Search Results
You are looking at 1 - 10 of 12 items for
- Author: Yun Zhang x
- Refine by access: All content x
Search for other papers by Esther Paulo in
Google Scholar
PubMed
Search for other papers by Dongmei Wu in
Google Scholar
PubMed
Search for other papers by Peter Hecker in
Google Scholar
PubMed
Search for other papers by Yun Zhang in
Google Scholar
PubMed
Search for other papers by Biao Wang in
Google Scholar
PubMed
Numerous studies have suggested that beige adipocyte abundance is correlated with improved metabolic performance, but direct evidence showing that beige adipocyte expansion protects animals from the development of obesity is missing. Previously, we have described that the liver kinase b1 (LKB1) regulates beige adipocyte renaissance in subcutaneous inguinal white adipose tissue (iWAT) through a class IIa histone deacetylase 4 (HDAC4)-dependent mechanism. This study investigates the physiological impact of persistent beige adipocyte renaissance in energy homeostasis in mice. Here we present that the transgenic mice H4-TG, overexpressing constitutively active HDAC4 in adipocytes, showed beige adipocyte expansion in iWAT at room temperature. H4-TG mice exhibited increased energy expenditure due to beige adipocyte expansion. They also exhibited reduced adiposity under both normal chow and high-fat diet (HFD) feeding conditions. Specific ablation of beige adipocytes reversed the protection against HFD-induced obesity in H4-TG mice. Taken together, our results directly demonstrate that beige adipocyte expansion regulates adiposity in mice and targeting beige adipocyte renaissance may present a novel strategy to tackle obesity in humans.
Search for other papers by Zhenhua Li in
Google Scholar
PubMed
Search for other papers by Tao Zhang in
Google Scholar
PubMed
Search for other papers by Hongyan Dai in
Google Scholar
PubMed
Search for other papers by Guanghui Liu in
Google Scholar
PubMed
Search for other papers by Haibin Wang in
Google Scholar
PubMed
Search for other papers by Yingying Sun in
Google Scholar
PubMed
Search for other papers by Yun Zhang in
Google Scholar
PubMed
Search for other papers by Zhiming Ge in
Google Scholar
PubMed
Search for other papers by Zhenhua Li in
Google Scholar
PubMed
Search for other papers by Tao Zhang in
Google Scholar
PubMed
Search for other papers by Hongyan Dai in
Google Scholar
PubMed
Search for other papers by Guanghui Liu in
Google Scholar
PubMed
Search for other papers by Haibin Wang in
Google Scholar
PubMed
Search for other papers by Yingying Sun in
Google Scholar
PubMed
Search for other papers by Yun Zhang in
Google Scholar
PubMed
Search for other papers by Zhiming Ge in
Google Scholar
PubMed
Apoptosis plays a critical role in the diabetic cardiomyopathy, and endoplasmic reticulum stress (ERS) is one of the intrinsic apoptosis pathways. Previous studies have shown that the endoplasmic reticulum becomes swollen and dilated in diabetic myocardium, and ERS is involved in heart failure and diabetic kidney. This study is aimed to demonstrate whether ERS is induced in myocardium of streptozotocin (STZ)-induced diabetic rats. We established a type 1 diabetic rat model, used echocardiographic evaluation, hematoxylin–eosin staining, and the terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify the existence of diabetic cardiomyopathy and enhanced apoptosis in the diabetic heart. We performed immunohistochemistry, western blot, and real-time PCR to analyze the hallmarks of ERS that include glucose-regulated protein 78, CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase12. We found these hallmarks to have enhanced expression in protein and mRNA levels in diabetic myocardium. Also, another pathway that can lead to cell death of ERS, c-Jun NH2-terminal kinase-dependent pathway, was also activated in diabetic heart. Those results suggested that ERS was induced in STZ-induced diabetic rats' myocardium, and ERS-associated apoptosis occurred in the pathophysiology of diabetic cardiomyopathy.
