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  • 1
    Online Resource
    Online Resource
    Anti-diabetic effects of astaxanthin on an STZ-induced diabetic model in rats
    Japan Endocrine Society ; 2021
    In:  Endocrine Journal Vol. 68, No. 4 ( 2021), p. 451-459
    Details
    In: Endocrine Journal, Japan Endocrine Society, Vol. 68, No. 4 ( 2021), p. 451-459
    Type of Medium: Online Resource
    ISSN: 0918-8959 , 1348-4540
    URL: Article
    DOI: 10.1507/endocrj.EJ20-0699
    Language: English
    Publisher: Japan Endocrine Society
    Publication Date: 2021
    detail.hit.zdb_id: 2133773-1
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  • 2
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    The Gut Microbiota and Its Metabolites, Novel Targets for Treating and Preventing Non‐Alcoholic Fatty Liver Disease
    Wiley ; 2020
    In:  Molecular Nutrition & Food Research Vol. 64, No. 17 ( 2020-09)
    Details
    In: Molecular Nutrition & Food Research, Wiley, Vol. 64, No. 17 ( 2020-09)
    Abstract: Non‐alcoholic fatty liver disease (NAFLD) is one of the most prevalent metabolic disorders worldwide, along with obesity and type 2 diabetes. NAFLD involves a series of liver abnormalities from simple hepatic steatosis to non‐alcoholic steatohepatitis, which can ultimately lead to liver cirrhosis and cancer. The gut–liver axis plays an important role in the development of NAFLD, which depends mainly on regulation of the gut microbiota and its bacterial products. These intestinal bacterial species and their metabolites, including bile acids, tryptophan catabolites, and branched‐chain amino acids, regulate adipose tissue and intestinal homeostasis and contribute to the pathogenesis of NAFLD/non‐alcoholic steatohepatitis. In this review, the current evidence regarding the key role of the gut microbiota and its metabolites in the pathogenesis and development of NAFLD is highlighted, and the advances in the progression and applied prospects of gut microbiota‐targeted dietary and exercise therapies is also discussed.
    Type of Medium: Online Resource
    ISSN: 1613-4125 , 1613-4133
    URL: Issue
    URL: Article
    DOI: 10.1002/mnfr.v64.17
    DOI: 10.1002/mnfr.202000375
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2160372-8
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  • 3
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    Lycopene Alleviates Obesity‐Induced Inflammation and Insulin Resistance by Regulating M1/M2 Status of Macrophages
    Wiley ; 2019
    In:  Molecular Nutrition & Food Research Vol. 63, No. 21 ( 2019-11)
    Details
    In: Molecular Nutrition & Food Research, Wiley, Vol. 63, No. 21 ( 2019-11)
    Abstract: Adipose tissue macrophage (ATM) recruitment and polarization are pivotal in the development of insulin resistance. However, treatment modalities targeting ATMs remain limited. The effects of lycopene, an antioxidant carotenoid compound, on adipose tissue inflammation and insulin resistance in high fat (HF)‐diet‐induced obese mice are examined. Methods and results C57BL/6J mice are fed an HF diet or an HF diet containing lycopene (HF+LY) for 8 weeks. Lycopene attenuates HF‐diet‐induced glucose intolerance and hyperinsulinemia. Compared with HF mice, HF+LY mice exhibit attenuated adipocyte hypertrophy and macrophage infiltration in epididymal white adipose tissue (eWAT) and hepatic steatosis and inflammation. Flow cytometry analysis of ATMs demonstrates that lycopene attenuated the increased number of ATMs in HF diet‐fed mice. In addition, HF+LY mice have 23% fewer M1‐polarized ATMs and 60% more M2‐polarized ATMs than HF mice, resulting in the predominance of M2 over M1 in the ATM population. M2‐dominant polarization is also seen in hepatic macrophages in HF+LY mice. Moreover, lycopene promotes IL‐4‐induced M2 polarization by increasing the phosphorylation levels of STAT6 and Akt in Raw 264.7 macrophages. Conclusions Lycopene facilitates M2‐dominant polarization in ATM, thereby attenuating HF diet‐induced inflammation and insulin resistance in eWAT and the liver.
