probiotic group, LL001 treatment improved alanine transaminase (87.3 ± 8.2 to 71.1 ± 6.0 U/L, P  = 0.01) and aspartate transaminase levels (64.9 ± 4.9 to 50.0 ± 3.5 U/L, P  < 0.01), LH001 group showed body weight reduction (78.4 ± 3.0 to 77.2 ± 2.8 kg, P  = 0.01), and PPKID7 reduced cholesterol levels (186.1 ± 7.0 to 178.0 ± 7.9 mmol/L, P  = 0.03). Probiotics treatment decreased the abundance of Proteobacteria and increased the abundance of Ruminococcaceae and Lachnospiraceae in the LL001 group. In the pre- and post-comparison of probiotic treatment at the level of the top 20 genera, a tendency was observed to decrease the genera Haemohlius and Ruminococcus_g2 while increasing the genus Bifidobacterium . Conclusion Eight weeks of probiotics supplementation was associated with changes in the stool microbiome and improvements in the blood biochemical parameters of MASLD. Registration number of clinical trial NCT04555434.

Loranthus parasiticus Merr. ( L. parasiticus ) is a semiparasitic plant and it has antidiabetic effects. But potential application of L. parasiticus to improve insulin sensitivity in mice with type 2 diabetes remains unexplored. Herein, we aimed to investigate the potential antidiabetic effects of L. parasiticus extract (LPE) on hyperglycemia and insulin sensitivity in C57BL/Ksj-db/db mice. C57BL/Ksj-db/db mice were divided into three groups: diabetic control, rosiglitazone, and LPE. Db/db-control group was fed a standard semi-synthetic diet (AIN-93 G), db/db-RG group was fed AIN-93 G supplemented with rosiglitazone (RG) (0.005%, w/w), and db/db-LPE group was fed AIN-93 G supplemented with LPE (0.5%, w/w) for 6 weeks. Mice supplemented with LPE exhibited significantly lower blood glucose and glycosylated hemoglobin levels than diabetic control mice. Compared with diabetic control mice, LPE-supplemented mice exhibited a significant reduction in the homeostatic index of insulin resistance. LPE supplementation stimulated the pIRS Tyr612 and Akt Ser473 , as well as the activation of PI3K in the skeletal muscle insulin signaling pathway. Furthermore, LPE supplementation significantly increased the pAMPK Thr172 and ACC Ser79 and the expression of plasma membrane GLUT4. LPE supplementation improves insulin sensitivity and alleviates hyperglycemia in diabetic mice.