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Article: Anti-Fibrotic Effects of DL-Glyceraldehyde in Hepatic Stellate Cells via Activation of ERK-JNK-Caspase-3 Signaling Axis.

Samsuzzaman, Md / Kim, Sun Yeou

2023 Volume 31, Issue 4, Page(s) 425–433

Abstract: During liver injury, hepatic stellate cells can differentiate into myofibroblast-like structures, which are more susceptible to proliferation, migration, and extracellular matrix generation, leading to liver fibrosis. Anaerobic glycolysis is associated ... ...

Abstract	During liver injury, hepatic stellate cells can differentiate into myofibroblast-like structures, which are more susceptible to proliferation, migration, and extracellular matrix generation, leading to liver fibrosis. Anaerobic glycolysis is associated with activated stellate cells and glyceraldehyde (GA) is an inhibitor of glucose metabolism. Therefore, this study aimed to investigate the anti-fibrotic effects of GA in human stellate LX-2 cells. In this study, we used cell viability, morphological analysis, fluorescence-activated cell sorting (FACS), western blotting, and qRT-PCR techniques to elucidate the molecular mechanism underlying the anti-fibrotic effects of GA in LX-2 cells. The results showed that GA significantly reduced cell density and inhibited cell proliferation and lactate levels in LX-2 cells but not in Hep-G2 cells. We found that GA prominently increased the activation of caspase-3/9 for apoptosis induction, and a pan-caspase inhibitor, Z-VAD-fmk, attenuated the cell death and apoptosis effects of GA, suggesting caspase-dependent cell death. Moreover, GA strongly elevated reactive oxygen species (ROS) production and notably increased the phosphorylation of ERK and JNK. Interestingly, it dramatically reduced α-SMA and collagen type I protein and mRNA expression levels in LX-2 cells. Thus, inhibition of ERK and JNK activation significantly rescued GA-induced cell growth suppression and apoptosis in LX-2 cells. Collectively, the current study provides important information demonstrating the anti-fibrotic effects of GA, a glycolytic metabolite, and demonstrates the therapeutic potency of metabolic factors in liver fibrosis.
Language	English
Publishing date	2023-04-10
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2734146-X
ISSN	2005-4483 ; 1976-9148
ISSN (online)	2005-4483
ISSN	1976-9148
DOI	10.4062/biomolther.2022.131
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Annona muricate

Lee, Heaji / Kim, Sun Yeou / Lim, Yunsook

Nutrients

2023 Volume 15, Issue 11

Abstract: Type 2 diabetes mellitus (T2DM) is related with the incidence of sarcopenia and cognitive impairment that reduces quality of life in the elderly. Recent evidence has demonstrated that sarcopenia is associated with cognitive dysfunction, and muscle- ... ...

Abstract	Type 2 diabetes mellitus (T2DM) is related with the incidence of sarcopenia and cognitive impairment that reduces quality of life in the elderly. Recent evidence has demonstrated that sarcopenia is associated with cognitive dysfunction, and muscle-derived endocrine factors might contribute to cognitive function by the skeletal muscle-brain endocrine loop. This study investigated the beneficial effects of
MeSH term(s)	Mice ; Animals ; Diabetes Mellitus, Type 2/complications ; Brain-Derived Neurotrophic Factor/metabolism ; Annona/metabolism ; Diabetes Mellitus, Experimental/complications ; Sarcopenia/complications ; Fibronectins/metabolism ; Quality of Life ; Muscle, Skeletal/metabolism ; Brain/metabolism ; Insulin/metabolism ; Dietary Supplements ; Energy Metabolism
Chemical Substances	Brain-Derived Neurotrophic Factor ; Fibronectins ; Insulin
Language	English
Publishing date	2023-05-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15112559
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Article ; Online: Anti-Glucotoxicity Effect of Phytoconstituents

Yadav, Neera / Palkhede, Jyoti Dnyaneshwar / Kim, Sun-Yeou

International journal of molecular sciences

2023 Volume 24, Issue 8

Abstract: The therapeutic benefits of phytochemicals in the treatment of various illnesses and disorders are well documented. They show significant promise for the discovery and creation of novel medications for treating a variety of human diseases. Numerous ... ...

