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https://www.readbyqxmd.com/read/27913296/regulation-of-skeletal-muscle-insulin-stimulated-signaling-through-the-mek-redd1-mtor-axis
#1
Cory M Dungan, David L Williamson
Recent findings in adipocytes suggest that mitogen-activated protein kinase (MAPK)/extracellular-regulated signaling kinase (ERK) kinase 1/2 (MEK1/2) signaling regulates regulated in development and DNA damage 1 (REDD1) protein expression. Similarly, our previous work show that a lack of REDD1 protein expression, and associated hyperactive basal mechanistic target of rapamycin (mTOR) signaling, limits skeletal muscle's response to insulin. Therefore, we sought to determine: 1) if MEK1/2 inhibition is sufficient to reduce REDD1 protein expression and subsequently insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation via negative feedback of hyperactive mTOR in REDD1 wild-type (WT) mice and 2) if rapamycin-mediated mTOR inhibition is sufficient to improve IRS-1 tyrosine phosphorylation in REDD1 knockout (KO) mice...
November 29, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27913274/two-grass-carp-ctenopharyngodon-idella-insulin-like-growth-factor-binding-protein-5-genes-exhibit-different-yet-conserved-functions-in-development-and-growth
#2
Guo-Dong Zheng, Chun-Xue Zhou, Si-Tong Lin, Jie Chen, Xia-Yun Jiang, Shu-Ming Zou
Insulin-like growth factor binding-protein 5 (igfbp5), the most conserved member of the IGFBP family in vertebrates, plays a critical role in controlling cell survival, growth, differentiation, and apoptosis. Here, we characterized the expression patterns of igfbp5a and igfbp5b in grass carp (Ctenopharyngodon idella), which are retained in many fish species, likely from the teleost-specific whole-genome duplication. Both igfbp5a and igfbp5b encode 268- and 263-aa peptides, respectively, which share a sequence identity of 71%...
November 29, 2016: Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology
https://www.readbyqxmd.com/read/27913104/d-ala2-gip-glu-pal-is-neuroprotective-in-a-chronic-parkinson-s-disease-mouse-model-and-increases-bndf-expression-while-reducing-neuroinflammation-and-lipid-peroxidation
#3
Yanwei Li, WeiZhen Liu, Lin Li, Christian Hölscher
Type 2 diabetes mellitus (T2DM) is a risk factor for Parkinson's disease (PD). Therefore, treatment to improve insulin resistance in T2DM may be useful for PD patients. Glucose dependent insulinotropic polypeptide (GIP) is a member of the incretin hormone family that can promote insulin release and improve insulin resistance. Several GIP analogues have been developed as potential treatments for T2DM. We had shown previously that D-Ala2-GIP-glu-PAL, a novel long-acting GIP analogue, can play a neuroprotective role in the PD mouse model induced by acute MPTP injection...
November 29, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27912756/mechanisms-of-inflammatory-responses-and-development-of-insulin-resistance-how-are-they-interlinked
#4
Kanwal Rehman, Muhammad Sajid Hamid Akash
BACKGROUND: Insulin resistance (IR) is one of the major hallmark for pathogenesis and etiology of type 2 diabetes mellitus (T2DM). IR is directly interlinked with various inflammatory responses which play crucial role in the development of IR. Inflammatory responses play a crucial role in the pathogenesis and development of IR which is one of the main causative factor for the etiology of T2DM. METHODS: A comprehensive online English literature was searched using various electronic search databases...
December 3, 2016: Journal of Biomedical Science
https://www.readbyqxmd.com/read/27910746/nutrition-and-diabetes-mellitus-how-are-they-interlinked
#5
Kanwal Rehman, Muhammad Sajid Hamid Akash
The prevalence of type 2 diabetes mellitus (T2DM) has risen exponentially, and the number of incidences increases every day. The purpose of this article is to summarize the experimental evidence supporting the important association between nutrition and diet-based therapy for the control and management of T2DM. Evidence from several in vitro, in vivo, and human studies broadly found that nutrition-based therapy enriched with several important phytochemical constituents modulates lipid and carbohydrate metabolism, and it ameliorates glucolipotoxicity and insulin resistance...
