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Jin Yu Department of Gynecology of Traditional Chinese Medicine, Changhai Hospital, Naval Medical University, Shanghai, China

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Yuhuan Liu Department of Gynecology and Obstetrics, Changhai Hospital, Naval Medical University, Shanghai, China

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Danying Zhang Department of Gynecology of Traditional Chinese Medicine, Changhai Hospital, Naval Medical University, Shanghai, China

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Dongxia Zhai Department of Gynecology of Traditional Chinese Medicine, Changhai Hospital, Naval Medical University, Shanghai, China

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Linyi Song Department of Gynecology of Traditional Chinese Medicine, Changhai Hospital, Naval Medical University, Shanghai, China

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Zailong Cai Department of Biochemistry and Molecular Biology, Naval Medical University, Shanghai, China

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Chaoqin Yu Department of Gynecology of Traditional Chinese Medicine, Changhai Hospital, Naval Medical University, Shanghai, China

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High androgen levels in patients suffering from polycystic ovary syndrome (PCOS) can be effectively reversed if the herb Scutellaria baicalensis is included in traditional Chinese medicine prescriptions. To characterize the effects of baicalin, extracted from S. baicalensis, on androgen biosynthesis in NCI-H295R cells and on hyperandrogenism in PCOS model rats and to elucidate the underlying mechanisms. The optimum concentration and intervention time for baicalin treatment of NCI-H295R cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and ELISA. The functional genes affected by baicalin were studied by gene expression profiling (GEP), and the key genes were identified using a dual luciferase assay, RNA interference technique and genetic mutations. Besides, hyperandrogenic PCOS model rats were induced and confirmed before and after baicalin intervention. As a result, baicalin decreased the testosterone concentrations in a dose- and time-dependent manner in NCI-H295R cells. GEP revealed that 3β-hydroxysteroid dehydrogenase type II (HSD3B2) was the key enzyme of androgen biosynthesis, and baicalin inhibited the expression of HSD3B2 by regulating the binding of transcription factor GATA-binding factor 1 (GATA1) to the HSD3B2 promoter. Hyperandrogenic PCOS model rats treated with baicalin significantly reversed the high androgen levels of serum and the abnormal ovarian status, restored the estrous cyclicity and decreased the expression of HSD3B2 in ovarian. In summary, our data revealed that GATA1 is an important transcription factor activating the HSD3B2 promoter in steroidogenesis, and baicalin will potentially be an effective therapeutic agent for hyperandrogenism in PCOS by inhibiting the recruitment of GATA1 to the HSD3B2 promoter in ovarian tissue.

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Shou-Si Lu
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Yun-Li Yu
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Hao-Jie Zhu Key Lab of Drug Metabolism and Pharmacokinetics, Department of Pharmaceutical and Biomedical Science, China Pharmaceutical University, Nanjing 210009, People's Republic of China

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Xiao-Dong Liu
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Li Liu
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Yao-Wu Liu
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Ping Wang
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Lin Xie
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Guang-Ji Wang
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Berberine (BBR), a hypoglycemic agent, has shown beneficial metabolic effects for anti-diabetes, but its precise mechanism was unclear. Glucagon-like peptide-1 (GLP-1) is considered to be an important incretin that can decrease hyperglycemia in the gastrointestinal tract after meals. The aim of this study was to investigate whether BBR exerts its anti-diabetic effects via modulating GCG secretion. Diabetes-like rats induced by streptozotocin received BBR (120 mg/kg per day, i.g) for 5 weeks. Two hours following the last dose, the rats were anaesthetized and received 2.5 g/kg glucose by gavage. At 15-minute and 30-minute after glucose load, blood samples, pancreas, and intestines were obtained to measure insulin and GCG using ELISA kit. The number of L cells in the ileum and β-cells in the pancreas were identified using immunohistology. The expression of proglucagon mRNA in the ileum was measured by RT-PCR. The results indicated that BBR treatment significantly increased GCG levels in plasma and intestine (P<0.05) accompanied with the increase of proglucagon mRNA expression and the number of L-cell compared with the controls (P<0.05). Furthermore, BBR increased insulin levels in plasma and pancreas as well as β-cell number in pancreas. The data support the hypothesis that the anti-diabetic effects of BBR may partly result from enhancing GCG secretion.

