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Impaired glucose regulation

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https://www.readbyqxmd.com/read/28634176/impact-of-glycemic-variability-on-chromatin-remodeling-oxidative-stress-and-endothelial-dysfunction-in-type-2-diabetic-patients-with-target-hba1c-levels
#1
Sarah Costantino, Francesco Paneni, Rodolfo Battista, Lorenzo Castello, Giuliana Capretti, Sergio Chiandotto, Luigi Tanese, Giulio Russo, Dario Pitocco, Gaetano A Lanza, Massimo Volpe, Thomas F Lüscher, Francesco Cosentino
Intensive glycemic control (IGC) targeting HbA1c fails to show an unequivocal reduction of macrovascular complications in type 2 diabetes (T2D), however the underlining mechanisms remain elusive. Epigenetic changes are emerging as important mediators of cardiovascular damage and may play a role in this setting. This study investigates whether epigenetic regulation of the adaptor protein p66(Shc), a key driver of mitochondrial oxidative stress, contributes to persistent vascular dysfunction in T2D patients despite IGC...
June 20, 2017: Diabetes
https://www.readbyqxmd.com/read/28631330/foxo-transcription-factors-at-the-interface-of-metabolism-and-cancer
#2
REVIEW
Wolfgang Link, Pablo J Fernandez-Marcos
Diabetes refers to a group of metabolic diseases characterized by impaired insulin signalling and high blood glucose. A growing body of epidemiological evidence links diabetes to several types of cancer but the underlying molecular mechanisms are poorly understood. The signalling cascade connecting insulin and FOXO proteins provides a compelling example for a conserved pathway at the interface between insulin signalling and cancer. FOXOs are transcription factors that orchestrate programs of gene expression known to control a variety of processes in response to cellular stress...
June 19, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28630133/dual-regulation-of-gluconeogenesis-by-insulin-and-glucose-in-the-proximal-tubules-of-the-kidney
#3
Motohiro Sasaki, Takayoshi Sasako, Naoto Kubota, Yoshitaka Sakurai, Iseki Takamoto, Tetsuya Kubota, Reiko Inagi, George Seki, Moritaka Goto, Kohjiro Ueki, Masaomi Nangaku, Takahito Jomori, Takashi Kadowaki
Growing attention has been focused on the roles of the proximal tubules (PTs) of the kidney in glucose metabolism, including the mechanism of regulation of gluconeogenesis. Here, we found that PT-specific IRS1/2 double-knockout mice, established by using the newly generated sodium-glucose cotransporter-2 (SGLT2)-Cre transgenic mice, exhibited impaired insulin signaling and upregulated gluconeogenic gene expression and renal gluconeogenesis, resulting in systemic insulin resistance. On the other hand, in streptozotocin-treated mice, although insulin action was impaired in the PTs, the gluconeogenic gene expression was unexpectedly downregulated in the renal cortex, which was restored by administration of an SGLT1/2 inhibitor...
June 19, 2017: Diabetes
https://www.readbyqxmd.com/read/28627974/microrna-132-protects-hippocampal-neurons-against-oxygen-glucose-deprivation-induced-apoptosis
#4
Zu-Zhen Sun, Zhan-Yun Lv, Wen-Jing Tian, Yan Yang
Hypoxic-ischemic brain injury (HIBI) results in death or long-term neurologic impairment in both adults and children. In this study, we investigated the effects of microRNA-132 (miR-132) dysregulation on oxygen-glucose deprivation (OGD)-induced apoptosis in fetal rat hippocampal neurons, in order to reveal the therapeutic potential of miR-132 on HIBI. MiR-132 dysregulation was induced prior to OGD exposure by transfection of primary fetal rat hippocampal neurons with miR-132 mimic or miR-132 inhibitor. The effects of miR-132 overexpression and suppression on OGD-stimulated hippocampal neurons were evaluated by detection of cell viability, apoptotic cells rate, and the expression of apoptosis-related proteins...
June 1, 2017: International Journal of Immunopathology and Pharmacology
https://www.readbyqxmd.com/read/28627674/mir-200c-serves-an-important-role-in-h5v-endothelial-cells-in-high-glucose-by-targeting-notch1
#5
Yunfeng Zhang, Qiang Guan, Xing Jin
Diabetic vasculopathy is the leading cause of impairment and death in diabetic patients, a variety of factors are involved in its underlying pathological process, however, endothelial cell (EC) dysfunction serves a significant role in the process. MicroRNAs (miRNAs) have emerged as potential therapeutic candidates, due to their ability to regulate multiple targets involved in ECs. The aim of the present study was to investigate the role of miR‑200c in regulating ECs in high glucose condition. To investigate the role of miR‑200c in regulating hyperglycemia induced ECs by targeting Notch1, ECs H5V cells were cultured in high sugar conditions to initiate the inhibition of Notch1, the same cells in normal medium as the control...
