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  • MDPI AG  (27)
  • Chen, Chun-Jung  (27)
  • 1
    Online Resource
    Online Resource
    Magnesium Lithospermate B Attenuates High-Fat Diet-Induced Muscle Atrophy in C57BL/6J Mice
    MDPI AG ; 2021
    In:  Nutrients Vol. 14, No. 1 ( 2021-12-27), p. 104-
    Details
    In: Nutrients, MDPI AG, Vol. 14, No. 1 ( 2021-12-27), p. 104-
    Abstract: Magnesium lithospermate B (MLB) is a primary hydrophilic component of Danshen, the dried root of Salvia miltiorrhiza used in traditional medicine, and its beneficial effects on obesity-associated metabolic abnormalities were reported in our previous study. The present study investigated the anti-muscle atrophy potential of MLB in mice with high-fat diet (HFD)-induced obesity. In addition to metabolic abnormalities, the HFD mice had a net loss of skeletal muscle weight and muscle fibers and high levels of muscle-specific ubiquitin E3 ligases, namely the muscle atrophy F-box (MAFbx) and muscle RING finger protein 1 (MuRF-1). MLB supplementation alleviated those health concerns. Parallel changes were revealed in high circulating tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), skeletal TNF receptor I (TNFRI), nuclear factor-kappa light chain enhancer of activated B cells (NF-κB), p65 phosphorylation, and Forkhead box protein O1 (FoxO1) as well as low skeletal phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt) phosphorylation. The study revealed that MLB prevented obesity-associated skeletal muscle atrophy, likely through the inhibition of MAFbx/MuRF-1-mediated muscular degradation. The activation of the PI3K-Akt-FoxO1 pathway and inhibition of the TNF-α/TNFRI/NF-κB pathway were assumed to be beneficial effects of MLB.
    Type of Medium: Online Resource
    ISSN: 2072-6643
    URL: Article
    DOI: 10.3390/nu14010104
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2518386-2
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  • 2
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    Olanzapine Induced Dysmetabolic Changes Involving Tissue Chromium Mobilization in Female Rats
    MDPI AG ; 2019
    In:  International Journal of Molecular Sciences Vol. 20, No. 3 ( 2019-02-01), p. 640-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 20, No. 3 ( 2019-02-01), p. 640-
    Abstract: Atypical antipsychotics, such as olanzapine, are commonly prescribed to patients with schizophrenic symptoms and other psychiatric disorders. However, weight gain and metabolic disturbance cause adverse effects, impair patient compliance and limit clinical utility. Thus, a better understanding of treatment-acquired adverse effects and identification of targets for therapeutic intervention are believed to offer more clinical benefits for patients with schizophrenia. Beyond its nutritional effects, studies have indicated that supplementation of chromium brings about beneficial outcomes against numerous metabolic disorders. In this study, we investigated whether olanzapine-induced weight gain and metabolic disturbance involved chromium dynamic mobilization in a female Sprague-Dawley rat model, and whether a dietary supplement of chromium improved olanzapine-acquired adverse effects. Olanzapine medicated rats experienced weight gain and adiposity, as well as the development of hyperglycemia, hyperinsulinemia, insulin resistance, hyperlipidemia, and inflammation. The olanzapine-induced metabolic disturbance was accompanied by a decrease in hepatic Akt and AMP-activated Protein Kinase (AMPK) actions, as well as an increase in serum interleukin-6 (IL-6), along with tissue chromium depletion. A daily intake of chromium supplements increased tissue chromium levels and thermogenic uncoupling protein-1 (UCP-1) expression in white adipose tissues, as well as improved both post-olanzapine weight gain and metabolic disturbance. Our findings suggest that olanzapine medicated rats showed a disturbance of tissue chromium homeostasis by inducing tissue depletion and urinary excretion. This loss may be an alternative mechanism responsible for olanzapine-induced weight gain and metabolic disturbance.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms20030640
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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  • 3
