Search results for: Leptin
#33634255 
2020/08/13
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Association of serum leptin with angiographically proven cardiovascular disease and with components of the metabolic syndrome: a cross-sectional study in East Azerbaijan.
Role of leptin is well documented in cardiometabolic diseases. The objective of this study was to investigate if the serum levels of leptin associates with the serum levels of markers related to cardiac and metabolic disorders in adults.Nafiseh Khanbabaei, Hossein Mozafar Saadati, Shahnam Valizadeh Shahbazloo, Reyhaneh Hoseinpoor, Seyed Hossein Naderi, Roya Taghvamanesh, Sakhavat Abolhasani
1993 related Products with: Association of serum leptin with angiographically proven cardiovascular disease and with components of the metabolic syndrome: a cross-sectional study in East Azerbaijan.
100 500 tests50 ul96 tests500 tests 50 UG
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#33634249 2021/01/25
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Nontuberculous mycobacterial lung infections in patients with eating disorders: plausible mechanistic links in a case series.
Nontuberculous mycobacteria (NTM) are widely distributed in the environment and are almost always acquired into the lungs by bioaerosol inhalation or aspiration of NTM-contaminated water, biofilms, and soil. NTM are increasingly recognized as causes of lung diseases in immunocompetent hosts, a not insignificant number of whom have a life-long or nearly life-long slender body habitus as well as thoracic cage abnormalities such as scoliosis and pectus excavatum. While several hypotheses have been offered to explain the purported increase in susceptibility to NTM lung disease in such individuals, the precise explanation remains unknown. We described three patients with eating disorders associated with severe malnutrition and either purging behaviors or other risks for aspiration who were diagnosed with NTM lung infections-the largest number of such patients to date in a single report. We discuss the clinical and experimental evidence that low body weight and chronic vomiting with attendant jeopardy for aspiration, as seen in patients with eating disorders, may represent risk factors for NTM lung disease. We also speculate the possibility of occult and undiagnosed eating disorders in some of the slender NTM lung disease patients with no known risk factors for the opportunistic infection other than their low body weight.Daniela E Grayeb, Edward D Chan, Leah M Swanson, Dennis G Gibson, Philip S Mehler
1891 related Products with: Nontuberculous mycobacterial lung infections in patients with eating disorders: plausible mechanistic links in a case series.
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#33633690 2021/02/09
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Tissue-Specific Approaches Reveal Diverse Metabolic Functions of Rho-Kinase 1.
Rho-kinase 1 (ROCK1) has been implicated in diverse metabolic functions throughout the body, with promising evidence identifying ROCK1 as a therapeutic target in diabetes and obesity. Considering these metabolic roles, several pharmacological inhibitors have been developed to elucidate the mechanisms underlying ROCK1 function. Y27632 and fasudil are two common ROCK1 inhibitors; however, they have varying non-specific selectivity to inhibit other AGC kinase subfamily members and whole-body pharmacological approaches lack tissue-specific insight. As a result, interpretation of studies with these inhibitors is difficult, and alternative approaches are needed to elucidate ROCK1's tissue specific metabolic functions. Fortunately, recent technological advances utilizing molecular carriers or genetic manipulation have facilitated discovery of ROCK1's tissue-specific mechanisms of action. In this article, we review the tissue-specific roles of ROCK1 in the regulation of energy balance and substrate utilization. We highlight prominent metabolic roles in liver, adipose, and skeletal muscle, in which ROCK1 regulates energy expenditure, glucose uptake, and lipid metabolism inhibition of AMPK2α and paradoxical modulation of insulin signaling. Compared to ROCK1's roles in peripheral tissues, we also describe contradictory functions of ROCK1 in the hypothalamus to increase energy expenditure and decrease food intake leptin signaling. Furthermore, dysregulated ROCK1 activity in either of these tissues results in metabolic disease phenotypes. Overall, tissue-specific approaches have made great strides in deciphering the many critical metabolic functions of ROCK1 and, ultimately, may facilitate the development of novel treatments for metabolic disorders.Taylor Landry, Daniel Shookster, Hu Huang
1284 related Products with: Tissue-Specific Approaches Reveal Diverse Metabolic Functions of Rho-Kinase 1.
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#33632534 2021/02/12
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Visceral adipose tissue glucose uptake is linked to prognosis in multiple myeloma patients: An exploratory study.
