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Lepr db

Lucy M Hinder, Phillipe D O'Brien, John M Hayes, Carey Backus, Andrew P Solway, Catrina Sims-Robinson, Eva L Feldman
Patients with the metabolic syndrome, 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 the metabolic syndrome, where improvement in weight and dyslipidemia more closely correlates with restoration of nerve function than improvement in glycemic status...
April 5, 2017: Disease Models & Mechanisms
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
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
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
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
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
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
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
Yang Sun, Yili Yang, Zhen Qin, Jinya Cai, Xiuming Guo, Yun Tang, Jingjing Wan, Ding-Feng Su, Xia Liu
The acute-phase protein orosomucoid (ORM) exhibits a variety of activities in vitro and in vivo, notably modulation of immunity and transportation of drugs. We found in this study that mice lacking ORM1 displayed aberrant energy homeostasis characterized by increased body weight and fat mass. Further investigation found that ORM, predominantly ORM1, is significantly elevated in sera, liver, and adipose tissues from the mice with high-fat diet (HFD)-induced obesity and db/db mice that develop obesity spontaneously due to mutation in the leptin receptor (LepR)...
June 2016: Diabetes
Yi Wang, Chengsheng Han, Wenzhen Zhu, Zhengxing Wu, Yanmei Liu, Liangyi Chen
Imbalanced glucagon and insulin release leads to the onset of type 2 diabetes. To pinpoint the underlying primary driving force, here we have developed a fast, non-biased optical method to measure ratios of pancreatic α- and β-cell mass and function simultaneously. We firstly label both primary α- and β-cells with the red fluorescent probe ZinRhodaLactam-1 (ZRL1), and then highlight α-cells by selectively quenching the ZRL1 signal from β-cells. Based on the signals before and after quenching, we calculate the ratio of the α-cell to β-cell mass within live islets, which we found matched the results from immunohistochemistry...
June 15, 2016: Journal of Cell Science
Omonseigho O Talton, Kathleen A Pennington, Kelly E Pollock, Keenan Bates, Lixin Ma, Mark R Ellersieck, Laura C Schulz
Maternal obesity and gestational diabetes are prevalent worldwide. Offspring of mothers with these conditions weigh more and are predisposed to metabolic syndrome. A hallmark of both conditions is maternal hyperleptinemia, but the role of elevated leptin levels during pregnancy on developmental programming is largely unknown. We previously found that offspring of hyperleptinemic mothers weighed less and had increased activity. The goal of this study was to determine whether maternal leptin affects offspring insulin sensitivity by investigating offspring glucose metabolism and lipid accumulation...
July 2016: Endocrinology
Elliott H Sohn, Hille W van Dijk, Chunhua Jiao, Pauline H B Kok, Woojin Jeong, Nazli Demirkaya, Allison Garmager, Ferdinand Wit, Murat Kucukevcilioglu, Mirjam E J van Velthoven, J Hans DeVries, Robert F Mullins, Markus H Kuehn, Reinier Otto Schlingemann, Milan Sonka, Frank D Verbraak, Michael David Abràmoff
Diabetic retinopathy (DR) has long been recognized as a microvasculopathy, but retinal diabetic neuropathy (RDN), characterized by inner retinal neurodegeneration, also occurs in people with diabetes mellitus (DM). We report that in 45 people with DM and no to minimal DR there was significant, progressive loss of the nerve fiber layer (NFL) (0.25 μm/y) and the ganglion cell (GC)/inner plexiform layer (0.29 μm/y) on optical coherence tomography analysis (OCT) over a 4-y period, independent of glycated hemoglobin, age, and sex...
May 10, 2016: Proceedings of the National Academy of Sciences of the United States of America
S Weisberg, R Leibel, D V Tortoriello
BACKGROUND: Type 2 diabetes stems from obesity-associated insulin resistance, and in the genetically susceptible, concomitant pancreatic β-cell failure can occur, which further exacerbates hyperglycemia. Recent work by our group and others has shown that the natural polyphenol curcumin attenuates the development of insulin resistance and hyperglycemia in mouse models of hyperinsulinemic or compensated type 2 diabetes. Although several potential downstream molecular targets of curcumin exist, it is now recognized to be a direct inhibitor of proteasome activity...