    Type of Medium: Online Resource
    ISSN: 1613-4125 , 1613-4133
    URL: Issue
    URL: Article
    DOI: 10.1002/mnfr.v63.21
    DOI: 10.1002/mnfr.201900602
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2160372-8
    SSG: 12
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  • 4
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    Xanthine Oxidase Inhibition Attenuates Insulin Resistance and Diet-Induced Steatohepatitis in Mice
    Elsevier BV ; 2019
    In:  SSRN Electronic Journal
    Details
    In: SSRN Electronic Journal, Elsevier BV
    Type of Medium: Online Resource
    ISSN: 1556-5068
    URL: Article
    DOI: 10.2139/ssrn.3391355
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
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  • 5
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    Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with vitamin E
    Springer Science and Business Media LLC ; 2015
    In:  Scientific Reports Vol. 5, No. 1 ( 2015-11-25)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 5, No. 1 ( 2015-11-25)
    Abstract: Hepatic insulin resistance and nonalcoholic steatohepatitis (NASH) could be caused by excessive hepatic lipid accumulation and peroxidation. Vitamin E has become a standard treatment for NASH. However, astaxanthin, an antioxidant carotenoid, inhibits lipid peroxidation more potently than vitamin E. Here, we compared the effects of astaxanthin and vitamin E in NASH. We first demonstrated that astaxanthin ameliorated hepatic steatosis in both genetically ( ob/ob ) and high-fat-diet-induced obese mice. In a lipotoxic model of NASH: mice fed a high-cholesterol and high-fat diet, astaxanthin alleviated excessive hepatic lipid accumulation and peroxidation, increased the proportion of M1-type macrophages/Kupffer cells and activated stellate cells to improve hepatic inflammation and fibrosis. Moreover, astaxanthin caused an M2-dominant shift in macrophages/Kupffer cells and a subsequent reduction in CD4 + and CD8 + T cell recruitment in the liver, which contributed to improved insulin resistance and hepatic inflammation. Importantly, astaxanthin reversed insulin resistance, as well as hepatic inflammation and fibrosis, in pre-existing NASH. Overall, astaxanthin was more effective at both preventing and treating NASH compared with vitamin E in mice. Furthermore, astaxanthin improved hepatic steatosis and tended to ameliorate the progression of NASH in biopsy-proven human subjects. These results suggest that astaxanthin might be a novel and promising treatment for NASH.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/srep17192
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2015
    detail.hit.zdb_id: 2615211-3
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  • 6
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    Online Resource
    DPP-4 Inhibition by Linagliptin Attenuates Obesity-Related Inflammation and Insulin Resistance by Regulating M1/M2 Macrophage Polarization
    American Diabetes Association ; 2016
    In:  Diabetes Vol. 65, No. 10 ( 2016-10-01), p. 2966-2979
    Details
    In: Diabetes, American Diabetes Association, Vol. 65, No. 10 ( 2016-10-01), p. 2966-2979
    Abstract: Dipeptidyl peptidase 4 (DPP-4) cleaves a large number of chemokine and peptide hormones involved in the regulation of the immune system. Additionally, DPP-4 may also be involved in macrophage-mediated inflammation and insulin resistance. Thus, the current study investigated the effect of linagliptin, an inhibitor of DPP-4, on macrophage migration and polarization in white adipose tissue (WAT) and liver of high-fat diet–induced obese (DIO) mice. DPP-4+ macrophages in lean and obese mice were quantified by fluorescence-activated cell sorting (FACS) analysis. DPP-4 was predominantly expressed in F4/80+ macrophages in crown-like structures compared with adipocytes in WAT of DIO mice. FACS analysis also revealed that, compared with chow-fed mice, DIO mice exhibited a significant increase in DPP-4+ expression in cells within adipose tissue macrophages (ATMs), particularly M1 ATMs. Linagliptin showed a greater DPP-4 inhibition and antioxidative capacity than sitagliptin and reduced M1-polarized macrophage migration while inducing an M2-dominant shift of macrophages within WAT and liver, thereby attenuating obesity-induced inflammation and insulin resistance. Loss of macrophage inflammatory protein-1α, a chemokine and DPP-4 substrate, in DIO mice abrogated M2 macrophage-polarizing and insulin-sensitizing effects of linagliptin. Therefore, the inhibition of DPP-4 by linagliptin reduced obesity-related insulin resistance and inflammation by regulating M1/M2 macrophage status.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db16-0317