The use of computerized tomography to opportunistically assess body composition has highlighted abnormalities such as low muscle mass and high adiposity may be hidden conditions in cancer patients. However, the role of skeletal muscle (SM), subcutaneous (SAT) and visceral (VAT) adipose tissue glucose uptake measured by F-fluorodeoxyglucose (F-FDG) positron emission tomography (PET)-CT on patient prognostication is unclear.Ademar Dantas da Cunha Júnior, Marina Nogueira Silveira, Maria Emilia Seren Takahashi, Edna Marina de Souza, Camila Mosci, Celso Dario Ramos, Sandra Regina Brambilla, Fernando Vieira Pericole, Carla M Prado, Maria Carolina Santos Mendes, José Barreto Campello Carvalheira
1120 related Products with: Visceral adipose tissue glucose uptake is linked to prognosis in multiple myeloma patients: An exploratory study.
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#33631239 2021/02/22
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ADIPOQ and LEP variants on asthma and atopy: genetic association modified by overweight.
Asthma and atopy are considered condition associated with obesity, being affected by genetic and environmental factors. The LEP and ADIPOQ genes, responsible for the expression and secretion of leptin and adiponectin, respectively, and polymorphisms in such genes have been linked to both diseases, independently, and also with the obesity-associated asthma phenotype in populations with high European ancestry and high-income countries. However, in mixed populations, there are few studies evaluating the impact of these variants in genes associated with the phenotype of asthma and obesity. Thus, the aim of this study was to investigate variants in LEP and ADIPOQ associated with asthma and atopy, and whether overweight modifies that effect.Raísa Santos Coelho, Ana Paula Castro Melo, Hátilla Dos Santos Silva, Rita De Cassia Ribeiro Silva, Sheila Maria Alvim Matos, Maurício Lima Barreto, Neuza Maria Alcântara-Neves, Camila Alexandrina Viana de Figueiredo, Ryan do Santos Costa
2163 related Products with: ADIPOQ and LEP variants on asthma and atopy: genetic association modified by overweight.
10 mg100 mg100ug200ul5mg100 mg 25 MG100ul25 mg200ug2.5 mg
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#33631197 2021/02/22
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Chemerin in inflammatory diseases.
Obesity is associated with a series of health problems. Adipocytes are a huge repository of energy as well as an important source of many adipokines. In obesity, adipocytes are dysfunctional with excessive production and secretion of pro-inflammatory adipokines, such as tumor necrosis factor α (TNF-α), leptin, and chemerin. Recent studies have revealed that chemerin plays an important role in modulating physiologic as well as pathophysiologic processes. For example, chemerin stimulates maturation and differentiation of pre-adipocytes, acts as a chemoattractant and facilitates innate and acquired immunity. Furthermore, chemerin participates in the early stage of acute inflammation by reacting with the ChemR23 receptor. In various inflammatory diseases, the serum chemerin is significantly increased. Additionally, chemerin is also considered as an important biomarker for benign and malignant tumors. Thus, elucidating the pathologic mechanisms of chemerin action may facilitate the development of new therapeutic modalities to treat diverse inflammatory diseases. In this review, we summarize current knowledge of chemerin and its role as an important regulator in modulating various inflammatory diseases. Mechanisms underlying chemerin function in diverse diseases are explored to better understand its biochemistry and mechanisms of action.Xin Su, Ye Cheng, Guoming Zhang, Bin Wang
1606 related Products with: Chemerin in inflammatory diseases.
2ug500 tests2ug2ug500 tests0.1 mg500 tests96 tests5ug2ug500 tests500 tests
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#33630762 2021/02/25
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Bardet-Biedl Syndrome proteins regulate intracellular signaling and neuronal function in patient-specific iPSC-derived neurons.