2016: Critical Reviews in Eukaryotic Gene Expression
https://www.readbyqxmd.com/read/27909910/biological-mechanisms-for-the-effect-of-obesity-on-cancer-risk-experimental-evidence
#6
Mauricio Berriel Diaz, Stephan Herzig, Tobias Schafmeier
Multiple epidemiological studies demonstrated that overweight and obesity significantly increase the risk of several types of cancer. As the prevalence of obesity is dramatically rising, it is expected that it will represent one of the major lifestyle-associated risk factors for cancer development in the near future. Numerous recent studies expanded knowledge about key players and pathways, which are deregulated in the obese state and potentially promote cancer initiation, progression and aggressiveness via remote and local effects...
2016: Recent Results in Cancer Research
https://www.readbyqxmd.com/read/27909723/inhibition-of-jnk-suppresses-autophagy-and-attenuates-insulin-resistance-in-a-rat-model-of-nonalcoholic-fatty-liver-disease
#7
Hua Yan, Yanqiong Gao, Ying Zhang
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, the pathological process of which is complex. Activation of the c‑Jun N‑terminal kinase (JNK) signaling pathway is associated with the mechanism underlying obesity-induced insulin resistance. Furthermore, the JNK signaling pathway and dysfunctional autophagy serve important roles in hepatic lipid metabolism. However, the exact role of JNK in autophagy and obesity‑induced insulin resistance is not fully understood. Therefore, the present study aimed to investigate the underlying mechanisms by which the JNK signaling pathway regulates autophagy and insulin resistance in fatty liver...
November 24, 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27908407/effects-of-fluoride-on-insulin-signaling-and-bone-metabolism-in-ovariectomized-rats
#8
Amanda Gomes Pereira, Fernando Yamamoto Chiba, Maria Sara de Lima Coutinho Mattera, Renato Felipe Pereira, Rita de Cássia Alves Nunes, Thaís Verônica Saori Tsosura, Roberta Okamoto, Doris Hissako Sumida
Fluoride is an essential trace element for the maintenance of bone health owing to its capacity to stimulate proliferation and osteoblastic activity that can lead to increased bone formation. However, excessive sodium fluoride (NaF) intake can impair carbohydrate metabolism thereby promoting hyperglycemia, insulin resistance, and changes in insulin signaling. Thus, this study aimed to evaluate the effect of chronic treatment with NaF in bone metabolism, insulin signaling, and plasma concentrations of glucose, insulin, tumor necrosis factor-α (TNF-α), osteocalcin (OCN), and fluoride in ovariectomized rats...
January 2017: Journal of Trace Elements in Medicine and Biology
https://www.readbyqxmd.com/read/27907247/ship2-structure-function-and-inhibition
#9
Mark P Thomas, Christophe Erneux, Barry V L Potter
SHIP2 is a phosphatase that acts at the 5-position of phosphatidylinositol 3,4,5-trisphosphate. It is one of several enzymes that catalyse dephosphorylation at the 5-position of phosphoinositides or inositol phosphates. SHIP2 has a confirmed role in opsismodysplasia, a disease of bone development, but also interacts with proteins involved in insulin signalling, cytoskeletal function (thus having an impact on endocytosis, adhesion, proliferation and apoptosis) and immune system function. The structure of three domains (constituting about 38% of the protein) is known...
November 30, 2016: Chembiochem: a European Journal of Chemical Biology
https://www.readbyqxmd.com/read/27907012/the-signature-of-microrna-dysregulation-in-muscle-paralyzed-by-spinal-cord-injury-includes-downregulation-of-micrornas-that-target-myostatin-signaling
#10
Rita De Gasperi, Zachary A Graham, Lauren M Harlow, William A Bauman, Weiping Qin, Christopher P Cardozo
Spinal cord injury (SCI) results in muscle atrophy, reduced force generation and an oxidative-to-glycolytic fiber type shift. The mechanisms responsible for these alterations remain incompletely understood. To gain new insights regarding mechanisms involved in deterioration of muscle after SCI, global expression profiles of miRs in paralyzed gastrocnemius muscle were compared between sham-operated (Sham) and spinal cord-transected (SCI) rats. Ingenuity Pathways Analysis of the altered miRs identified signaling via insulin, IGF-1, integrins and TGF-β as being significantly enriched for target genes...