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    Characterization of Collapsin Response Mediator Protein 2 in Colorectal Cancer Progression in Subjects with Diabetic Comorbidity
    MDPI AG ; 2022
    In:  Cells Vol. 11, No. 4 ( 2022-02-18), p. 727-
    Details
    In: Cells, MDPI AG, Vol. 11, No. 4 ( 2022-02-18), p. 727-
    Abstract: Background: Common demographic risk factors are identified in colorectal cancer (CRC) and type 2 diabetes mellitus (DM), nevertheless, the molecular link and mechanism for CRC-DM comorbidity remain elusive. Dysregulated glycogen synthase kinase-3 beta under metabolic imbalance is suggested to accelerate CRC pathogenesis/progression via regulating collpasin response mediator protein-2 (CRMP2). Accordingly, roles of CRMP2 in CRC and CRC-DM patients were investigated for elucidating the molecular convergence of CRC and DM. Methods: CRMP2 profile in tumor tissues from CRC and CRC-DM patients was investigated to explore the link between CRC and DM etiology. Meanwhile, molecular mechanism of glucose to regulate CRMP2 profile and CRC characteristics was examined in vitro and in vivo. Results: CRMP2 was significantly lower in tumor lesions and associated with advanced tumor stage in CRC-DM patients. Physiological hyperglycemia suppressed CRMP2 expression/activity and augmented malignant characteristics of CRC cells. Hyperglycemia promotes actin de-polymerization, cytoskeleton flexibility and cell proliferation/metastasis by downregulating CRMP2 profile and thus contributes to CRC disease progression. Conclusions: This study uncovers molecular evidence to substantiate and elucidate the link between CRC and T2DM, as well as characterizing the roles of CRMP2 in CRC-DM. Accordingly, altered metabolic adaptations are promising targets for anti-diabetic and cancer strategies.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells11040727
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2661518-6
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  • 4
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    Association between Ultraviolet B Exposure Levels and Depression in Taiwanese Adults: A Nested Case–Control Study
    MDPI AG ; 2022
    In:  International Journal of Environmental Research and Public Health Vol. 19, No. 11 ( 2022-06-03), p. 6846-
    Details
    In: International Journal of Environmental Research and Public Health, MDPI AG, Vol. 19, No. 11 ( 2022-06-03), p. 6846-
    Abstract: Depression is a common mental disorder that affects more than 264 million people worldwide. Anxiety, diabetes, Alzheimer’s disease, myocardial infarction, and cancer, among other disorders, are known to increase the risk of depression. Exposure to ultraviolet B (UVB) can cause human serotonin levels to increase. The vitamin D pathway is one mechanism through which ultraviolet light absorbed through the skin can affect mood; however, UVB exposure is known to increase the risk of cancer. In this study, we explored the effects of prolonged exposure to UVB on depression. Data were retrieved from the Taiwan National Health Insurance Research Database for 2008 to 2013. Each patient with depression was matched 1:4 with a comparison patient by sex and age (±5 years); thus, the study included 23,579 patients with depression and 94,316 healthy controls for comparison. The patients had been exposed to UVB for at least 1 year to observe the cumulative effect of UVB exposure. Based on the World Health Organization UV index, we divided the observation period data into five UV levels: low, moderate, high, very high, and extreme. A multivariate Poisson regression model was used to assess the risk of depression according to UVB exposure level, adjusting for sex, age, income, urbanization level, month, and comorbidities. The results revealed that the incidence rate ratio (IRR) for patients with depression was 0.889 for moderate levels (95% CI 0.835–0.947), 1.134 for high levels (95% CI: 1.022–1.260), 1.711 for very high levels (95% CI: 1.505–1.945), and 2.785 for extreme levels (95% CI: 2.439–3.180) when compared to low levels. Moderate levels of UVB lowered the risk of depression, while high levels of UVB gradually increased the risk. We propose that UVB at normal concentrations can effectively improve depression. However, exposure to high concentrations of UVB damage DNA results in physical diseases such as skin cancer, which increase the risk of depression.
