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https://www.readbyqxmd.com/read/28969688/praziquantel-treatment-after-schistosoma-japonicum-infection-maintains-hepatic-insulin-sensitivity-and-improves-glucose-metabolism-in-mice
#1
Xiaofeng Luo, Yuxiao Zhu, Ran Liu, Jingwei Song, Fan Zhang, Wenyue Zhang, Zhipeng Xu, Min Hou, Bingya Yang, Lin Chen, Minjun Ji
BACKGROUND: Epidemiological studies in China have revealed that Schistosoma japonicum infection is inversely correlated with metabolic syndrome, even after repeated chemotherapy with praziquantel (PZQ). We investigated the effect of chronic S. japonicum infection, PZQ chemotherapy, and soluble egg antigen (SEA) treatment on whole-body metabolic homeostasis and hepatic insulin sensitivity in mouse models. RESULTS: Infection with S. japonicum was found to increase whole-body and hepatic insulin sensitivity in mice...
October 2, 2017: Parasites & Vectors
https://www.readbyqxmd.com/read/28954992/nonconcordant-regulation-of-mitochondrial-respiratory-complexes-in-the-kidneys-of-5-6-nephrectomized-mice
#2
Yukie Nakashita, Tomoya Sano, Hiroaki Yoshioka, Tomoki Shimada, Ryotaro Hori, Makoto Usami, Yasuhiro Hamada
Hyperglycemia induces nonconcordant regulation of renal mitochondrial respiratory complexes, increases oxidative stress, and causes diabetic nephropathy. Hypertension is a complication associated with diabetes and involves glomerular hyperfiltration, the effects of which on mitochondrial respiratory complexes are not well understood. To investigate the effect of glomerular hyperfiltration on renal mitochondrial respiratory complexes, we used the 5/6 nephrectomized BKS. Cg-Dock7(m)+/+Lepr(db)/J, Dock7(m)+/+Lepr(db) mice (db/m-5/6Nx mice) as a model for glomerular hyperfiltration...
2017: Journal of Medical Investigation: JMI
https://www.readbyqxmd.com/read/28938561/preventive-effects-of-the-sodium-glucose-cotransporter-2-inhibitor-tofogliflozin-on-diethylnitrosamine-induced-liver-tumorigenesis-in-obese-and-diabetic-mice
#3
Koki Obara, Yohei Shirakami, Akinori Maruta, Takayasu Ideta, Tsuneyuki Miyazaki, Takahiro Kochi, Hiroyasu Sakai, Takuji Tanaka, Mitsuru Seishima, Masahito Shimizu
Sodium glucose cotransporter 2 inhibitors are expected to ameliorate the abnormalities associated with metabolic syndrome including non-alcoholic fatty liver disease. In this study, we investigated the effects of the sodium glucose cotransporter 2 inhibitor tofogliflozin on the development of non-alcoholic fatty liver disease-related liver tumorigenesis in C57BL/KsJ-+Lepr (db) /+Lepr (db) obese and diabetic mice. The direct effects of tofogliflozin on human liver cancer cell proliferation were also evaluated...
August 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/28893589/leptin-status-alters-buprenorphine-induced-antinociception-in-obese-mice-with-dysfunctional-leptin-receptors
#4
Zachary Glovak, Sara Mihalko, Helen A Baghdoyan, Ralph Lydic
Buprenorphine is an opiate used for pain management and to treat opiate addiction. The cytokine leptin can modulate nociception, but the extent to which buprenorphine-induced antinociception varies as a function of leptin signaling has not been characterized. Four congenic mouse lines with phenotypes that include differences in body weight and leptin status were used to test the hypothesis that the antinociceptive effects of buprenorphine vary as function of sex and leptin signaling. Each mouse line was comprised of males (n=12) and females (n=12) for a total of 96 animals...