2016: PloS One
https://www.readbyqxmd.com/read/27906714/central-nervous-system-regulation-of-hepatic-lipid-and-lipoprotein-metabolism
#11
Jennifer Taher, Sarah Farr, Khosrow Adeli
PURPOSE OF REVIEW: Hepatic lipid and lipoprotein metabolism is an important determinant of fasting dyslipidemia and the development of fatty liver disease. Although endocrine factors like insulin have known effects on hepatic lipid homeostasis, emerging evidence also supports a regulatory role for the central nervous system (CNS) and neuronal networks. This review summarizes evidence implicating a bidirectional liver-brain axis in maintaining metabolic lipid homeostasis, and discusses clinical implications in insulin-resistant states...
November 30, 2016: Current Opinion in Lipidology
https://www.readbyqxmd.com/read/27906690/the-long-road-to-leptin
#12
Jeffrey Friedman
Leptin is an adipose tissue hormone that functions as an afferent signal in a negative feedback loop that maintains homeostatic control of adipose tissue mass. This endocrine system thus serves a critical evolutionary function by protecting individuals from the risks associated with being too thin (starvation) or too obese (predation and temperature dysregulation). Mutations in leptin or its receptor cause massive obesity in mice and humans, and leptin can effectively treat obesity in leptin-deficient patients...
December 1, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27906092/alterations-to-mtorc1-signaling-in-the-skeletal-muscle-differentially-affect-whole-body-metabolism
#13
Maitea Guridi, Barbara Kupr, Klaas Romanino, Shuo Lin, Denis Falcetta, Lionel Tintignac, Markus A Rüegg
BACKGROUND: The mammalian target of rapamycin complex 1 (mTORC1) is a central node in a network of signaling pathways controlling cell growth and survival. This multiprotein complex integrates external signals and affects different nutrient pathways in various organs. However, it is not clear how alterations of mTORC1 signaling in skeletal muscle affect whole-body metabolism. RESULTS: We characterized the metabolic phenotype of young and old raptor muscle knock-out (RAmKO) and TSC1 muscle knock-out (TSCmKO) mice, where mTORC1 activity in skeletal muscle is inhibited or constitutively activated, respectively...
March 21, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27905558/microrna-mir-34-provides-robustness-to-environmental-stress-response-via-the-daf-16-network-in-c-elegans
#14
Meltem Isik, T Keith Blackwell, Eugene Berezikov
Diverse stresses and aging alter expression levels of microRNAs, suggesting a role for these posttranscriptional regulators of gene expression in stress modulation and longevity. Earlier studies demonstrated a central role for the miR-34 family in promoting cell cycle arrest and cell death following stress in human cells. However, the biological significance of this response was unclear. Here we show that in C. elegans mir-34 upregulation is necessary for developmental arrest, correct morphogenesis, and adaptation to a lower metabolic state to protect animals against stress-related damage...
December 1, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27904654/augmentation-of-histone-deacetylase-3-hdac3-epigenetic-signature-at-the-interface-of-proinflammation-and-insulin-resistance-in-patients-with-type-2-diabetes
#15
Chandrakumar Sathishkumar, Paramasivam Prabu, Mahalingam Balakumar, Raji Lenin, Durai Prabhu, Ranjith Mohan Anjana, Viswanathan Mohan, Muthuswamy Balasubramanyam
BACKGROUND: A role of proinflammation has been implicated in the pathogenesis of diabetes, but the up-stream regulatory signals and molecular signatures are poorly understood. While histone modifications such as changes in histone deacetylase (HDAC) are emerging as novel epigenetic biomarkers, there is lack of studies to demonstrate their clinical relevance in diabetes. Therefore, we investigated the extent of HDAC machinery and inflammatory signals in peripheral blood mononuclear cells (PBMCs) from patients with type 2 diabetes mellitus (T2DM) compared to control subjects...
