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Article ; Online: Expression of apelin‑13 and its negative correlation with TGF‑β1 in patients with diabetic kidney disease.

Wang, Qi / Liu, Xujing / Zhai, Aihua / Xu, Hua / Ma, Shizhan / Liu, Yulin

2024 Volume 27, Issue 3, Page(s) 110

Abstract: Diabetic kidney disease (DKD) is a severe microvascular complication of diabetes, one key feature of which includes renal fibrosis. As apelin is an adipokine closely related to diabetes, the present study aimed to evaluate apelin-13 expression levels and ...

Abstract	Diabetic kidney disease (DKD) is a severe microvascular complication of diabetes, one key feature of which includes renal fibrosis. As apelin is an adipokine closely related to diabetes, the present study aimed to evaluate apelin-13 expression levels and the relationship between apelin-13 and disease indicators in patients with diabetic kidney disease (DKD). The present case-control study enrolled 70 patients with diabetes, including 31 with diabetic kidney disease (DKD group), 39 without DKD (non-DKD group) and 30 healthy controls. The levels of serum apelin-13 and TGF-β1, the key driver of renal fibrosis, were determined by ELISA. Additionally, age, mean disease duration, weight, blood pressure, fasting blood glucose, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein, cholesterol, urea nitrogen, blood creatinine and 24-hour urinary total protein (24-h UTP) were recorded. The results demonstrated that apelin-13 and TGF-β1 expression levels, age, blood pressure, fasting blood glucose, cholesterol and blood urea nitrogen levels were significantly higher in patients with diabetes compared with the healthy controls (P<0.05). Moreover, apelin-13 and TGF-β1 expression levels, mean disease duration, systolic pressure, blood creatinine, blood urea nitrogen and 24-h UTP were significantly higher in the DKD group compared with the non-DKD group (P<0.05). The estimated glomerular filtration rate (eGFR) was significantly reduced in the DKD group compared with the non-DKD group (P<0.05). Correlation analysis demonstrated a negative correlation between apelin-13 and eGFR expression and a positive correlation between apelin-13 expression and 24-h UTP in both the DKD and non-DKD groups (P<0.05). A negative correlation was also demonstrated between apelin-13 and TGF-β1 expression levels in the DKD group and non-DKD groups (both P<0.05). In conclusion, apelin-13 and TGF-β1 expression levels were significantly higher in the DKD group compared with those in the non-DKD group. Additionally, apelin-13 expression was negatively correlated with TGF-β1 expression in the DKD and non-DKD groups. Therefore, apelin-13 could potentially be used in the future as an indicator of renal fibrosis or destruction in patients with DKD. The present trial was retrospectively registered in the Chinese Clinical Trial Registry (trial registration no. ChiCTR2200060945) on 14.06.2022.
Language	English
Publishing date	2024-01-23
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2024.12398
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Article: Exploring the link between obesity and hypothyroidism in autoimmune thyroid diseases: a metabolic perspective.

Jing, Mengzhe / Shao, Shanshan / Ma, Shizhan / Gao, Ling / Wang, Qian / Zhou, Meng

Frontiers in molecular biosciences

2024 Volume 11, Page(s) 1379124

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2024-04-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2024.1379124
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Article: The effect of

Wu, Dongming / Zhang, Zhenyuan / Sun, Wenxiu / Yan, Yong / Jing, Mengzhe / Ma, Shizhan

Frontiers in endocrinology

2023 Volume 14, Page(s) 1130350

Abstract: Background: Previous research has shown a tight relationship between the G0/G1 switch gene 2 (G0S2) and metabolic diseases such as non-alcoholic fatty liver disease (NAFLD) and obesity and diabetes, and insulin resistance has been shown as the major ... ...