Abstract	The therapeutic benefits of phytochemicals in the treatment of various illnesses and disorders are well documented. They show significant promise for the discovery and creation of novel medications for treating a variety of human diseases. Numerous phytoconstituents have shown antibiotic, antioxidant, and wound-healing effects in the conventional system. Traditional medicines based on alkaloids, phenolics, tannins, saponins, terpenes, steroids, flavonoids, glycosides, and phytosterols have been in use for a long time and are crucial as alternative treatments. These phytochemical elements are crucial for scavenging free radicals, capturing reactive carbonyl species, changing protein glycation sites, inactivating carbohydrate hydrolases, fighting pathological conditions, and accelerating the healing of wounds. In this review, 221 research papers have been reviewed. This research sought to provide an update on the types and methods of formation of methylglyoxal-advanced glycation end products (MGO-AGEs) and molecular pathways induced by AGEs during the progression of the chronic complications of diabetes and associated diseases as well as to discuss the role of phytoconstituents in MGO scavenging and AGEs breaking. The development and commercialization of functional foods using these natural compounds can provide potential health benefits.
MeSH term(s)	Humans ; Pyruvaldehyde/metabolism ; Glycation End Products, Advanced/metabolism ; Magnesium Oxide ; Diabetes Mellitus
Chemical Substances	Pyruvaldehyde (722KLD7415) ; Glycation End Products, Advanced ; Magnesium Oxide (3A3U0GI71G)
Language	English
Publishing date	2023-04-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24087672
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Article ; Online: Solanum melongena extract supplementation protected skeletal muscle and brain damage by regulation of BDNF/PGC1α/irisin pathway via brain function-related myokines in high-fat diet induced obese mice.

Lee, Heaji / Kim, Sun Yeou / Lim, Yunsook

The Journal of nutritional biochemistry

2023 Volume 124, Page(s) 109537

Abstract: In this study, we investigated the protective effects of SM on skeletal muscle and brain damage by regulation of BDNF/PGC1α/irisin pathway via brain function related myokines in high-fat diet-induced OB mice. OB was induced by high-fat diet for 6 weeks. ... ...

Abstract	In this study, we investigated the protective effects of SM on skeletal muscle and brain damage by regulation of BDNF/PGC1α/irisin pathway via brain function related myokines in high-fat diet-induced OB mice. OB was induced by high-fat diet for 6 weeks. SM extract (SME) was administered with 200 mg/kg BW (LSM) and 500 mg/kg BW (HSM) by oral gavage every day for 12 weeks. Behavior tests such as grip strength, Y-maze, and passive avoidance test were conducted to analyze muscle and cognitive function. Histopathological changes in skeletal muscle and brain were examined by hematoxylin and eosin staining and the protein levels of biomarkers related to oxidative stress, inflammation, protein degradation, neuro-plasticity, and cell cycling were measured by western blot. SME regulated morphological changes (muscle cross-sectional area: 1.23%, 1.40%; density of neurons in hippocampus:1.74%, 1.73%) in T2DM mice. Importantly, SME supplementation significantly increased several muscle-derived myokines which might influence the expression of neuronal markers in OB mice (FGF21: 1.27%, 1.34%; PGC1α: 1.0%, 1.32%; IRISIN: 1.9%, 1.08%; BDNF: 1.35%, 1.23%). Accordingly, SME activated hippocampal neurotrophic factors including BDNF (1.0%, 1.2%) and its associated PGC1α/irisin pathway (PGC1α :1.1%, 1.1%; IRISIN:1.1%, 0.9%) significantly. This study demonstrated the possibliy that protective myokines increased by SME supplementation may contribute to neuro-protection in OB mice. Taken together, the current study suggests that SME can be used to prevent skeletal muscle and brain damage in OB by protecting against oxidative stress and inflammatin via modulation of the BDNF/PGC1α/irisin pathway in the therapeutic approach of obese patients.
MeSH term(s)	Humans ; Mice ; Animals ; Fibronectins/metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Myokines ; Mice, Obese ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Solanum melongena/metabolism ; Diet, High-Fat/adverse effects ; Muscle, Skeletal/metabolism ; Brain/metabolism ; Dietary Supplements
Chemical Substances	Fibronectins ; Brain-Derived Neurotrophic Factor ; Myokines ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1014929-6
ISSN	1873-4847 ; 0955-2863
ISSN (online)	1873-4847
ISSN	0955-2863
DOI	10.1016/j.jnutbio.2023.109537
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Article ; Online: Lespedeza bicolor extract supplementation reduced hyperglycemia-induced skeletal muscle damage by regulation of AMPK/SIRT/PGC1α–related energy metabolism in type 2 diabetic mice

Lee, Heaji / Kim, Sun Yeou / Lim, Yunsook

Nutrition Research. 2023 Feb., v. 110 p.1-13

2023

Abstract: Lespedeza bicolor (LB) is known to have antidiabetic activities; however, the underlying molecular mechanisms of LB in hyperglycemia-induced skeletal muscle damage is unclear. Inflammation and oxidative stress caused by type 2 diabetes mellitus (T2DM) ... ...