2016: Clinical Epigenetics
https://www.readbyqxmd.com/read/27903748/hepatic-expression-of-adenovirus-36-e4orf1-improves-glycemic-control-and-promotes-glucose-metabolism-via-akt-activation
#16
Travis B McMurphy, Wei Huang, Run Xiao, Xianglan Liu, Nikhil V Dhurandhar, Lei Cao
Considering that impaired proximal insulin signaling is linked with diabetes, approaches that enhance glucose disposal independent of insulin signaling are attractive. In vitro data indicate that the E4ORF1 peptide derived from human adenovirus 36 (Ad36) interacts with cells from adipose tissue, skeletal muscle and liver to enhance glucose disposal, independent of proximal insulin signaling. Adipocyte-specific expression of Ad36E4ORF1 improved hyperglycemia in mice. To determine the hepatic interaction of Ad36E4ORF1 in enhancing glycemic control, we expressed E4ORF1 of Ad36 or adenovirus 5, or fluorescent tag alone using recombinant adeno-associated viral vector in the livers of three mouse models...
November 30, 2016: Diabetes
https://www.readbyqxmd.com/read/27901601/activation-of-estrogen-response-element-independent-er%C3%AE-signaling-protects-female-mice-from-diet-induced-obesity
#17
Ali Yasrebi, Janelle A Rivera, Elizabeth A Krumm, Jennifer A Yang, Troy A Roepke
17β-estradiol (E2) regulates central and peripheral mechanisms that control energy and glucose homeostasis predominantly through estrogen receptor α (ERα) acting via receptor binding to estrogen response elements (ERE). ERα signaling is also involved in mediating the effects of E2 on diet-induced obesity (DIO), although the roles of ERE-dependent and -independent ERα signaling in ameliorating the effects of DIO remain largely unknown. We hypothesize that ERE-dependent ERα signaling is necessary to ameliorate the effects of DIO...
November 30, 2016: Endocrinology
https://www.readbyqxmd.com/read/27901270/adipose-tissue-inflammation-by-intermittent-hypoxia-mechanistic-link-between-obstructive-sleep-apnoea-and-metabolic-dysfunction
#18
Silke Ryan
Obstructive sleep apnoea (OSA) is a highly prevalent condition and recognized as a major public health burden conveying a significant risk of cardiometabolic diseases and mortality. Type 2 diabetes (T2D), insulin resistance (IR) and glucose tolerance are common in subjects with OSA and this association is at least in part independent of the effects of obesity. Continuous positive airway pressure (CPAP) is the treatment of choice for the majority of patients with OSA but the benefit of CPAP on glycaemic health is uncertain...
November 29, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27900351/data-for-differentially-expressed-micrornas-in-saturated-fatty-acid-palmitate-treated-hepg2-cells
#19
Won-Mo Yang, Kyung-Ho Min, Wan Lee
Certain microRNAs (miRNAs) targeting the molecules in the insulin signaling cascades are dysregulated by saturated fatty acids (SFA), which can lead to insulin resistance and type 2 diabetes. This article reports the accompanying data collected using miRNAs microarrays to identify the changes in miRNA expression in HepG2 cells treated with SFA palmitate. Differentially expressed miRNA analyses in HepG2 cells showed that a range of upregulated (>1.5-fold) or downregulated (<0.5-fold) miRNAs. Further extensive insights into the implications of miRNAs, particularly miR-1271, in HepG2 cells can be found in "MiR-1271 upregulated by saturated fatty acid palmitate provokes impaired insulin signaling by repressing INSR and IRS-1 expression in HepG2 cells" (W...
December 2016: Data in Brief
https://www.readbyqxmd.com/read/27899484/lack-of-cul4b-in-adipocytes-promotes-ppar%C3%AE-mediated-adipose-tissue-expansion-and-insulin-sensitivity
#20
Peishan Li, Yu Song, Wenying Zan, Liping Qin, Shuang Han, Baichun Jiang, Hao Dou, Changshun Shao, Yaoqin Gong
Obesity and obesity-associated diseases are linked to dysregulation of peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway. Identification of the factors that regulate PPARγ expression and activity is crucial for combating obesity. However, the ubiquitin E3 ligases that target PPARγ for proteasomal degradation have been rarely identified and their functions in vivo have not been characterized. Here we report that CUL4B-RING E3 ligase (CRL4B) negatively regulates PPARγ by promoting its polyubiquitination and proteasomal degradation...
November 29, 2016: Diabetes
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