Abstract	Background: Previous research has shown a tight relationship between the G0/G1 switch gene 2 (G0S2) and metabolic diseases such as non-alcoholic fatty liver disease (NAFLD) and obesity and diabetes, and insulin resistance has been shown as the major risk factor for both NAFLD and T2DM. However, the mechanisms underlying the relationship between G0S2 and insulin resistance remain incompletely understood. Our study aimed to confirm the effect of G0S2 on insulin resistance, and determine whether the insulin resistance in mice fed a high-fat diet (HFD) results from G0S2 elevation. Methods: In this study, we extracted livers from mice that consumed HFD and received tail vein injections of AD-G0S2/Ad-LacZ, and performed a proteomics analysis. Results: Proteomic analysis revealed that there was a total of 125 differentially expressed proteins (DEPs) (56 increased and 69 decreased proteins) among the identified 3583 proteins. Functional enrichment analysis revealed that four insulin signaling pathway-associated proteins were significantly upregulated and five insulin signaling pathway -associated proteins were significantly downregulated. Conclusion: These findings show that the DEPs, which were associated with insulin resistance, are generally consistent with enhanced insulin resistance in G0S2 overexpression mice. Collectively, this study demonstrates that G0S2 may be a potential target gene for the treatment of obesity, NAFLD, and diabetes.
MeSH term(s)	Animals ; Mice ; Cell Cycle Proteins/genetics ; Diet, High-Fat/adverse effects ; Insulin ; Insulin Resistance/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Obesity/complications ; Proteomics
Chemical Substances	Cell Cycle Proteins ; Insulin ; G0S2 protein, mouse
Language	English
Publishing date	2023-03-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1130350
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Article ; Online: Association of Obesity Based on Different Metabolic Status with Risk of Gout Occurrence in Patients: A National Study.

Wang, Yanyan / Fan, Xiude / Hou, Xu / Liu, Luna / Ma, Shizhan / Han, Junming / Wang, Zhixiang

Endocrine, metabolic & immune disorders drug targets

2023

Abstract: Background: Obesity often co-exists with metabolic abnormalities, but the results of studies on the relationship between obesity, metabolic abnormalities and the risk of gout are inconsistent.: Objective: We aimed to study whether there was a mutual ... ...

Abstract	Background: Obesity often co-exists with metabolic abnormalities, but the results of studies on the relationship between obesity, metabolic abnormalities and the risk of gout are inconsistent. Objective: We aimed to study whether there was a mutual regulation between obesity, metabolic abnormalities and the risk of gout. Method: We conducted a cross-sectional study to expound the association between obesity based on different metabolic statuses and the risk of gout. Patients were derived from Nationwide Readmission Database (2018 sample). Results: A total of 9,668,330 records were recruited for analysis from January to December. The risk of gout in the obesity group, metabolic abnormalities group and obesity combined with metabolic abnormalities group was 1.67 times (OR=1.67, 95%CI 1.64-1.70), 3.12 times (OR=3.12, 95%CI 3.09-3.15) and 4.27 times (OR=4.27, 95%CI 4.22-4.32) higher than that in the normal control group. For different metabolic components, OR value was highest in hypertension group (OR=2.65, 95%CI 2.60-2.70 and OR=4.85, 95%CI 4.73-4.97), followed by dyslipidemia group (OR=2.23, 95%CI 2.16-2.30 and OR=3.74, 95%CI 3.55-3.95) and in hyperglycemia group (OR=1.73, 95%CI 1.66-1.80 and OR=2.94, 95%CI 2.78-3.11). Fewer components of metabolic syndrome were associated with a lower risk of gout in both nonobese and obese patients. Conclusion: When metabolic abnormalities were present, obesity induced a higher risk of gout. Different components of metabolic abnormalities had different effects on the risk of gout occurrence, and the number of metabolic abnormalities was closely related to the risk of gout occurrence. Follow-up and intervention methods targeting obesity and metabolic abnormalities should be considered for patients with gout.
Language	English
Publishing date	2023-09-11
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2228325-0
ISSN	2212-3873 ; 1871-5303
ISSN (online)	2212-3873
ISSN	1871-5303
DOI	10.2174/1871530323666230911140635
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Article: Association between Regional Body Muscle Mass and Non-Alcoholic Fatty Liver Disease: An Observational Study Using Data from the REACTION Study.