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Shuisheng Li State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Yong Zhang State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Yun Liu State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Xigui Huang State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Weiren Huang State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Danqi Lu State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Pei Zhu State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Yu Shi State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Christopher H K Cheng State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Xiaochun Liu State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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Haoran Lin State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China
State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China

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To ascertain the neuroendocrine function of the kisspeptin/GPR54 system in non-mammalian species, full-length cDNAs encoding for Kiss1 and Kiss2 as well as their putative cognate receptors GPR54a and GPR54b, were isolated from goldfish (Carassius auratus). The deduced protein sequences between Kiss1 and Kiss2 in goldfish share very low similarity, but their putative mature peptides (kisspeptin-10) are relatively conserved. RT-PCR analysis demonstrated that the goldfish kiss1 gene (gfkiss1) is highly expressed in the optic tectum-thalamus, intestine, kidney, and testis, while the goldfish kiss2 gene (gfkiss2) is mainly detected in the hypothalamus, telencephalon, optic tectum thalamus, adipose tissue, kidney, heart, and gonads. The two receptor genes (gfgpr54a and gfgpr54b) are highly expressed in the brain regions including telencephalon, optic tectum thalamus, and hypothalamus. Both mature goldfish kisspeptin-10 peptides (gfKiss1–10 and gfKiss2–10) are biologically active as they could functionally interact with the two goldfish receptors expressed in cultured eukaryotic cells to trigger the downstream signaling pathways with different potencies. The actions of gfKiss1–10 and gfKiss2–10 on LH secretion were further investigated in vitro and in vivo. Intraperitoneal administration of gfKiss1–10 to sexually mature female goldfish could increase the serum LH levels. However, this peptide does not significantly influence LH release from goldfish pituitary cells in primary culture, indicating that the peptide does not exert its actions at the pituitary level. On the other hand, gfKiss2–10 appears to be a much less potent peptide as it exhibits no significant in vivo bioactivity and is also inactive on the primary pituitary cells.

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M Candolfi Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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G Jaita Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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D Pisera Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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L Ferrari Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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C Barcia Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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C Liu Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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J Yu Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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G Liu Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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M G Castro Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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A Seilicovich Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Buenos Aires (C1121ABG), Argentina
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

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Our previous work showed that tumor necrosis factor (TNF)-α and FasL induce apoptosis of anterior pituitary cells. To further analyze the effect of these proapoptotic factors, we infected primary cultures from rat anterior pituitary, GH3 and AtT20 cells with first-generation adenoviral vectors encoding TNF-α, FasL or, as a control, β-galactosidase (β-Gal), under the control of the human cytomegalovirus promoter. Successful expression of the encoded transgenes was determined by immunocytochemistry. Although we observed basal expression of TNF-α and FasL in control cultures of anterior pituitary cells, fluorescence-activated cell sorting (FACS) cell cycle analysis showed that the overexpression of TNF-α or FasL increases the percentage of hypodiploid lactotropes and somatotropes. Nuclear morphology and TUNEL staining revealed that the cells undergo an apoptotic death process. We detected strong immunoreactivity for TNFR1 and Fas in the somatolactotrope cell line GH3. TNF-α, but not FasL, was expressed in control cultures of GH3 cells. The infection of GH3 cells with adenovirus encoding TNF-α or FasL increased the percentages of hypodiploid and TUNEL-positive cells. TNF-α or FasL immunoreactivity was not observed in the corticotrope cell line AtT20. However, adenovirus encoding TNF-α or FasL efficiently transduced these cells and increased the percentages of hypodiploid and TUNEL-positive cells. The expression of β-Gal was detected in all these cultures but did not affect cell viability. In conclusion, these results suggest that death signaling cascades triggered by TNF receptor 1 (TNFR1) and Fas are present in both normal and tumoral pituitary cells. Therefore, overexpression of proapoptotic factors could be a useful tool in the therapy of pituitary adenomas.

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Can Liu Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Mian Zhang Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Meng-yue Hu Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Hai-fang Guo Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Jia Li Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Yun-li Yu Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Shi Jin Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Xin-ting Wang Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Li Liu Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Xiao-dong Liu Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China

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Panax ginseng is one of the most popular herbal remedies. Ginsenosides, major bioactive constituents in P. ginseng, have shown good antidiabetic action, but the precise mechanism was not fully understood. Glucagon-like peptide-1 (GLP1) is considered to be an important incretin that can regulate glucose homeostasis in the gastrointestinal tract after meals. The aim of this study was to investigate whether ginseng total saponins (GTS) exerts its antidiabetic effects via modulating GLP1 release. Ginsenoside Rb1 (Rb1), the most abundant constituent in GTS, was selected to further explore the underlying mechanisms in cultured NCI-H716 cells. Diabetic rats were developed by a combination of high-fat diet and low-dose streptozotocin injection. The diabetic rats orally received GTS (150 or 300 mg/kg) daily for 4 weeks. It was found that GTS treatment significantly ameliorated hyperglycemia and dyslipidemia, accompanied by a significant increase in glucose-induced GLP1 secretion and upregulation of proglucagon gene expression. Data from NCI-H716 cells showed that both GTS and Rb1 promoted GLP1 secretion. It was observed that Rb1 increased the ratio of intracellular ATP to ADP concentration and intracellular Ca2 + concentration. The metabolic inhibitor azide (3 mM), the KATP channel opener diazoxide (340 μM), and the Ca2 + channel blocker nifedipine (20 μM) significantly reversed Rb1-mediated GLP1 secretion. All these results drew a conclusion that ginsenosides stimulated GLP1 secretion both in vivo and in vitro. The antidiabetic effects of ginsenosides may be a result of enhanced GLP1 secretion.