November 1, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28885548/novel-insights-into-the-adipokinome-of-obese-and-obese-diabetic-mouse-models
#5
Birgit Knebel, Simon Goeddeke, Gereon Poschmann, Daniel F Markgraf, Sylvia Jacob, Ulrike Nitzgen, Waltraud Passlack, Christina Preuss, Hans-Dieter Dicken, Kai Stühler, Sonja Hartwig, Stefan Lehr, Jorg Kotzka
The group of adipokines comprises hundreds of biological active proteins and peptides released from adipose tissue. Alterations of those complex protein signatures are suggested to play a crucial role in the pathophysiology of multifactorial, metabolic diseases. We hypothesized that also the pathophysiology of type-2-diabetes is linked to the dysregulation of the adipocyte secretome. To test this, we investigated mouse models with monogenic defects in leptin signaling which are susceptible to adipositas (C57BL/6 Cg-Lep(ob) (obob)) or adipositas with diabetes (C57BL/KS Cg-Lepr(db) (dbdb)) according to their genetic background...
September 8, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28865861/liver-transcriptome-analysis-reveals-important-factors-involved-in-the-metabolic-adaptation-of-the-transition-cow
#6
N-T Ha, C Drögemüller, C Reimer, F Schmitz-Hsu, R M Bruckmaier, H Simianer, J J Gross
During early lactation, dairy cows experience a severe metabolic load often resulting in the development of various diseases. The inevitable deficiency in nutrients and energy at the onset of lactation requires an optimal adaptation of the hepatic metabolism to overcome metabolic stress. We conducted a whole-liver transcriptome analysis for the transition cow to identify novel factors crucial for metabolic adaptation. Liver samples were obtained from 6 Red Holstein dairy cows (parity 2 to 7, mean ± standard deviation: 3...
November 2017: Journal of Dairy Science
https://www.readbyqxmd.com/read/28852138/inhibition-of-gdf8-myostatin-accelerates-bone-regeneration-in-diabetes-mellitus-type-2
#7
Christoph Wallner, Henriette Jaurich, Johannes Maximilian Wagner, Mustafa Becerikli, Kamran Harati, Mehran Dadras, Marcus Lehnhardt, Björn Behr
Metabolic diseases like diabetes mellitus cause bone healing deficiencies. We found significant impairment of bone regeneration, osteogenic differentiation and proliferation in diabetic bone. Moreover recent studies suggest a highly underestimated importance of GDF8 (Myostatin) in bone metabolism. Our goal was to analyze the role of GDF8 as a regulator of osteogenic differentiation, proliferation and bone regeneration. We used a murine tibial defect model in diabetic (Lepr(db-/-)) mice. Myostatin-Inhibitor Follistatin was administered in tibial bony defects of diabetic mice...
August 29, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28793909/-6-gingerol-from-zingiber-officinale-potentiates-glp-1-mediated-glucose-stimulated-insulin-secretion-pathway-in-pancreatic-%C3%AE-cells-and-increases-rab8-rab10-regulated-membrane-presentation-of-glut4-transporters-in-skeletal-muscle-to-improve-hyperglycemia-in
#8
Mehdi Bin Samad, Md Nurul Absar Bin Mohsin, Bodiul Alam Razu, Mohammad Tashnim Hossain, Sinayat Mahzabeen, Naziat Unnoor, Ishrat Aklima Muna, Farjana Akhter, Ashraf Ul Kabir, J M A Hannan
BACKGROUND: [6]-Gingerol, a major component of Zingiber officinale, was previously reported to ameliorate hyperglycemia in type 2 diabetic mice. Endocrine signaling is involved in insulin secretion and is perturbed in db/db Type-2 diabetic mice. [6]-Gingerol was reported to restore the disrupted endocrine signaling in rodents. In this current study on Lepr(db/db) diabetic mice, we investigated the involvement of endocrine pathway in the insulin secretagogue activity of [6]-Gingerol and the mechanism(s) through which [6]-Gingerol ameliorates hyperglycemia...