Du, Jing / Ma, Shizhan / Fang, Li / Zhao, Meng / Yuan, Zhongshang / Cheng, Yiping / Zhao, Jiajun / Fan, Xiude / Guo, Qingling / Wu, Zhongming

Journal of personalized medicine

2023 Volume 13, Issue 2

Abstract: Background and aims: ...

Abstract	Background and aims:
Language	English
Publishing date	2023-01-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm13020209
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Article: Therapeutic targets of hypercholesterolemia: HMGCR and LDLR.

Ma, Shizhan / Sun, Wenxiu / Gao, Ling / Liu, Shudong

Diabetes, metabolic syndrome and obesity : targets and therapy

2019 Volume 12, Page(s) 1543–1553

Abstract: Cholesterol homeostasis is critical and necessary for the body's functions. Hypercholesterolemia can lead to significant clinical problems, such as cardiovascular disease (CVD). 3-Hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) and low-density ... ...

Abstract	Cholesterol homeostasis is critical and necessary for the body's functions. Hypercholesterolemia can lead to significant clinical problems, such as cardiovascular disease (CVD). 3-Hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) and low-density lipoprotein cholesterol receptor (LDLR) are major points of control in cholesterol homeostasis. We summarize the regulatory mechanisms of HMGCR and LDLR, which may provide insight for new drug design and development.
Language	English
Publishing date	2019-08-21
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2494854-8
ISSN	1178-7007
ISSN	1178-7007
DOI	10.2147/DMSO.S219013
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Article ; Online: Gut dysbiosis is associated with primary hypothyroidism with interaction on gut-thyroid axis.

Su, Xinhuan / Zhao, Ying / Li, Yang / Ma, Shizhan / Wang, Zhe

Clinical science (London, England : 1979)

2020 Volume 134, Issue 12, Page(s) 1521–1535

Abstract: Background Previous studies have shown that the gut microbiome is associated with thyroid diseases, including Graves' disease, Hashimoto's disease, thyroid nodules, and thyroid cancer. However, the association between intestinal flora and primary ... ...

Abstract	Background Previous studies have shown that the gut microbiome is associated with thyroid diseases, including Graves' disease, Hashimoto's disease, thyroid nodules, and thyroid cancer. However, the association between intestinal flora and primary hypothyroidism remains elusive. We aimed to characterize gut microbiome in primary hypothyroidism patients. Methods Fifty-two primary hypothyroidism patients and 40 healthy controls were recruited. The differences in gut microbiota between the two groups were analyzed by 16S rRNA sequencing technology. Fecal microbiota transplantation (FMT) was performed in mice using flora from both groups; changes in thyroid function were then assessed in the mice. Results There were significant differences in α and β diversities of gut microbiota between primary hypothyroidism patients and healthy individuals. The random forest analysis indicated that four intestinal bacteria (Veillonella, Paraprevotella, Neisseria, and Rheinheimera) could distinguish untreated primary hypothyroidism patients from healthy individuals with the highest accuracy; this was confirmed by receiver operator characteristic curve analysis. The short chain fatty acid producing ability of the primary hypothyroidism patients' gut was significantly decreased, which resulted in the increased serum lipopolysaccharide (LPS) levels. The FMT showed that mice receiving the transplant from primary hypothyroidism patients displayed decreased total thyroxine levels. Conclusions Our study suggests that primary hypothyroidism causes changes in gut microbiome. In turn, an altered flora can affect thyroid function in mice. These findings could help understand the development of primary hypothyroidism and might be further used to develop potential probiotics to facilitate the adjuvant treatment of this disease.
MeSH term(s)	Adult ; Animals ; Case-Control Studies ; Dysbiosis/complications ; Fatty Acids/metabolism ; Fecal Microbiota Transplantation ; Female ; Gastrointestinal Microbiome ; Gastrointestinal Tract/pathology ; Humans ; Hypothyroidism/complications ; Male ; Metagenomics ; Mice, Inbred BALB C ; Phylogeny ; ROC Curve ; Thyroid Gland/pathology
Chemical Substances	Fatty Acids
Language	English
Publishing date	2020-06-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	206835-7
ISSN	1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
ISSN (online)	1470-8736
ISSN	0301-0538 ; 0009-0360 ; 0143-5221
DOI	10.1042/CS20200475
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Article: Single-Cell Sequencing Analysis of the db/db Mouse Hippocampus Reveals Cell-Type-Specific Insights Into the Pathobiology of Diabetes-Associated Cognitive Dysfunction.