Search for other papers by Jacob C Garza in
Google Scholar
PubMed
Search for other papers by Chung Sub Kim in
Google Scholar
PubMed
Search for other papers by Jing Liu in
Google Scholar
PubMed
Search for other papers by Wei Zhang in
Google Scholar
PubMed
Search for other papers by Xin-Yun Lu in
Google Scholar
PubMed
Pharmacological and genetic studies have suggested that melanocortin-4 receptor (MC4R) signaling in the paraventricular nucleus of hypothalamus (PVN) regulates appetite and energy balance. However, the specific role of MC4R signaling in PVN neurons in these processes remains to be further elucidated in normally developed animals. In the present study, we employed RNA interference to determine whether MC4R knockdown in the PVN modulates food intake and body weight in adult rats. Adeno-associated viral (AAV) vectors encoding short hairpin RNAs targeting MC4R (AAV-shRNA-MC4R) were generated to induce MC4R knockdown in the PVN. By in situ hybridization, we detected a high-level expression of Dicer, a key enzyme required for shRNA-mediated gene silencing, along the entire rostrocaudal extent of the PVN. Bilateral injection of AAV-shRNA-MC4R vectors into the PVN of the adult rat resulted in significant and specific reduction of MC4R mRNA expression. Animals with MC4R knockdown exhibited an increase in food intake and excessive body weight gain when exposed to a high-fat diet. Our results provide evidence that AAV-mediated silencing of MC4R on PVN neurons promotes hyperphagia and obesity in response to the dietary challenge in the adult animal.
Search for other papers by Hongyu Su in
Google Scholar
PubMed
Search for other papers by Xueyi Chen in
Google Scholar
PubMed
Department of Obstetrics and Gynecology, First Hospital of Soochow University, Suzhou, Jiangsu, China
Search for other papers by Yueming Zhang in
Google Scholar
PubMed
Search for other papers by Linglu Qi in
Google Scholar
PubMed
Search for other papers by Yun He in
Google Scholar
PubMed
Search for other papers by Juanxiu Lv in
Google Scholar
PubMed
Search for other papers by Yingying Zhang in
Google Scholar
PubMed
Search for other papers by Xiang Li in
Google Scholar
PubMed
Search for other papers by Jiaqi Tang in
Google Scholar
PubMed
Search for other papers by Zhice Xu in
Google Scholar
PubMed
Cerebral circulation is important in fetal brain development, and angiotensin II (Ang II) plays vital roles in regulation of adult cerebral circulation. However, functions of Ang II in fetal cerebral vasculature and influences of in utero hypoxia on Ang II-mediated fetal cerebral vascular responses are largely unknown. This study investigated the effects and mechanisms of in utero hypoxia on fetal middle cerebral arteries (MCA) via Ang II. Near-term ovine fetuses were exposed to in utero hypoxia, and fetal MCA responses to Ang II were tested for vascular tension, calcium transient, and molecular analysis. Ang II caused significant dose-dependent contraction in control fetal MCA. Ang II-induced MCA constriction was decreased significantly in hypoxic fetuses. Neither losartan (AT1R antagonist, 10−5 mol/L) nor PD123,319 (AT2R antagonist, 10−5 mol/L) altered Ang II-mediated contraction in fetal MCA. Phenylephrine-mediated constriction was also significantly weaker in hypoxic fetuses. Bay K8644 caused similar contractions between the two groups. Protein expression of L-type voltage-dependent calcium channels was unchanged. There were no differences in caffeine-mediated vascular tension or calcium transients. Contraction induced by PDBu (PKC agonist) was obviously weaker in hypoxic MCA. Protein expression of PKCβ was reduced in the hypoxic compared with the control, along with no differences in phosphorylation levels. The results showed that fetal MCA was functionally responsive to Ang II near term. Intrauterine hypoxia reduced the vascular agonist-mediated contraction in fetal MCA, probably via decreasing PKCβ and its phosphorylation, which might play protective effects on fetal cerebral circulation against transient hypoxia.