Abstract	Lespedeza bicolor (LB) is known to have antidiabetic activities; however, the underlying molecular mechanisms of LB in hyperglycemia-induced skeletal muscle damage is unclear. Inflammation and oxidative stress caused by type 2 diabetes mellitus (T2DM) not only contributes to insulin resistance, but also promotes muscle atrophy via decreased muscle protein synthesis and increased protein degradation, leading to frailty and sarcopenia. In this study, we hypothesized that LB extract (LBE) supplementatin has an ameliorative effect on hyperglycemia-induced skeletal muscle damage by activation of 5′ adenosine monophosphate-activated protein kinase (AMPK)/sirtuin (SIRT)/proliferator-activated receptor γ coactivator 1α (PGC1α)–associated energy metabolism in mice with T2DM. Diabetes was induced by a high-fat diet with a 2-time streptozotoxin injection (30 mg/kg body weight) in male C57BL/6J mice. After diabetes was induced (fasting blood glucose level ≥140 mg/dL), the mice were administered with LBE at a low dose (100 mg/kg/d) or high dose (250 mg/kg/d) by gavage for 12 weeks. LBE supplementation ameliorated glucose tolerance and hemoglobin A1c (%) in mice with T2DM. Moreover, LBE supplementation upregulated protein levels of insulin receptor subunit-1 and Akt accompanied by increased translocation of glucose transporter 4 in mice with T2DM. Furthermore, LBE increased mitochondrial biogenesis by activating SIRT1, SIRT3, SIRT4, and peroxisome PGC1α in diabetic skeletal muscle. Meanwhile, LBE supplementation reduced oxidative stress and inflammation in mice with T2DM. Taken together, the current study suggested that LBE could be a potential therapeutic to prevent skeletal muscle damage by regulation AMPK/SIRT/PGC1α–related energy metabolism in T2DM.
Keywords	AMP-activated protein kinase ; Lespedeza bicolor ; biogenesis ; blood glucose ; body weight ; energy metabolism ; glucose tolerance ; glucose transporters ; glycohemoglobin ; high fat diet ; hyperglycemia ; inflammation ; insulin receptors ; insulin resistance ; males ; mitochondria ; muscle protein ; noninsulin-dependent diabetes mellitus ; nutrition research ; oxidative stress ; protein degradation ; protein synthesis ; sarcopenia ; skeletal muscle ; therapeutics ; Type 2 diabetes mellitus ; Insulin signaling ; 4-HNE ; AMPK ; AUC ; BW ; CON ; DMC ; FBG ; Foxo3a ; GLUT ; HbA1c ; HL ; HO-1 ; IL-6 ; LB ; LBE ; LL ; MuRF1 ; MCP-1 ; NQO1 ; OGTT ; PGC1α ; ROS ; SIRT ; T2DM ; IR ; IRS ; TNF-α
Language	English
Dates of publication	2023-02
Size	p. 1-13.
Publishing place	Elsevier Inc.
Document type	Article ; Online
ZDB-ID	582432-1
ISSN	1879-0739 ; 0271-5317
ISSN (online)	1879-0739
ISSN	0271-5317
DOI	10.1016/j.nutres.2022.12.007
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Glyoxal-derived advanced glycation end products (GO-AGEs) with UVB critically induce skin inflammaging: in vitro and in silico approaches.

Sultana, Razia / Parveen, Amna / Kang, Min-Cheol / Hong, Seong-Min / Kim, Sun Yeou

Scientific reports

2024 Volume 14, Issue 1, Page(s) 1843

Abstract: Advanced glycation end products (AGEs) have potential implications on several diseases including skin inflammation and aging. AGEs formation can be triggered by several factors such as UVB, glyoxal and methylglyoxal etc. However, little attention has ... ...