    Type of Medium: Online Resource
    ISSN: 1660-4601
    URL: Article
    DOI: 10.3390/ijerph19116846
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2175195-X
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  • 5
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    Air Pollutant Particles, PM2.5, Exposure and Glaucoma in Patients with Diabetes: A National Population-Based Nested Case–Control Study
    MDPI AG ; 2021
    In:  International Journal of Environmental Research and Public Health Vol. 18, No. 18 ( 2021-09-21), p. 9939-
    Details
    In: International Journal of Environmental Research and Public Health, MDPI AG, Vol. 18, No. 18 ( 2021-09-21), p. 9939-
    Abstract: The global prevalence of diabetes mellitus (DM) has reached 20%. Air pollutants with a particle size of less than 2.5 μm (PM2.5) are a globally recognized risk factor for diabetes and glaucoma. We examined whether the risk of glaucoma would decrease or increase when patients with DM were exposed to different PM2.5 concentrations. Data were obtained from the National Health Insurance Research Database (NHIRD) of Taiwan and the Air Quality Monitoring Network between 2008 and 2013. This nested case–control study involved 197 DM patients with glaucoma and 788 DM patients without glaucoma. Cases and controls were matched (1:4) by gender, age (±5 years), and index date (±6 months), and their data were entered in a logistic regression model adjusted for gender, age, urbanization level, income level, and comorbidities. The odds ratio (OR) of glaucoma at PM2.5 exposure concentration in the fourth quartile (Q4) compared with in the first quartile (Q1) was 1.7 (95% CI: 1.084–2.764). For glaucoma risk, the OR was 1.013 (95% CI: 1.006–1.020) at a PM2.5 exposure concentration in Q1, 1.004 (95% CI: 1.001–1.007) in the third quartile (Q3), and 1.003 (95% CI: 1.001–1.004) in Q4. In the subgroup analysis of patients living in non-emerging towns and non-agricultural towns, the OR for glaucoma in Q4 compared with in Q1 was 2.1 (95% CI: 1.229–3.406) and 1.8 (95% CI: 1.091–2.803), respectively (p trend = 0.001 and 0.011). For patients without migraine, the OR for glaucoma was 1.7 (95% CI: 1.074–2.782; p = 0.006). These results demonstrate that, for patients with DM, PM2.5 increased the risk of glaucoma and PM2.5 was an independent risk factor for glaucoma in patients with DM.
    Type of Medium: Online Resource
    ISSN: 1660-4601
    URL: Article
    DOI: 10.3390/ijerph18189939
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
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  • 6
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    Proinflammatory Responses of 1-Nitropyrene against RAW264.7 Macrophages through Akt Phosphorylation and NF-κB Pathways
    MDPI AG ; 2021
    In:  Toxics Vol. 9, No. 11 ( 2021-10-21), p. 276-
    Details
    In: Toxics, MDPI AG, Vol. 9, No. 11 ( 2021-10-21), p. 276-
    Abstract: Air pollution is a major environmental and public health problem worldwide. A nitro-polycyclic aromatic hydrocarbon and the most abundant air pollutant in diesel engine exhaust, 1-nitropyrene (1-NP), is caused by the incomplete combustion of carbonaceous organic substances. Macrophages are effector cells of the innate immune cells that provide resistance in the peripheral tissue. The overactivation of macrophages results in inflammation. The generation of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumour necrosis factor alpha, is induced by 1-NP in a concentration-dependent manner in macrophages. In this study, the production of proinflammatory mediators, such as nitrogen oxide and prostaglandin E2, was induced by 1-NP in a concentration-dependent manner through the expression of iNOS and COX2. The generation of proinflammatory cytokines, iNOS, and COX2 was induced by 1-NP through nuclear factor (NF)-κB p65 phosphorylation and the degradation of its upstream factor, IκB. Finally, Akt phosphorylation was induced by 1-NP in a concentration-dependent manner. These findings suggest that 1-NP exhibits a proinflammatory response through the NF-κB pathway activation due to Akt phosphorylation.