Ma, Shizhan / Bi, Wenkai / Liu, Xueying / Li, Shangbin / Qiu, Yaxin / Huang, Chengcheng / Lv, Renjun / Yin, Qingqing

Frontiers in endocrinology

2022 Volume 13, Page(s) 891039

Abstract: Diabetes-associated cognitive decline (DCD), is one of the complications of diabetes, which is characterized by a series of neurophysiological and pathological abnormalities. However, the exact pathogenesis of DCD is still unknown. Single-cell RNA ... ...

Abstract	Diabetes-associated cognitive decline (DCD), is one of the complications of diabetes, which is characterized by a series of neurophysiological and pathological abnormalities. However, the exact pathogenesis of DCD is still unknown. Single-cell RNA sequencing (scRNA-seq) could discover unusual subpopulations, explore functional heterogeneity and identify signaling pathways and potential markers. The aim of this research was to provide deeper opinion into molecular and cellular changes underlying DCD, identify different cellular types of the diabetic mice hippocampus at single-cell level, and elucidate the factors mediating the pathogenesis of DCD. To elucidate cell specific gene expression changes in the hippocampus of diabetic encephalopathy. Single-cell RNA sequencing of hippocampus from db/m and db/db mice was carried out. Subclustering analysis was performed to further describe microglial cell subpopulations. Interestingly using immunohistochemistry, these findings were confirmed at the protein level. Single cell analysis yielded transcriptome data for 14621 hippocampal cells and defined 11 different cell types. Analysis of differentially expressed genes in the microglia compartments indicated that infection- and immune system process- associated terms, oxidative stress and inflammation play vital roles in the progression of DCD. Compared with db/m mouse, experiments at the protein level supported the activation of microglia, increased expression of inflammatory factors and oxidative stress damage in the hippocampus of db/db mouse. In addition, a major finding of our research was the subpopulation of microglia that express genes related to pro-inflammatory disease-associated microglia (DAM). Our research reveals pathological alterations of inflammation and oxidative stress mediated hippocampal damage in the db/db mice, and may provide potential diagnostic biomarkers and therapeutic interventions for DCD.
MeSH term(s)	Animals ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/genetics ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/metabolism ; Hippocampus/metabolism ; Inflammation/metabolism ; Mice ; Single-Cell Analysis
Language	English
Publishing date	2022-06-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2022.891039
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Article ; Online: The effect of hyperthyroidism on cognitive function, neuroinflammation, and necroptosis in APP/PS1 mice.

Lou, Kai / Liu, Shudong / Zhang, Fengxia / Sun, Wenxiu / Su, Xinhuan / Bi, Wenkai / Yin, Qingqing / Qiu, Yaxin / Zhang, Zhenyuan / Jing, Mengzhe / Ma, Shizhan

Journal of translational medicine

2023 Volume 21, Issue 1, Page(s) 657

Abstract: Background: Increasing evidence has linked the thyroid dysfunction to the pathogenesis of dementia. Evidence from clinical studies has demonstrated that hypothyroidism is related to an increased risk of dementia. But the association of hyperthyroidism ... ...