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Sheng-Gao Tang School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China

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Xiao-Yu Liu School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China

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Ji-Ming Ye Molecular Pharmacology for Diabetes, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia

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Ting-Ting Hu School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China

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Ying-Ying Yang School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China

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Ting Han School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China

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Wen Tan Institute of Biomedical & Pharmaceutical Science, Guangdong University of Technology, Guangzhou, China

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Diabetes-induced injury of myocardium, defined as diabetic cardiomyopathy (DCM), accounts for significant mortality and morbidity in diabetic population. Alleviation of DCM by a potent drug remains considerable interests in experimental and clinical researches because hypoglycemic drugs cannot effectively control this condition. Here, we explored the beneficial effects of isosteviol sodium (STVNa) on type 1 diabetes-induced DCM and the potential mechanisms involved. Male Wistar rats were induced to diabetes by injection of streptozotocin (STZ). One week later, diabetic rats were randomly grouped to receive STVNa (STZ/STVNa) or its vehicle (STZ). After 11 weeks of treatment or 11 weeks treatment following 4 weeks of removal of the treatment, the cardiac function and structure were evaluated and related mechanisms were investigated. In diabetic rats, oxidative stress, inflammation, blood glucose and plasma advanced glycation end products (AGEs) were significantly increased, whereas superoxide dismutase 2 (SOD-2) expression and activity were decreased. STVNa treatment inhibited cardiac hypertrophy, fibrosis and inflammation, showed similar ratio of heart to body weight and antioxidant capacities almost similar to the normal controls, which can be sustained at least 4 weeks. Moreover, STVNa inhibited diabetes-inducted stimulation of both extracellular signal-regulated kinase (ERK) and nuclear factor κB (NF-κB) signal pathways. However, blood glucose, plasma AGE and insulin levels were not altered by STVNa treatment. These results indicate that STVNa may be developed into a potent therapy for DCM. The mechanism underlying this therapeutic effect involves the suppression of oxidative stress and inflammation by inhibiting ERK and NF-κB without changing blood glucose or AGEs.

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Lin-Yu Jin Department of spinal surgery, Peking University People’s Hospital, Peking University, Beijing, China
Department of spinal surgery, enji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China

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Zhen-Dong Lv Department of spinal surgery, enji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China

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Xin-Jin Su Department of spinal surgery, enji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China

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Shuai Xu Department of spinal surgery, Peking University People’s Hospital, Peking University, Beijing, China

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Hai-Ying Liu Department of spinal surgery, Peking University People’s Hospital, Peking University, Beijing, China

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Xin-Feng Li Department of spinal surgery, enji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China

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Estrogen receptors (ERs) regulate the development of the growth plate (GP) by binding to estrogen, a phenomenon that determines the growth of skeletal bone. However, the exact mechanisms underlying the regulatory effects of ERs on axial and appendicular growth plates during puberty remain unclear. In the present study, the strategy of ERβ blocking resulted in increased longitudinal elongation of the appendicular bone (P < 0.01), whereas ERα blocking suppressed appendicular elongation (P < 0.05). Blocking both ERs did not have opposite effects on axial longitudinal growth. The expression of chondrocyte proliferation genes including collagen II, aggrecan, and Sox9 and hypertrophic marker genes including collagen X, MMP13, and Runx2 was significantly increased in the growth plate of female mice treated with ERβ antagonist compared with that in the GP of control mice (P < 0.05). There were no significant differences in local insulin-like growth factor 1 (IGF-1) expression among these groups (P > 0.05), and Indian hedgehog protein (Ihh) and parathyroid-related protein (PTHrP) expressions differed among these groups (P < 0.05). ERs appeared not to affect axial bone growth during puberty in female mice (P > 0.05). Our data show that the blocking of different ER subtypes might have a region-specific influence on longitudinal appendicular and axial growth.