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Search for other papers by Chang-Jiang Li in
Google Scholar
PubMed
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Search for other papers by Hui-Wen Sun in
Google Scholar
PubMed
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Search for other papers by Fa-Liang Zhu in
Google Scholar
PubMed
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Search for other papers by Liang Chen in
Google Scholar
PubMed
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Search for other papers by Yuan-Yuan Rong in
Google Scholar
PubMed
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Search for other papers by Yun Zhang in
Google Scholar
PubMed
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
Search for other papers by Mei Zhang in
Google Scholar
PubMed
In this study, we investigated the in vivo role of adiponectin, an adipocytokine, on the development of atherosclerosis in rabbits mainly using adenovirus expressing adiponectin gene (Ad-APN) and intravascular ultrasonography. Serum adiponectin concentrations in rabbits after Ad-APN local transfer to abdominal aortas increased about nine times as much as those before transfer (P < 0.01), about ten times as much as the levels of endogenous adiponectin in adenovirus expressing β-galactosidase gene (Ad-β gal) treated rabbits (P < 0.01), and about four times as much as those in the aorta of non-injured rabbits on a normal cholesterol diet (P < 0.01). Ultrasonography revealed a significantly reduced atherosclerotic plaque area in abdominal aortas of rabbits infected through intima with Ad-APN, by 35.2% compared with the area before treatment (P < 0.01), and by 35.8% compared with that in Ad-β gal-treated rabbits (P < 0.01). In rabbits infected through adventitia, Ad-APN treatment reduced plaque area by 28.9% as compared with the area before treatment (P < 0.01) and 25.6% compared with that in Ad-β gal-treated rabbits (P < 0.01). Adiponectin significantly suppressed the mRNA expression of vascular cell adhesion molecule-1 (VCAM-1) by 18.5% through intima transfer (P < 0.05) and 26.9% through adventitia transfer (P < 0.01), and intercellular adhesion molecule-1 (ICAM-1) by 40.7% through intima transfer (P < 0.01), and 30.7% through adventitia transfer (P < 0.01). However, adiponectin had no effect on the expression of types I and III collagen. These results suggest that local adiponectin treatment suppresses the development of atherosclerosis in vivo in part by attenuating the expression of VCAM-1 and ICAM-1 in vascular walls.
Search for other papers by Jian-Ting Ke in
Google Scholar
PubMed
Search for other papers by Mi Li in
Google Scholar
PubMed
Search for other papers by Shi-Qing Xu in
Google Scholar
PubMed
Search for other papers by Wen-Jian Zhang in
Google Scholar
PubMed
Search for other papers by Yong-Wei Jiang in
Google Scholar
PubMed
Search for other papers by Lan-yun Cheng in
Google Scholar
PubMed
Search for other papers by Li Chen in
Google Scholar
PubMed
Search for other papers by Jin-Ning Lou in
Google Scholar
PubMed
Search for other papers by Wei Wu in
Google Scholar
PubMed
The efficacy of gliquidone for the treatment of diabetic nephropathy was investigated by implanting micro-osmotic pumps containing gliquidone into the abdominal cavities of Goto-Kakizaki (GK) rats with diabetic nephropathy. Blood glucose, 24 h urinary protein, and 24 h urinary albumin levels were measured weekly. After 4 weeks of gliquidone therapy, pathological changes in the glomerular basement membrane (GBM) were examined using an electron microscope. Real-time PCR, western blotting, and immunohistochemistry were employed to detect glomerular expression of receptors for advanced glycation end products (RAGE) (AGER), protein kinase C β (PKCβ), and protein kinase A (PKA) as well as tubular expression of the albumin reabsorption-associated proteins: megalin and cubilin. Human proximal tubular epithelial cells (HK-2 cells) were used to analyze the effects of gliquidone and advanced glycation end products (AGEs) on the expression of megalin and cubilin and on the absorption of albumin. Gliquidone lowered blood glucose, 24 h urinary protein, and 24 h urinary albumin levels in GK rats with diabetic nephropathy. The level of plasma C-peptide increased markedly and GBM and podocyte lesions improved dramatically after gliquidone treatment. Glomerular expression of RAGE and PKCβ decreased after gliquidone treatment, while PKA expression increased. AGEs markedly suppressed the expression of megalin and cubulin and the absorption of albumin in HK-2 cells in vitro, whereas the expression of megalin and cubilin and the absorption of albumin were all increased in these cells after gliquidone treatment. In conclusion, gliquidone treatment effectively reduced urinary protein in GK rats with diabetic nephropathy by improving glomerular lesions and promoting tubular reabsorption.
Search for other papers by Shuisheng Li in
Google Scholar
PubMed
Search for other papers by Yong Zhang in
Google Scholar
PubMed
Search for other papers by Yun Liu in
Google Scholar
PubMed
Search for other papers by Xigui Huang in
Google Scholar
PubMed
Search for other papers by Weiren Huang in
Google Scholar
PubMed
Search for other papers by Danqi Lu in
Google Scholar
PubMed
Search for other papers by Pei Zhu in
Google Scholar
PubMed
Search for other papers by Yu Shi in
Google Scholar
PubMed
Search for other papers by Christopher H K Cheng in
Google Scholar
PubMed
Search for other papers by Xiaochun Liu in
Google Scholar
PubMed
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
Search for other papers by Haoran Lin in
Google Scholar
PubMed
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.