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2016
    detail.hit.zdb_id: 1501252-9
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  • 7
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    Online Resource
    Adipose Tissue Macrophage Phenotypes and Characteristics: The Key to Insulin Resistance in Obesity and Metabolic Disorders
    Wiley ; 2020
    In:  Obesity Vol. 28, No. 2 ( 2020-02), p. 225-234
    Details
    In: Obesity, Wiley, Vol. 28, No. 2 ( 2020-02), p. 225-234
    Abstract: Obesity is one of the most serious global health problems, with an incidence that increases yearly and coincides with the development of a variety of associated comorbidities (e.g., type 2 diabetes, nonalcoholic fatty liver disease, some immune‐related disorders). Although many studies have investigated the pathogenesis of overweight and obesity, multiple regulatory factors underlying the onset of obesity‐related metabolic disorders remain elusive. Macrophages contribute to modulation of obesity‐related inflammation and insulin resistance (IR); adipose tissue macrophages are particularly important in this context. Based on newly identified links between the chemokine system and obesity, macrophage polarization has become an essential target of new therapies for obesity‐related IR. The findings of multiple studies imply that variations in gut microbiota and its metabolites might contribute to the regulation of obesity and related metabolic disorders. Recently, several novel antidiabetic drugs, applied as treatment for weight loss, were shown to be effective for obesity‐induced IR and other comorbidities. The present review will discuss the properties and functions of macrophages in adipose tissue under conditions of obesity from three perspectives: the chemokine system, the gut microbiota, and antidiabetic drug application. It is proposed that macrophages might be a key therapeutic target for obesity‐induced complications.
    Type of Medium: Online Resource
    ISSN: 1930-7381 , 1930-739X
    URL: Issue
    URL: Article
    DOI: 10.1002/oby.v28.2
    DOI: 10.1002/oby.22674
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2027211-X
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  • 8
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    Online Resource
    DPP-4 Inhibition with Anagliptin Reduces Lipotoxicity-Induced Insulin Resistance and Steatohepatitis in Male Mice
    The Endocrine Society ; 2020
    In:  Endocrinology Vol. 161, No. 10 ( 2020-10-01)
    Details
    In: Endocrinology, The Endocrine Society, Vol. 161, No. 10 ( 2020-10-01)
    Abstract: Excessive hepatic lipid accumulation drives the innate immune system and aggravates insulin resistance, hepatic inflammation, and fibrogenesis, leading to nonalcoholic steatohepatitis (NASH). Dipeptidyl peptidase-4 (DPP-4) regulates glucose metabolism and is expressed in many different cell types, including the cells of the immune system. In addition, DPP-4 may be involved in macrophage-mediated inflammation and insulin resistance. This study investigated the effects of anagliptin (Ana), an inhibitor of DPP-4, on macrophage polarity and phenotype in the livers of mice with steatohepatitis. We investigated the effects of Ana on steatohepatitis induced via a high-cholesterol high-fat (CL) diet or a choline-deficient L-amino acid-defined, high-fat (CDAHF) diet. DPP-4 activity, liver histology, and insulin sensitivity were evaluated, and liver DPP-4+ macrophages were quantified using fluorescence-activated cell sorting (FACS). Liver and plasma DPP-4 activity increased significantly in mice on both diets. FACS revealed that, compared with chow-fed mice, the CL-fed mice exhibited a significant increase in the proportion of DPP-4+ liver macrophages, particularly the M1-type macrophages. Ana decreased hepatic lipid and M1 macrophage accumulation and stimulated M2 macrophage accumulation in the liver, thereby attenuating insulin resistance, steatohepatitis, and fibrosis. Importantly, Ana alleviated hepatic fibrosis and steatohepatitis in mice fed CL diet and CDAHF diet. Using Ana to inhibit DPP-4 reduced lipotoxicity-induced hepatic insulin resistance through regulating the M1/M2 macrophage status.