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Dan Wang Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China

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Chu-Dan Liu Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China

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Meng-Li Tian Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China

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Cheng-Quan Tan Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China

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Gang Shu Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China

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Qing-Yan Jiang Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China

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Lin Zhang Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China

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Yu-Long Yin Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, Institute of Subtropical Animal Nutrition and Feed, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China
Key Laboratory of Agro-Ecological Processes in Subtropical Region, Laboratory of Animal Nutritional Physiology and Metabolic Process, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha, Hunan, China

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Dietary fibers and their microbial fermentation products short-chain fatty acids promote metabolic benefits, but the underlying mechanisms are still unclear. Recent studies indicate that intestinal lipid handling is under regulatory control and has broad influence on whole body energy homeostasis. Here we reported that dietary inulin and propionate significantly decreased whole body fat mass without affecting food intake in mice fed with chow diet. Meanwhile, triglyceride (TG) content was decreased and lipolysis gene expression, such as adipose triglyceride lipase (A tgl), hormone-sensitive lipase (H sl) and lysosomal acid lipase (L al) was elevated in the jejunum and ileum of inulin- and propionate-treated mice. In vitro studies on Caco-2 cells showed propionate directly induced enterocyte Atgl, Hsl and Lal gene expression and decreased TG content, via activation of phosphorylation of AMP-activated protein kinase (p-AMPK) and lysine-specific demethylase 1 (LSD1). Moreover, inulin and propionate could increase intestinal lipolysis under high-fat diet (HFD)-fed condition which contributed to the prevention of HFD-induced obesity. Our study suggests that dietary fiber inulin and its microbial fermentation product propionate can regulate metabolic homeostasis through regulating intestinal lipid handling, which may provide a novel therapeutic target for both prevention and treatment of obesity.

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Xuanchun Wang Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Wei Gong Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Yu Liu Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Zhihong Yang Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Wenbai Zhou Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Mei Wang Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Zhen Yang Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Jie Wen Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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Renming Hu Department of Endocrinology, Huashan Hospital, Institute of Endocrinology and Diabetology at Fudan University, Shanghai Medical College, Fudan University, Shanghai 200040, People's Republic of China

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We report the identification of a novel secreted peptide, INM02. The mRNA transcript of human INM02 gene is about 3.0 kb. Its open-reading frame contains 762 bps and encodes a protein of 254 amino acids. Northern blot analysis demonstrates that INM02 mRNA is widely expressed in rat tissues, especially with abundant quantities in pancreatic islets, testis, and bladder tissue. We have expressed recombinant INM02 protein and generated rabbit anti-INM02 polyclonal antibodies. We show here that INM02 could be detectable in human serum by ELISA. We also present evidence that INM02 mRNA expression could be regulated by glucose. Experiments on both MIN6 cells and intact isolated islets demonstrate that INM02 mRNA levels are increased more than threefold by high glucose (25 mM) when compared with low glucose (5.5 mM). ELISA analysis shows that secretion of INM02 is significantly augmented by high glucose in vitro. It is speculated that as a novel secreted protein, INM02 is associated with functions of pancreatic islets, especially of β-cells.

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Qin Yin Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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Jun Gu Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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Pengju Ren Department of Orthopedics, The Shanghai Tenth People’s Hospital of Tongji University, Shanghai, China

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Zhiqiang Guan Department of Dermatology, Xuzhou Municipal Hospital Affiliated to Xuzhou Medical University, Xuzhou, Jiangsu, China

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Yongxiang Wang Department of Orthopedics, Clinical Medical College, Yangzhou University, Yangzhou, China
Department of Orthopedics, Northern Jiangsu People’s Hospital, Yangzhou, China

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Ruijun Bai Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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Yu Liu Department of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow University, Wuxi, Jiangsu, China

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The role of this study was to evaluate the impact of gut microbiota depletion on the progression of osteoarthritis (OA) and osteoporosis (OP). We conducted an experimental mouse model of OA and OP over an 8-week period. The model involved destabilization of the medial meniscus and bilateral ovariectomy (OVX). To deplete the gut microbiota, we administered a course of antibiotics for 8 weeks. The severity of OA was assessed through micro-CT scanning, X-rays, and immunohistochemical staining. Microbiome analysis was performed using PCR of 16S DNA on fecal samples, and the levels of serum lipopolysaccharide, interleukin 6, tumor necrosis factor-α (TNF-α), osteocalcin, and estrogen were measured using enzyme-linked immunosorbent assay. We found that in comparison to the OVX+OA group, the OVX+OA+ABT group exhibited increased bone mineral density (P < 0.0001), bone volume fraction (P = 0.0051), and trabecular number (P = 0.0023) in the metaphyseal bone. Additionally, cartilage injury and levels of matrix metalloproteinase 13 were reduced in the OVX+OA+ABT group compared to the OVX+OA group. Moreover, the OVX+OA+ABT group demonstrated decreased relative abundance of Bacteroidetes, serum lipopolysaccharide (P = 0.0005), TNF-α (P < 0.0001), CTX-1 (P = 0.0002), and increased expression of bone formation markers. These findings were further supported by correlation network analyses. Depletion of gut microbiota was shown to protect against bone loss and cartilage degradation by modulating the composition of the gut microbiota in osteoporosis and osteoarthritis.

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