Bardet-Biedl Syndrome (BBS) is a rare autosomal recessive disorder caused by mutations in genes encoding components of the primary cilium and characterized by hyperphagic obesity. To investigate the molecular basis of obesity in human BBS, we developed a cellular model of BBS using induced pluripotent stem cell (iPSCs)-derived hypothalamic arcuate-like neurons. BBS mutations BBS1M390R and BBS10C91fsX95 did not affect neuron differentiation efficiency but caused morphological defects including impaired neurite outgrowth and longer primary cilia. Single-cell RNA sequencing of BBS1M390R hypothalamic neurons identified several downregulated pathways including insulin and cAMP signaling, and axon guidance. Additional studies demonstrated that BBS1M390R and BBS10C91fsX95 mutations impaired insulin signaling in both human fibroblasts and iPSC-derived neurons. Overexpression of intact BBS10 fully restored insulin signaling by restoring insulin receptor tyrosine phosphorylation in BBS10C91fsX95 neurons. Moreover, mutations in BBS1 and BBS10 impaired leptin-mediated p-STAT3 activation in iPSC-derived hypothalamic neurons. Correction of the BBS mutation by CRISPR rescued leptin signaling. POMC expression and neuropeptide production were decreased in BBS1M390R and BBS10C91fsX95 iPSC-derived hypothalamic neurons. In the aggregate, these data provide insights into the anatomic and functional mechanisms by which components of the BBSome in CNS primary cilia mediate effects on energy homeostasis.Liheng Wang, Yang Liu, George Stratigopoulos, Sunil K Panigrahi, Lina Sui, Charles A LeDuc, Hannah J Glover, Maria Caterina De Rosa, Lisa C Burnett, Damian J Williams, Linshan Shang, Robin Goland, Stephen H Tsang, Sharon L Wardlaw, Dieter Egli, Deyou Zheng, Claudia A Doege, Rudolph L Leibel
2129 related Products with: Bardet-Biedl Syndrome proteins regulate intracellular signaling and neuronal function in patient-specific iPSC-derived neurons.
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#33628645 2021/02/16
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Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets.
"Quantile-dependent expressivity" occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g., C-reactive protein, CRP) is high or low relative to its distribution. We have previously shown that the heritabilities () of coffee and alcohol consumption, postprandial lipemia, lipoproteins, leptin, adiponectin, adiposity, and pulmonary function are quantile-specific. Whether CRP heritability is quantile-specific is currently unknown.Paul T Williams
1552 related Products with: Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets.
1 kit96T2 Pieces/Box0.1mg100 ug1 Set101 Set1 Set50 1 Set
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#33627868 2021/02/24
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A mechanosensitive peri-arteriolar niche for osteogenesis and lymphopoiesis.
Stromal cells in adult bone marrow that express leptin receptor (LEPR) are a critical source of growth factors, including stem cell factor (SCF), for the maintenance of haematopoietic stem cells and early restricted progenitors. LEPR cells are heterogeneous, including skeletal stem cells and osteogenic and adipogenic progenitors, although few markers have been available to distinguish these subsets or to compare their functions. Here we show that expression of an osteogenic growth factor, osteolectin, distinguishes peri-arteriolar LEPR cells poised to undergo osteogenesis from peri-sinusoidal LEPR cells poised to undergo adipogenesis (but retaining osteogenic potential). Peri-arteriolar LEPRosteolectin cells are rapidly dividing, short-lived osteogenic progenitors that increase in number after fracture and are depleted during ageing. Deletion of Scf from adult osteolectin cells did not affect the maintenance of haematopoietic stem cells or most restricted progenitors but depleted common lymphoid progenitors, impairing lymphopoiesis, bacterial clearance, and survival after acute bacterial infection. Peri-arteriolar osteolectin cell maintenance required mechanical stimulation. Voluntary running increased, whereas hindlimb unloading decreased, the frequencies of peri-arteriolar osteolectin cells and common lymphoid progenitors. Deletion of the mechanosensitive ion channel PIEZO1 from osteolectin cells depleted osteolectin cells and common lymphoid progenitors. These results show that a peri-arteriolar niche for osteogenesis and lymphopoiesis in bone marrow is maintained by mechanical stimulation and depleted during ageing.Bo Shen, Alpaslan Tasdogan, Jessalyn M Ubellacker, Jingzhu Zhang, Elena D Nosyreva, Liming Du, Malea M Murphy, Shuiqing Hu, Yating Yi, Nergis Kara, Xin Liu, Shay Guela, Yuemeng Jia, Vijayashree Ramesh, Claire Embree, Evann C Mitchell, Yunduo C Zhao, Lining A Ju, Zhao Hu, Genevieve M Crane, Zhiyu Zhao, Ruhma Syeda, Sean J Morrison