    Type of Medium: Online Resource
    ISSN: 0013-7227 , 1945-7170
    URL: Article
    DOI: 10.1210/endocr/bqaa139
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2020
    detail.hit.zdb_id: 2011695-0
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  • 9
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    Online Resource
    Empagliflozin reverses obesity and insulin resistance through fat browning and alternative macrophage activation in mice fed a high-fat diet
    BMJ ; 2019
    In:  BMJ Open Diabetes Research & Care Vol. 7, No. 1 ( 2019-10), p. e000783-
    Details
    In: BMJ Open Diabetes Research & Care, BMJ, Vol. 7, No. 1 ( 2019-10), p. e000783-
    Abstract: We reported previously that empagliflozin—a sodium-glucose cotransporter (SGLT) 2 inhibitor—exhibited preventive effects against obesity. However, it was difficult to extrapolate these results to human subjects. Here, we performed a therapeutic study, which is more relevant to clinical situations in humans, to investigate antiobesity effects of empagliflozin and illustrate the mechanism underlying empagliflozin-mediated enhanced fat browning in obese mice. Research design and methods After 8 weeks on a high-fat diet (HFD), C57BL/6J mice exhibited obesity, accompanied by insulin resistance and low-grade chronic inflammation. Cohorts of obese mice were continued on the HFD for an additional 8-week treatment period with or without empagliflozin. Results Treatment with empagliflozin for 8 weeks markedly increased glucose excretion in urine, and suppressed HFD-induced weight gain, insulin resistance and hepatic steatosis. Notably, empagliflozin enhanced oxygen consumption and carbon dioxide production, leading to increased energy expenditure. Consistently, the level of uncoupling protein 1 expression was increased in both brown and white (WAT) adipose tissues of empagliflozin-treated mice. Furthermore, empagliflozin decreased plasma levels of interleukin (IL)-6 and monocyte chemoattractant protein-1, but increased plasma levels of IL-33 and adiponectin in obese mice. Finally, we found that empagliflozin reduced M1-polarized macrophage accumulation, while inducing the anti-inflammatory M2 phenotype of macrophages in the WAT and liver, thereby attenuating obesity-related chronic inflammation. Conclusions Treatment with empagliflozin attenuated weight gain by increasing energy expenditure and adipose tissue browning, and alleviated obesity-associated inflammation and insulin resistance by alternative macrophage activation in the WAT and liver of obese mice.
    Type of Medium: Online Resource
    ISSN: 2052-4897
    URL: Article
    DOI: 10.1136/bmjdrc-2019-000783
    Language: English
    Publisher: BMJ
    Publication Date: 2019
    detail.hit.zdb_id: 2732918-5
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  • 10
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    Online Resource
    Significant dissociation of expression patterns of the basic helix–loop–helix transcription factors Dec1 and Dec2 in rat kidney
    The Company of Biologists ; 2011
    In:  Journal of Experimental Biology Vol. 214, No. 8 ( 2011-04-15), p. 1257-1263
    Details
    In: Journal of Experimental Biology, The Company of Biologists, Vol. 214, No. 8 ( 2011-04-15), p. 1257-1263
    Abstract: Dec1 and Dec2 are regulators of the mammalian molecular clock that show robust circadian rhythms in the suprachiasmatic nucleus and various peripheral tissues. Although the expression of Dec1 and Dec2 is altered by multiple stimuli in different organs, their transcriptional regulatory mechanisms have not been fully elucidated for the kidney. In the present study, we describe for the first time significant dissociation of expression patterns with arrhythmic expression of Dec1 and rhythmic expression of Dec2 in rat kidney under a normal light–dark (LD) cycle. Daytime restricted feeding (RF) significantly altered the expression patterns of these two clock genes, and even induced circadian expression of Dec1 with an amplitude of 2.2 on day 3 and 4.2 on day 7. However, when a reversed feeding schedule was coupled with a reversed LD cycle, the expression of Dec1 but not Dec2 reverted to being arrhythmic. Moreover, exogenous injection of the glucocorticoid analogue dexamethasone (Dex) at certain times of the day resulted in rhythmic expression of Dec1, which was similar to that seen following RF for 7 days. In contrast, endogenous disruption of glucocorticoids by adrenalectomy abolished RF-induced rhythmic expression of Dec1 in the kidney. These observations suggest the existence of a glucocorticoid gating mechanism in the circadian expression of Dec1 in rat kidney.
    Type of Medium: Online Resource
    ISSN: 1477-9145 , 0022-0949
    URL: Article
    DOI: 10.1242/jeb.052100
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2011
    detail.hit.zdb_id: 1482461-9
    SSG: 12
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