Abstract	Advanced glycation end products (AGEs) have potential implications on several diseases including skin inflammation and aging. AGEs formation can be triggered by several factors such as UVB, glyoxal and methylglyoxal etc. However, little attention has been paid to glyoxal-derived AGEs (GO-AGEs) and UVB-induced skin inflammaging, with none have investigated together. This study aimed to investigate the possible role of GO-AGEs and UVB in skin inflammaging focusing on revealing its molecular mechanisms. The effects of GO-AGEs in the presence or absence of UVB were studied by using enzyme linked immunosorbent assay, western blotting, qPCR, flow cytometry and in silico approaches. In HaCaT cells, GO-AGEs in the presence of UVB irradiation (125 mJ/cm
MeSH term(s)	Humans ; Glyoxal ; Molecular Docking Simulation ; Skin ; Dermatitis ; Interleukin-1beta ; Glycation End Products, Advanced
Chemical Substances	Glyoxal (50NP6JJ975) ; Interleukin-1beta ; Glycation End Products, Advanced
Language	English
Publishing date	2024-01-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-52037-z
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Article ; Online: Antidepressive Effect of Natural Products and Their Derivatives Targeting BDNF-TrkB in Gut-Brain Axis.

Liaqat, Humna / Parveen, Amna / Kim, Sun-Yeou

International journal of molecular sciences

2022 Volume 23, Issue 23

Abstract: Modern neurological approaches enable detailed studies on the pathophysiology and treatment of depression. An imbalance in the microbiota-gut-brain axis contributes to the pathogenesis of depression. This extensive review aimed to elucidate the ... ...

Abstract	Modern neurological approaches enable detailed studies on the pathophysiology and treatment of depression. An imbalance in the microbiota-gut-brain axis contributes to the pathogenesis of depression. This extensive review aimed to elucidate the antidepressive effects of brain-derived neurotrophic factor (BDNF)-targeting therapeutic natural products and their derivatives on the gut-brain axis. This information could facilitate the development of novel antidepressant drugs. BDNF is crucial for neuronal genesis, growth, differentiation, survival, plasticity, and synaptic transmission. Signaling via BDNF and its receptor tropomyosin receptor kinase B (TrkB) plays a vital role in the etiopathogenesis of depression and the therapeutic mechanism of antidepressants. This comprehensive review provides information to researchers and scientists for the identification of novel therapeutic approaches for neuropsychiatric disorders, especially depression and stress. Future research should aim to determine the possible causative role of BDNF-TrkB in the gut-brain axis in depression, which will require further animal and clinical research as well as the development of analytical approaches.
Language	English
Publishing date	2022-11-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232314968
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Article: The Activation of Nrf2/HO-1 by 8-Epi-7-deoxyloganic Acid Attenuates Inflammatory Symptoms through the Suppression of the MAPK/NF-κB Signaling Cascade in In Vitro and In Vivo Models.

Simu, Shakina Yesmin / Alam, Md Badrul / Kim, Sun Yeou

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 9

Abstract: In this study, we examined the ameliorative effects of 8-epi-7-deoxyloganic acid (DLA), an iridoid glycoside, on oxidative stress and inflammation in both LPS-stimulated macrophages and mice with carrageenan-induced inflammation. DLA decreased oxidative ... ...

Abstract	In this study, we examined the ameliorative effects of 8-epi-7-deoxyloganic acid (DLA), an iridoid glycoside, on oxidative stress and inflammation in both LPS-stimulated macrophages and mice with carrageenan-induced inflammation. DLA decreased oxidative stress through the up-regulation of heme oxygenase-1 (HO-1) via the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), leading to the suppression of reactive oxygen species (ROS) and nitric oxide generation (NO). In addition, DLA inhibited the activation of mitogen-activated protein kinases (MAPKs) and the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, resulting in a decreased production of the proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and -6 (IL-6), as well as of monocyte chemoattractant protein-1 (MCP-1). In addition, DLA effectively inhibited the generation of nitric oxide (NO) and prostaglandin E2 (PGE2) by inhibiting the expression of the upstream genes inducible nitric oxidase (iNOS) and cyclooxygenase-2 (COX-2). DLA demonstrated powerful anti-inflammatory and antioxidant properties and thus appears as an intriguing prospective therapeutic treatment.
Language	English
Publishing date	2022-09-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11091765
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Article ; Online: Neuroprotective Natural Products' Regulatory Effects on Depression via Gut-Brain Axis Targeting Tryptophan.

Liaqat, Humna / Parveen, Amna / Kim, Sun Yeou

Nutrients

2022 Volume 14, Issue 16

Abstract: L-tryptophan (Trp) contributes to regulating bilateral communication of the gut-brain axis. It undergoes three major metabolic pathways, which lead to formation of kynurenine, serotonin (5-HT), and indole derivatives (under the control of the microbiota). ...