Abstract	Background: Increasing evidence has linked the thyroid dysfunction to the pathogenesis of dementia. Evidence from clinical studies has demonstrated that hypothyroidism is related to an increased risk of dementia. But the association of hyperthyroidism with dementia is largely unknown. Methods: We used the adenovirus containing thyrotropin receptor (TSHR) amino acid residues 1-289 (Ad-TSHR289)-induced Graves' disease (GD) phenotype in Alzheimer's disease (AD) model mice (APP/PS1 mice) to evaluate the effect of hyperthyroidism on the cognitive function and β-amyloid (Aβ) accumulation. Results: GD mice exhibited a stable long-term hyperthyroidism and cognitive deficits. Single Cell RNA-sequencing analysis indicated that microglia function played a critical role in the pathophysiological processes in GD mice. Neuroinflammation and polarization of microglia (M1/M2 phenotype) and activated receptor-interacting serine/threonine protein kinase 3 (RIPK3)/mixed lineage kinase domain-like pseudo-kinase (MLKL)-mediated necroptosis contributed to the pathological process, including Aβ deposition and neuronal loss. RIPK3 inhibitor could inhibit GD-mediated Aβ accumulation and neuronal loss. Conclusions: Our findings reveal that GD hyperthyroidism aggravates cognitive deficits in AD mice and induces Aβ deposition and neuronal loss by inducing neuroinflammation and RIPK3/MLKL-mediated necroptosis.
MeSH term(s)	Animals ; Mice ; Necroptosis ; Neuroinflammatory Diseases ; Hyperthyroidism/complications ; Cognition ; Graves Disease ; Alzheimer Disease/complications
Language	English
Publishing date	2023-09-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2118570-0
ISSN	1479-5876 ; 1479-5876
ISSN (online)	1479-5876
ISSN	1479-5876
DOI	10.1186/s12967-023-04511-x
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Article ; Online: TSH promotes adiposity by inhibiting the browning of white fat.

Zhang, Jianmei / Wu, Huixiao / Ma, Shizhan / Gao, Ling / Yu, Chunxiao / Jing, Fei / Zhao, Jiajun

Adipocyte

2020 Volume 9, Issue 1, Page(s) 264–278

Abstract: Adiposity is caused by an imbalance between energy intake and consumption. Promotion of the browning of white fat increases energy expenditure and could combat adiposity. Thyroid-stimulating hormone (TSH) has been confirmed to positively correlate with ... ...

Abstract	Adiposity is caused by an imbalance between energy intake and consumption. Promotion of the browning of white fat increases energy expenditure and could combat adiposity. Thyroid-stimulating hormone (TSH) has been confirmed to positively correlate with adiposity. However, the putative connection between TSH and white adipose browning has never been explored. In this study, we sought to assess the effect of TSH on white adipose tissue browning and energy metabolism. Subclinical hypothyroidism mice, thyroid-specific
MeSH term(s)	Adipocytes, Brown/metabolism ; Adipogenesis ; Adipose Tissue, Brown/drug effects ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/drug effects ; Adipose Tissue, White/metabolism ; Adiposity/drug effects ; Animals ; Biomarkers ; Cell Differentiation ; Energy Metabolism/genetics ; Male ; Metabolic Diseases/etiology ; Metabolic Diseases/metabolism ; Mice ; Mice, Transgenic ; Receptors, Thyrotropin/genetics ; Receptors, Thyrotropin/metabolism ; Thermogenesis ; Thyrotropin/metabolism ; Thyrotropin/pharmacology
Chemical Substances	Biomarkers ; Receptors, Thyrotropin ; Thyrotropin (9002-71-5)
Language	English
Publishing date	2020-06-20
Publishing country	United States
Document type	Journal Article
ISSN	2162-397X
ISSN (online)	2162-397X
DOI	10.1080/21623945.2020.1783101
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