August 9, 2017: BMC Complementary and Alternative Medicine
https://www.readbyqxmd.com/read/28580288/restoration-of-lepr-in-%C3%AE-cells-of-lepr-null-mice-does-not-prevent-hyperinsulinemia-and-hyperglycemia
#9
Anna M D'souza, Timothy J Kieffer
OBJECTIVE: The adipose-derived hormone leptin plays an important role in regulating body weight and glucose homeostasis. Leptin receptors are expressed in the central nervous system as well as peripheral tissues involved in regulating glucose homeostasis, including insulin-producing β cells of the pancreas. Previous studies assessing the role of leptin receptors in β cells used Cre-loxP to disrupt the leptin receptor gene (Lepr) in β cells, but variable results were obtained. Furthermore, recombination of Lepr was observed in the hypothalamus or exocrine pancreas, in addition to the β cells, and Lepr in non-β cells may have compensated for the loss of Lepr in β cells, thus making it difficult to assess the direct effects of Lepr in β cells...
June 2017: Molecular Metabolism
https://www.readbyqxmd.com/read/28577176/complement-c5a-induces-mesenchymal-stem-cell-apoptosis-during-the-progression-of-chronic-diabetic-complications
#10
Ming Zhu, Xiao He, Xiao-Hui Wang, Wei Qiu, Wei Xing, Wei Guo, Tian-Chen An, Luo-Quan Ao, Xue-Ting Hu, Zhan Li, Xiao-Ping Liu, Nan Xiao, Jian Yu, Hong Huang, Xiang Xu
AIMS/HYPOTHESIS: Regeneration and repair mediated by mesenchymal stem cells (MSCs) are key self-protection mechanisms against diabetic complications, a reflection of diabetes-related cell/tissue damage and dysfunction. MSC abnormalities have been reported during the progression of diabetic complications, but little is known about whether a deficiency in these cells plays a role in the pathogenesis of this disease. In addition to MSC resident sites, peripheral circulation is a major source of MSCs that participate in the regeneration and repair of damaged tissue...
June 3, 2017: Diabetologia
https://www.readbyqxmd.com/read/28438610/hyperglycemia-increases-interstitial-cells-of-cajal-via-mapk1-and-mapk3-signaling-to-etv1-and-kit-leading-to-rapid-gastric-emptying
#11
Yujiro Hayashi, Yoshitaka Toyomasu, Siva Arumugam Saravanaperumal, Michael R Bardsley, John A Smestad, Andrea Lorincz, Seth T Eisenman, Gianluca Cipriani, Molly H Nelson Holte, Fatimah J Al Khazal, Sabriya A Syed, Gabriella B Gajdos, Kyoung Moo Choi, Gary J Stoltz, Katie E Miller, Michael L Kendrick, Brian P Rubin, Simon J Gibbons, Adil E Bharucha, David R Linden, Louis James Maher, Gianrico Farrugia, Tamas Ordog
BACKGROUND & AIMS: Depletion of interstitial cells of Cajal (ICCs) is common in diabetic gastroparesis. However, in approximately 20% of patients with diabetes, gastric emptying (GE) is accelerated. GE also occurs faster in obese individuals, and is associated with increased blood levels of glucose in patients with type 2 diabetes. To understand the fate of ICCs in hyperinsulinemic, hyperglycemic states characterized by rapid GE, we studied mice with mutation of the leptin receptor (Lepr(db/db)), which in our colony had accelerated GE...
August 2017: Gastroenterology
https://www.readbyqxmd.com/read/28381495/dietary-reversal-of-neuropathy-in-a-murine-model-of-prediabetes-and-metabolic-syndrome
#12
Lucy M Hinder, Phillipe D O'Brien, John M Hayes, Carey Backus, Andrew P Solway, Catrina Sims-Robinson, Eva L Feldman
Patients with metabolic syndrome, which is defined as obesity, dyslipidemia, hypertension and impaired glucose tolerance (IGT), can develop the same macro- and microvascular complications as patients with type 2 diabetes, including peripheral neuropathy. In type 2 diabetes, glycemic control has little effect on the development and progression of peripheral neuropathy, suggesting that other metabolic syndrome components may contribute to the presence of neuropathy. A parallel phenomenon is observed in patients with prediabetes and metabolic syndrome, where improvement in weight and dyslipidemia more closely correlates with restoration of nerve function than improvement in glycemic status...