    Type of Medium: Online Resource
    ISSN: 2305-6304
    URL: Article
    DOI: 10.3390/toxics9110276
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2733883-6
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  • 7
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    Interleukin-4 Improves Metabolic Abnormalities in Leptin-Deficient and High-Fat Diet Mice
    MDPI AG ; 2020
    In:  International Journal of Molecular Sciences Vol. 21, No. 12 ( 2020-06-23), p. 4451-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 21, No. 12 ( 2020-06-23), p. 4451-
    Abstract: Obesity is a metabolic disorder that results from complex interactions between genetic predisposition and dietary factors. Interleukin-4 (IL-4), besides its role in immunity, has metabolic effects on insulin efficacy. We studied the effects of IL-4 on metabolic abnormalities in a mice model of obesity involving leptin deficiency and leptin resistance. Leptin-deficient 145E and leptin-resistant high-fat diet (HFD) mice showed lower levels of circulating IL-4. 145E and HFD mice showed a number of abnormalities: Obesity, hyperglycemia, hyperinsulinemia, insulin resistance, dyslipidemia, liver injury, and adiposity with concurrent inflammation, decreases in Akt, signal transducer and activator of transcription 3 (STAT3), and STAT6 phosphorylation in the hypothalamus, liver, and epididymal fat. Independent of leptin-deficient obesity and dietary obesity, a course of 8-week IL-4 supplementation improved obesity and impairment in Akt, STAT3, and STAT6 signaling. Amelioration of cytokine expression, despite variable extents, was closely linked with the actions of IL-4. Additionally, the browning of white adipocytes by IL-4 was found in epididymal white adipose tissues and 3T3-L1 preadipocytes. Chronic exercise, weight management, and probiotics are recommended to overweight patients and IL-4 signaling is associated with clinical improvement. Thus, IL-4 could be a metabolic regulator and antiobesity candidate for the treatment of obesity and its complications.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms21124451
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2019364-6
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  • 8
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    Aspirin Mitigated Tumor Growth in Obese Mice Involving Metabolic Inhibition
    MDPI AG ; 2020
    In:  Cells Vol. 9, No. 3 ( 2020-02-28), p. 569-
    Details
    In: Cells, MDPI AG, Vol. 9, No. 3 ( 2020-02-28), p. 569-
    Abstract: Obesity is associated with a wide range of chronic diseases, including cancer. It has been noted that the integration of metabolic mechanisms in obese patients may predispose them to suffer from cancer incidence and its progression. Thus, a better understanding of metabolic alterations in obesity, along with the development of feasible therapeutic approaches for intervention, are theoretically relevant to the prevention and treatment of cancer malignancy. Using a syngeneic tumor model involving Lewis Lung Carcinoma (LLC) cells and C57BL/6 mice fed with a high fat diet, obesity was found to be associated with dysregulated glucose and glutamine metabolism, inflammation, along with platelet activation and the promotion of tumor growth. Tumor-bearing lowered glucose levels while moderately increasing inflammation, platelet activation, and glutamine levels. The antiplatelet drug aspirin, mitigated tumor growth in obese mice, paralleled by a decrease in systemic glucose, insulin, inflammation, platelet activation, glutamine and tumor expression of cell proliferation, aerobic glycolysis, glutaminolysis, platelets, and leukocyte molecules. The anti- and pro-cell proliferation, aerobic glycolysis, and glutaminolysis effects of aspirin and glutamine were further demonstrated in a LLC cell study. Although there remains limitations to our experiments, glucose and glutamine metabolism are proposed targets for the anticancer effects of aspirin.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells9030569
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
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  • 9
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    Jak2 Inhibitor AG490 Improved Poststroke Central and Peripheral Inflammation and Metabolic Abnormalities in a Rat Model of Ischemic Stroke