Abstract	L-tryptophan (Trp) contributes to regulating bilateral communication of the gut-brain axis. It undergoes three major metabolic pathways, which lead to formation of kynurenine, serotonin (5-HT), and indole derivatives (under the control of the microbiota). Metabolites from the principal Trp pathway, kynurenic acid and quinolinic acid, exhibit neuroprotective activity, while picolinic acid exhibits antioxidant activity, and 5-HT modulates appetite, sleep cycle, and pain. Abnormality in Trp plays crucial roles in diseases, including depression, colitis, ulcer, and gut microbiota-related dysfunctions. To address these diseases, the use of natural products could be a favorable alternative because they are a rich source of compounds that can modulate the activity of Trp and combat various diseases through modulating different signaling pathways, including the gut microbiota, kynurenine pathway, and serotonin pathway. Alterations in the signaling cascade pathways via different phytochemicals may help us explore the deep relationships of the gut-brain axis to study neuroprotection. This review highlights the roles of natural products and their metabolites targeting Trp in different diseases. Additionally, the role of Trp metabolites in the regulation of neuroprotective and gastroprotective activities is discussed. This study compiles the literature on novel, potent neuroprotective agents and their action mechanisms in the gut-brain axis and proposes prospective future studies to identify more pharmaceuticals based on signaling pathways targeting Trp.
MeSH term(s)	Biological Products ; Brain-Gut Axis ; Depression ; Kynurenine/metabolism ; Neuroprotective Agents ; Serotonin/metabolism ; Tryptophan/metabolism
Chemical Substances	Biological Products ; Neuroprotective Agents ; Serotonin (333DO1RDJY) ; Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX)
Language	English
Publishing date	2022-08-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14163270
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Article ; Online: Lespedeza bicolor extract supplementation reduced hyperglycemia-induced skeletal muscle damage by regulation of AMPK/SIRT/PGC1α-related energy metabolism in type 2 diabetic mice.

Lee, Heaji / Kim, Sun Yeou / Lim, Yunsook

Nutrition research (New York, N.Y.)

2022 Volume 110, Page(s) 1–13

Abstract	Lespedeza bicolor (LB) is known to have antidiabetic activities; however, the underlying molecular mechanisms of LB in hyperglycemia-induced skeletal muscle damage is unclear. Inflammation and oxidative stress caused by type 2 diabetes mellitus (T2DM) not only contributes to insulin resistance, but also promotes muscle atrophy via decreased muscle protein synthesis and increased protein degradation, leading to frailty and sarcopenia. In this study, we hypothesized that LB extract (LBE) supplementatin has an ameliorative effect on hyperglycemia-induced skeletal muscle damage by activation of 5' adenosine monophosphate-activated protein kinase (AMPK)/sirtuin (SIRT)/proliferator-activated receptor γ coactivator 1α (PGC1α)-associated energy metabolism in mice with T2DM. Diabetes was induced by a high-fat diet with a 2-time streptozotoxin injection (30 mg/kg body weight) in male C57BL/6J mice. After diabetes was induced (fasting blood glucose level ≥140 mg/dL), the mice were administered with LBE at a low dose (100 mg/kg/d) or high dose (250 mg/kg/d) by gavage for 12 weeks. LBE supplementation ameliorated glucose tolerance and hemoglobin A1c (%) in mice with T2DM. Moreover, LBE supplementation upregulated protein levels of insulin receptor subunit-1 and Akt accompanied by increased translocation of glucose transporter 4 in mice with T2DM. Furthermore, LBE increased mitochondrial biogenesis by activating SIRT1, SIRT3, SIRT4, and peroxisome PGC1α in diabetic skeletal muscle. Meanwhile, LBE supplementation reduced oxidative stress and inflammation in mice with T2DM. Taken together, the current study suggested that LBE could be a potential therapeutic to prevent skeletal muscle damage by regulation AMPK/SIRT/PGC1α-related energy metabolism in T2DM.
MeSH term(s)	Animals ; Male ; Mice ; AMP-Activated Protein Kinases/metabolism ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Dietary Supplements ; Energy Metabolism ; Hyperglycemia/metabolism ; Lespedeza/chemistry ; Mice, Inbred C57BL ; Muscle, Skeletal ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Plant Extracts/pharmacology
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31) ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Plant Extracts
Language	English
Publishing date	2022-12-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	582432-1
ISSN	1879-0739 ; 0271-5317
ISSN (online)	1879-0739
ISSN	0271-5317
DOI	10.1016/j.nutres.2022.12.007
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