June 15, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28627440/microrna-21-regulates-hepatic-glucose-metabolism-by-targeting-foxo1
#6
Ailing Luo, Haibo Yan, Jichao Liang, Chunyuan Du, Xuemei Zhao, Lijuan Sun, Yong Chen
Abnormal activation of hepatic gluconeogenesis is a major contributor to fasting hyperglycemia in type 2 diabetes; however, the potential role of microRNAs in gluconeogenesis remains unclear. Here, we showed that hepatic expression levels of microRNA-21 (miR-21) were decreased in db/db and high-fat diet (HFD)-induced diabetic mice. Adenovirus-mediated overexpression of miR-21 decreased the expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) and inhibited glucose production in primary mouse hepatocytes...
June 13, 2017: Gene
https://www.readbyqxmd.com/read/28624907/dityrosine-administration-induces-dysfunction-of-insulin-secretion-accompanied-by-diminished-thyroid-hormones-t3-function-in-pancreas-of-mice
#7
Yin-Yi Ding, Zhu-Qing Li, Xiang-Rong Cheng, Yu-Mei Ran, Sha-Ji Wu, Yonghui Shi, Guowei Le
Oxidized tyrosine products are commonly found in food with high protein content and have been demonstrated to cause damage of liver and kidney in our previous studies. Dityrosine (Dityr) is a typical oxidized tyrosine product. Due to its structural homology with thyroid hormones T3, we assumed that one of the endocrine systems most likely considered in connection with its disruption by Dityr may be the T3 action. T3 plays important roles in insulin synthesis, and thyroid hormone resistance (RTH) is associated with the impairment of glucose metabolism...
June 17, 2017: Amino Acids
https://www.readbyqxmd.com/read/28624434/brain-glucose-metabolism-role-of-wnt-signaling-in-the-metabolic-impairment-in-alzheimer-s-disease
#8
REVIEW
Pedro Cisternas, Nibaldo C Inestrosa
The brain is an organ that has a high demand for glucose. In the brain, glucose is predominantly used in energy production, with almost 70% of the energy used by neurons. The importance of the energy requirement in neurons is clearly demonstrated by the fact that all neurodegenerative disorders exhibit a critical metabolic impairment that includes decreased glucose uptake/utilization and decreased mitochondrial activity, with a consequent diminution in ATP production. In fact, in Alzheimer's disease, the measurement of the general metabolic rate of the brain has been reported to be an accurate tool for diagnosis...
June 15, 2017: Neuroscience and Biobehavioral Reviews
https://www.readbyqxmd.com/read/28620389/2-deoxy-d-glucose-treatment-decreases-anti-inflammatory-m2-macrophage-polarization-in-mice-with-tumor-and-allergic-airway-inflammation
#9
Qingjie Zhao, Zhulang Chu, Linnan Zhu, Tao Yang, Peng Wang, Fang Liu, Ying Huang, Fang Zhang, Xiaodong Zhang, Wenjun Ding, Yong Zhao
As important effector cells in inflammation, macrophages can be functionally polarized into either inflammatory M1 or alternatively activated anti-inflammatory M2 phenotype depending on surroundings. The key roles of glycolysis in M1 macrophage polarization have been well defined. However, the relationship between glycolysis and M2 polarized macrophages is still poorly understood. Here, we report that 2-deoxy-d-glucose (2-DG), an inhibitor of the glycolytic pathway, markedly inhibited the expressions of Arg, Ym-1, Fizz1, and CD206 molecules, the hall-markers for M2 macrophages, during macrophages were stimulated with interleukin 4...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28614797/neuropeptide-y-expression-marks-partially-differentiated-%C3%AE-cells-in-mice-and-humans
#10
Pope Rodnoi, Mohan Rajkumar, Abu Saleh Md Moin, Senta K Georgia, Alexandra E Butler, Sangeeta Dhawan
β Cells are formed in embryonic life by differentiation of endocrine progenitors and expand by replication during neonatal life, followed by transition into functional maturity. In this study, we addressed the potential contribution of neuropeptide Y (NPY) in pancreatic β cell development and maturation. We show that NPY expression is restricted from the progenitor populations during pancreatic development and marks functionally immature β cells in fetal and neonatal mice and humans. NPY expression is epigenetically downregulated in β cells upon maturation...