Department of Endocrinology, FuJian Union hospital, Fuzhou, P R China
Search for other papers by Binbin Guan in
Google Scholar
PubMed
Search for other papers by Wenyi Li in
Google Scholar
PubMed
Search for other papers by Fengying Li in
Google Scholar
PubMed
Search for other papers by Yun Xie in
Google Scholar
PubMed
Search for other papers by Qicheng Ni in
Google Scholar
PubMed
Search for other papers by Yanyun Gu in
Google Scholar
PubMed
Search for other papers by Xiaoying Li in
Google Scholar
PubMed
Search for other papers by Qidi Wang in
Google Scholar
PubMed
Search for other papers by Hongli Zhang in
Google Scholar
PubMed
Search for other papers by Guang Ning in
Google Scholar
PubMed
The cellular and molecular mechanisms of glucose-stimulated β-cell proliferation are poorly understood. Recently, secreted frizzled-related protein 5 (encoded by Sfrp5; a Wnt signaling inhibitor) has been demonstrated to be involved in β-cell proliferation in obesity. A previous study demonstrated that glucose enhanced Wnt signaling to promote cell proliferation. We hypothesized that inhibition of SFRP5 contributes to glucose-stimulated β-cell proliferation. In this study, we found that the Sfrp5 level was significantly reduced in high glucose-treated INS-1 cells, primary rat β-cells, and islets isolated from glucose-infused rats. Overexpression of SFRP5 diminished glucose-stimulated proliferation in both INS-1 cells and primary β-cells, with a concomitant inhibition of the Wnt signaling pathway and decreased cyclin D2 expression. In addition, we showed that glucose-induced Sfrp5 suppression was modulated by the PI3K/AKT pathway. Therefore, we conclude that glucose inhibits Sfrp5 expression via the PI3K/AKT pathway and hence promotes rat pancreatic β-cell proliferation.
Search for other papers by Yong Zhang in
Google Scholar
PubMed
Search for other papers by Yun Liu in
Google Scholar
PubMed
Search for other papers by Xigui Huang in
Google Scholar
PubMed
Search for other papers by Xiaochun Liu in
Google Scholar
PubMed
Search for other papers by Baowei Jiao in
Google Scholar
PubMed
Search for other papers by Zining Meng in
Google Scholar
PubMed
Search for other papers by Pei Zhu in
Google Scholar
PubMed
Search for other papers by Shuisheng Li in
Google Scholar
PubMed
State Key Laboratory of Biocontrol, Department of Biochemistry, College of Ocean, School of Life Sciences, Institute of Aquatic Economic Animals, and the Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-Sen University, Guangzhou 510275, China
Search for other papers by Haoran Lin in
Google Scholar
PubMed
Search for other papers by Christopher H K Cheng in
Google Scholar
PubMed
Two GPR39 transcripts, designated as sbGPR39-1a and sbGPR39-1b, were identified in black seabream (Acanthopagrus schlegeli). The deduced amino acid (aa) sequence of sbGPR39-1a contains 423 residues with seven putative transmembrane (TM) domains. On the other hand, sbGPR39-1b contains 284 aa residues with only five putative TM domains. Northern blot analysis confirmed the presence of two GPR39 transcripts in the seabream intestine, stomach, and liver. Apart from seabream, the presence of two GPR39 transcripts was also found to exist in a number of teleosts (zebrafish and pufferfish) and mammals (human and mouse). Analysis of the GPR39 gene structure in different species suggests that the two GPR39 transcripts are generated by alternative splicing. When the seabream receptors were expressed in cultured HEK293 cells, Zn2 + could trigger sbGPR39-1a signaling through the serum response element pathway, but no such functionality could be detected for the sbGPR39-1b receptor. The two receptors were found to be differentially expressed in seabream tissues. sbGPR39-1a is predominantly expressed in the gastrointestinal tract. On the other hand, sbGPR39-1b is widely expressed in most central and peripheral tissues except muscle and ovary. The expression of sbGPR39-1a in the intestine and the expression of sbGPR39-1b in the hypothalamus were decreased significantly during food deprivation in seabream. On the contrary, the expression of the GH secretagogue receptors (sbGHSR-1a and sbGHSR-1b) was significantly increased in the hypothalamus of the food-deprived seabream. The reciprocal regulatory patterns of expression of these two genes suggest that both of them are involved in controlling the physiological response of the organism during starvation.