April 25, 2016: Nutrition & Diabetes
Christoph Wallner, Stephanie Abraham, Johannes Maximilian Wagner, Kamran Harati, Britta Ismer, Lukas Kessler, Hannah Zöllner, Marcus Lehnhardt, Björn Behr
UNLABELLED: Bone regeneration is typically a reliable process without scar formation. The endocrine disease type 2 diabetes prolongs and impairs this healing process. In a previous work, we showed that angiogenesis and osteogenesis-essential steps of bone regeneration-are deteriorated, accompanied by reduced proliferation in type 2 diabetic bone regeneration. The aim of the study was to improve these mechanisms by local application of adipose-derived stem cells (ASCs) and facilitate bone regeneration in impaired diabetic bone regeneration...
June 2016: Stem Cells Translational Medicine
Caifeng Yan, Weifeng Xu, Yujie Huang, Min Li, Yachen Shen, Hui You, Xiubin Liang
Many studies have provided evidence to demonstrate the beneficial renal effects of resveratrol (RESV) due to its antioxidant character and its capacity for activation of surtuin 1. However, the molecular mechanisms underlying the protective role of RESV against kidney injury are still incompletely understood. The present study used Lepr db/db (db/db) and Lepr db/m (db/m) mice as models to evaluate the effect of RESV on diabetic nephropathy (DN). RESV reduced proteinuria and attenuated the progress of renal fibrosis in db/db mice...
June 2016: Molecular Endocrinology
Harry Jung, Hajin Nam, Jun-Gyo Suh
The C57BLKS/J-Lepr(db) mouse has a point mutation in the leptin receptor gene and is one of the most useful animal model for non-insulin dependent diabetes mellitus in human. Since the homozygote of C57BLKS/J-Lepr(db) mouse is infertile, detection of point mutation in the leptin receptor gene is important for efficient maintaining strains as well as mass production of homozygotes. To develop a rapid and efficient genotyping method for C57BLKS/J-Lepr(db) mouse, the tetra-primer amplification-refractory mutation system polymerase chain reaction (ARMS-PCR) was used...
March 2016: Laboratory Animal Research
Oanh H Do, Jenny E Gunton, Herbert Y Gaisano, Peter Thorn
AIMS/HYPOTHESIS: Type 2 diabetes is a progressive disease that increases morbidity and the risk of premature death. Glucose dysregulation, such as elevated fasting blood glucose, is observed prior to diabetes onset. A decline in beta cell insulin secretion contributes to the later stages of diabetes, but it is not known what, if any, functional beta cell changes occur in prediabetes and early disease. METHODS: The Lepr (db) mouse (age 13-18 weeks) was used as a model of type 2 diabetes and a two-photon granule fusion assay was used to characterise the secretory response of pancreatic beta cells...
June 2016: Diabetologia
Stacey Hokke, Nicole Arias, James A Armitage, Victor G Puelles, Karen Fong, Stefania Geraci, Norbert Gretz, John F Bertram, Luise A Cullen-McEwen
BACKGROUND: Animal studies report a nephron deficit in offspring exposed to maternal diabetes, yet are limited to models of severe hyperglycaemia which do not reflect the typical clinical condition and which are associated with fetal growth restriction that may confound nephron endowment. We aimed to assess renal morphology and function in offspring of leptin receptor deficient mice (Lepr(db) /+) and hypothesised that exposure to impaired maternal glucose tolerance (IGT) would be detrimental to the developing kidney...
April 2, 2016: Diabetes/metabolism Research and Reviews
Aaron R Cox, Carol J Lam, Matthew M Rankin, Kourtney A King, Pan Chen, Ramon Martinez, Changhong Li, Jake A Kushner
AIMS/HYPOTHESIS: Understanding the developmental biology of beta cell regeneration is critical for developing new diabetes therapies. Obesity is a potent but poorly understood stimulus for beta cell expansion. Current models of obesity are complicated by developmental compensation or concurrent diabetes, limiting their usefulness for identifying the lineage mechanism(s) of beta cell expansion. We aimed to determine whether acute inducible obesity stimulates beta cell expansion and to determine the lineage mechanism of beta cell growth in obesity...
June 2016: Diabetologia
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