    MDPI AG ; 2021
    In:  Antioxidants Vol. 10, No. 12 ( 2021-12-07), p. 1958-
    Details
    In: Antioxidants, MDPI AG, Vol. 10, No. 12 ( 2021-12-07), p. 1958-
    Abstract: Poststroke hyperglycemia and inflammation have been implicated in the pathogenesis of stroke. Janus Kinase 2 (Jak2), a catalytic signaling component for cytokine receptors such as Interleukin-6 (IL-6), has inflammatory and metabolic properties. This study aimed to investigate the roles of Jak2 in poststroke inflammation and metabolic abnormality in a rat model of permanent cerebral ischemia. Pretreatment with Jak2 inhibitor AG490 ameliorated neurological deficit, brain infarction, edema, oxidative stress, inflammation, caspase-3 activation, and Zonula Occludens-1 (ZO-1) reduction. Moreover, in injured cortical tissues, Tumor Necrosis Factor-α, IL-1β, and IL-6 levels were reduced with concurrent decreased NF-κB p65 phosphorylation, Signal Transducers and Activators of Transcription 3 phosphorylation, Ubiquitin Protein Ligase E3 Component N-Recognin 1 expression, and Matrix Metalloproteinase activity. In the in vitro study on bEnd.3 endothelial cells, AG490 diminished IL-6-induced endothelial barrier disruption by decreasing ZO-1 decline. Metabolically, administration of AG490 lowered fasting glucose, with improvements in glucose intolerance, plasma-free fatty acids, and plasma C Reactive Proteins. In conclusion, AG490 improved the inflammation and oxidative stress of neuronal, hepatic, and muscle tissues of stroke rats as well as impairing insulin signaling in the liver and skeletal muscles. Therefore, Jak2 blockades may have benefits for combating poststroke central and peripheral inflammation, and metabolic abnormalities.
    Type of Medium: Online Resource
    ISSN: 2076-3921
    URL: Article
    DOI: 10.3390/antiox10121958
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2704216-9
    SSG: 15,3
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  • 10
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    18β-Glycyrrhetinic Acid Protects against Cholestatic Liver Injury in Bile Duct-Ligated Rats
    MDPI AG ; 2022
    In:  Antioxidants Vol. 11, No. 5 ( 2022-05-12), p. 961-
    Details
    In: Antioxidants, MDPI AG, Vol. 11, No. 5 ( 2022-05-12), p. 961-
    Abstract: 18β-Glycyrrhetinic acid is a nutraceutical agent with promising hepatoprotective effects. Its protective mechanisms against cholestatic liver injury were further investigated in a rodent model of extrahepatic cholestasis caused by Bile Duct Ligation (BDL) in rats. The daily oral administration of 18β-Glycyrrhetinic acid improved liver histology, serum biochemicals, ductular reaction, oxidative stress, inflammation, apoptosis, impaired autophagy, and fibrosis. 18β-Glycyrrhetinic acid alleviated the BDL-induced hepatic and systemic retention of bile acids, matrix-producing cell activation, hepatic collagen deposition, Transforming Growth Factor beta-1/Smad activation, malondialdehyde elevation, glutathione reduction, High Mobility Group Box-1/Toll-Like Receptor-4 activation, NF-κB activation, inflammatory cell infiltration/accumulation, Interleukin-1β expression, Signal Transducer and Activator of Transcription-1 activation, Endoplasmic Reticulum stress, impairment autophagy, and caspase 3 activation. Conversely, the protein expression of Sirt1, Farnesoid X Receptor, nuclear NF-E2-Related Factor-2, Transcription Factor EB, bile acid efflux transporters, and LC3-II, as well as the protein phosphorylation of AMP-Activated Protein Kinase, was promoted in 18β-Glycyrrhetinic acid-treated BDL rats. The hepatoprotective effects of 18β-Glycyrrhetinic acid in the present investigation correlated well with co-activation and possible interactions among Sirt, FXR, and Nrf2. The concurrent or concomitant activation of Sirt1, FXR, and Nrf2 not only restored the homeostatic regulation of bile acid metabolism, but also alleviated oxidative stress, inflammation, apoptosis, impaired autophagy, and fibrosis.
    Type of Medium: Online Resource
    ISSN: 2076-3921
    URL: Article
    DOI: 10.3390/antiox11050961
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2704216-9
    SSG: 15,3
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