June 1, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28256636/elevated-fibroblast-growth-factor-21-fgf21-in-obese-insulin-resistant-states-is-normalised-by-the-synthetic-retinoid-fenretinide-in-mice
#13
Nicola Morrice, George D Mcilroy, Seshu R Tammireddy, Jennifer Reekie, Kirsty D Shearer, Mary K Doherty, Mirela Delibegović, Phillip D Whitfield, Nimesh Mody
Fibroblast growth factor 21 (FGF21) has emerged as an important beneficial regulator of glucose and lipid homeostasis but its levels are also abnormally increased in insulin-resistant states in rodents and humans. The synthetic retinoid Fenretinide inhibits obesity and improves glucose homeostasis in mice and has pleotropic effects on cellular pathways. To identify Fenretinide target genes, we performed unbiased RNA-seq analysis in liver from mice fed high-fat diet ± Fenretinide. Strikingly, Fgf21 was the most downregulated hepatic gene...
March 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28194019/il-25-stimulates-m2-macrophage-polarization-and-thereby-promotes-mitochondrial-respiratory-capacity-and-lipolysis-in-adipose-tissues-against-obesity
#14
Juan Feng, Lingyi Li, Zhiying Ou, Qiao Li, Baoyong Gong, Zhenxian Zhao, Weiwei Qi, Ti Zhou, Jun Zhong, Weibin Cai, Xia Yang, Aiping Zhao, Guoquan Gao, Zhonghan Yang
Obesity and associated metabolic diseases are characterized by a chronic low-grade inflammatory state with the infiltration of many inflammatory cells, especially macrophages. Immune molecules, including some cytokines, have a close relationship with metabolism. Interleukin (IL)-25 is a member of the IL-17 cytokine family that can regulate macrophages and alleviate some metabolic dysfunction; however, its role and mechanisms in lipid metabolism remain to be extensively clarified. Human serum and liver biopsy specimens, high-fat diet-induced obesity mice and DB/DB (Lepr-/-) animal models were used to examine IL-25 expression in obesity and nonalcoholic fatty liver diseases (NAFLD)...
February 13, 2017: Cellular & Molecular Immunology
https://www.readbyqxmd.com/read/27895822/linagliptin-alleviates-fatty-liver-disease-in-diabetic-db-db-mice
#15
Svetlana V Michurina, Irina Ju Ishenko, Vadim V Klimontov, Sergey A Archipov, Natalia E Myakina, Marina A Cherepanova, Eugenii L Zavjalov, Galina V Koncevaya, Vladimir I Konenkov
AIM: To study the effects of linagliptin on the structural signs of non-alcoholic fatty liver disease (NAFLD) in db/db mice. METHODS: Male diabetic db/db mice (BKS.Cg-Dock7(m+)/(+)Lepr(db)/J) aged 10 wk received the dipeptidyl peptidase 4 (DPP4) inhibitor linagliptin (10 mg/kg) or saline as a placebo once per day by gavage for 8 wk. Intact db/db mice served as controls. Structural changes in the liver were analyzed from light and electron microscopic images of sections from intact, placebo-treated and linagliptin-treated animals...
November 15, 2016: World Journal of Diabetes
https://www.readbyqxmd.com/read/27855316/a-high-fat-diet-temporarily-renders-sod1-deficient-mice-resistant-to-an-oxidative-insult
#16
Junitsu Ito, Naoki Ishii, Ryusuke Akihara, Jaeyong Lee, Toshihiro Kurahashi, Takujiro Homma, Ryo Kawasaki, Junichi Fujii
Patients with nonalcoholic fatty liver disease may subsequently develop nonalcoholic steatohepatitis after suffering from a second insult, such as oxidative stress. Aim of this study was to investigate the pathogenesis of the liver injury caused when lipids accumulate under conditions of intrinsic oxidative stress using mice that are deficient in superoxide dismutase 1 (SOD1) and the leptin receptor (Lepr). We established Sod1(-/-)::Lepr(db/db) mice and carried out analyses of four groups of genetically modified mice, namely, wild type, Sod1(-/-), Lepr(db/db) and Sod1(-/-)::Lepr(db/db) mice...
November 3, 2016: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/27698916/diet-and-genetically-induced-obesity-produces-alterations-in-the-microbiome-inflammation-and-wnt-pathway-in-the-intestine-of-apc-1638n-mice-comparisons-and-contrasts
#17
Wei Liu, Jimmy W Crott, Lin Lyu, Anna C Pfalzer, Jinchao Li, Sang-Woon Choi, Yingke Yang, Joel B Mason, Zhenhua Liu
Obesity is an established risk factor for colorectal cancer (CRC). Our previous study indicated that obesity increases activity of the pro-tumorigenic Wnt-signaling. Presently, we sought to further advance our understanding of the mechanisms by which obesity promotes CRC by examining associations between microbiome, inflammation and Wnt-signaling in Apc(+/1638N) mice whose obesity was induced by one of two modalities, diet- or genetically-induced obesity. Three groups were employed: Apc(+/1638N)Lepr(+/+) fed a low fat diet (10% fat), Apc(+/1638N)Lepr(+/+) fed a high fat diet (60% fat, diet-induced obesity), and Apc(+/1638N)Lepr(db/db) fed a low fat diet (genetically-induced obesity)...
2016: Journal of Cancer
https://www.readbyqxmd.com/read/27678013/xenograft-of-microencapsulated-sertoli-cells-restores-glucose-homeostasis-in-db-db-mice-with-spontaneous-diabetes-mellitus
#18
Giovanni Luca, Iva Arato, Francesca Mancuso, Mario Calvitti, Giulia Falabella, Giuseppe Murdolo, Giuseppe Basta, Don F Cameron, Barbara C Hansen, Francesca Fallarino, Tiziano Baroni, Maria Chiara Aglietti, Cristina Tortoioli, Maria Bodo, Riccardo Calafiore
BACKGROUND: Increased abdominal fat and chronic inflammation in the expanded adipose tissue of obesity contribute to the development of insulin resistance and type 2 diabetes mellitus (T2D). The emerging immunoregulatory and anti-inflammatory properties of Sertoli cells have prompted their application to experimental models of autoimmune/inflammatory disorders, including diabetes. The main goal of this work was to verify whether transplantation of microencapsulated prepubertal porcine Sertoli cells (MC-SC) in the subcutaneous abdominal fat depot of spontaneously diabetic and obese db/db mice (homozygous for the diabetes spontaneous mutation [Lepr(db) ]) would: (i) improve glucose homeostasis and (ii) modulate local and systemic immune response and adipokines profiles...
November 2016: Xenotransplantation
https://www.readbyqxmd.com/read/27382383/erratum-rapid-and-efficient-identification-of-the-mouse-leptin-receptor-mutation-c57blks-j-lepr-db-by-tetra-primer-amplification-refractory-mutation-system-polymerase-chain-reaction-arms-pcr-analysis
#19
https://www.readbyqxmd.com/read/27207656/obesity-promotes-phip-induced-small-intestinal-carcinogenesis-in-hcyp1a-db-db-mice-involvement-of-mutations-and-dna-hypermethylation-of-apc
#20
Hong Wang, Anna Liu, Yingyi Kuo, Eric Chi, Xu Yang, Lanjing Zhang, Chung S Yang
Obesity is associated with an increased risk of cancer. To study the promotion of dietary carcinogen-induced gastrointestinal cancer by obesity, we employed 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) to induce intestinal tumorigenesis in CYP1A-humanized (hCYP1A) mice, in which mouse Cyp1a1/1a2 was replaced with human CYP1A1/1A2 Obesity was introduced in hCYP1A mice by breeding with Lepr(db/+) mice to establish the genetically induced obese hCYP1A-Lepr(db/db) mice or by feeding hCYP1A mice a high-fat diet...
July 2016: Carcinogenesis
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