June 15, 2017: JCI Insight
https://www.readbyqxmd.com/read/28614714/dectin-1-activation-exacerbates-obesity-and-insulin-resistance-in-the-absence-of-myd88
#11
Angela Castoldi, Vinicius Andrade-Oliveira, Cristhiane Favero Aguiar, Mariane Tami Amano, Jennifer Lee, Marcelli Terumi Miyagi, Marcela Teatin Latância, Tarcio Teodoro Braga, Marina Burgos da Silva, Aline Ignácio, Joanna Darck Carola Correia Lima, Flavio V Loures, José Antonio T Albuquerque, Marina Barguil Macêdo, Rafael Ribeiro Almeida, Jonas W Gaiarsa, Luis A Luévano-Martínez, Thiago Belchior, Meire Ioshie Hiyane, Gordon D Brown, Marcelo A Mori, Christian Hoffmann, Marília Seelaender, Willian T Festuccia, Pedro Manoel Moraes-Vieira, Niels Olsen Saraiva Câmara
The underlying mechanism by which MyD88 regulates the development of obesity, metainflammation, and insulin resistance (IR) remains unknown. Global deletion of MyD88 in high-fat diet (HFD)-fed mice resulted in increased weight gain, impaired glucose homeostasis, elevated Dectin-1 expression in adipose tissue (AT), and proinflammatory CD11c+ AT macrophages (ATMs). Dectin-1 KO mice were protected from diet-induced obesity (DIO) and IR and had reduced CD11c+ AT macrophages. Dectin-1 antagonist improved glucose homeostasis and decreased CD11c+ AT macrophages in chow- and HFD-fed MyD88 KO mice...
June 13, 2017: Cell Reports
https://www.readbyqxmd.com/read/28612564/-study-on-relationship-between-serum-25-hydroxyvitamin-d3-concentration-and-glucose-metabolism
#12
Wei Gao, Yang-Fan Fei, Chun Wang, Da-Wei Chen, Guan-Jian Liu, Xing-Wu Ran
OBJECTIVES: To investigate the relationship between serum 25-hydroxyvitamin D3 [25(OH)D3 ] concentration and glucose metabolism. METHODS: This cross-sectional survey recruited 668 participants, and the demographic and clinical characteristics of the participants were obtained from questionnaires. Physical examination and blood biochemical examination were performed, then the participants were divided into three groups as normal glucose tolerant (NGT) group, impaired glucose regulation(IGR) group, and diabetes mellitus (DM) group...
January 2017: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
https://www.readbyqxmd.com/read/28611026/map4k4-impairs-energy-metabolism-in-endothelial-cells-and-promotes-insulin-resistance-in-obesity
#13
Rachel J Roth Flach, Marina T DiStefano, Laura V Danai, Ozlem Senol-Cosar, Joseph C Yawe, Mark Kelly, Lorena Garcia Menendez, Michael P Czech
The blood vasculature responds to insulin, influencing hemodynamic changes in the periphery, which promotes tissue nutrient and oxygen delivery and thus metabolic function. The lymphatic vasculature regulates fluid and lipid homeostasis, and impaired lymphatic function can contribute to atherosclerosis and obesity. Recent studies have suggested a role for endothelial cell (EC) Mitogen activated protein kinase kinase kinase kinase 4 (Map4k4) in developmental angiogenesis and lymphangiogenesis as well as atherosclerosis...
June 13, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28608812/quantification-of-bone-fatty-acid-metabolism-and-its-regulation-by-adipocyte-lipoprotein-lipase
#14
Alexander Bartelt, Till Koehne, Klaus Tödter, Rudolph Reimer, Brigitte Müller, Friederike Behler-Janbeck, Joerg Heeren, Ludger Scheja, Andreas Niemeier
Adipocytes are master regulators of energy homeostasis. Although the contributions of classical brown and white adipose tissue (BAT and WAT, respectively) to glucose and fatty acid metabolism are well characterized, the metabolic role of adipocytes in bone marrow remains largely unclear. Here, we quantify bone fatty acid metabolism and its contribution to systemic nutrient handling in mice. Whereas in parts of the skeleton the specific amount of nutrients taken-up from the circulation was lower than in other metabolically active tissues such as BAT or liver, the overall contribution of the skeleton as a whole organ was remarkable, placing it among the top organs involved in systemic glucose as well as fatty acid clearance...
June 13, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28607108/kv2-1-clustering-contributes-to-insulin-exocytosis-and-rescues-human-%C3%AE-cell-dysfunction
#15
Jianyang Fu, Xiaoqing Dai, Gregory Plummer, Kunimasa Suzuki, Austin Bautista, John M Githaka, Laura Senior, Mette Jensen, Dafna Greitzer-Antes, Jocelyn E Manning Fox, Herbert Y Gaisano, Christopher B Newgard, Nicolas Touret, Patrick E MacDonald
Insulin exocytosis is regulated by ion channels that control excitability and Ca(2+) influx. Channels also play an increasingly appreciated role in microdomain structure. In this study, we examine the mechanism by which the voltage-dependent K(+) (Kv) channel Kv2.1 (KCNB1) facilitates depolarization-induced exocytosis in INS 832/13 cells and β-cells from human donors with and without type 2 diabetes (T2D). We find that Kv2.1, but not Kv2.2 (KCNB2), forms clusters of 6-12 tetrameric channels at the plasma membrane and facilitates insulin exocytosis...
June 12, 2017: Diabetes
https://www.readbyqxmd.com/read/28606928/mtor-controls-chrebp-transcriptional-activity-and-pancreatic-%C3%AE-cell-survival-under-diabetic-stress
#16
Gia Cac Chau, Dong Uk Im, Tong Mook Kang, Jeong Mo Bae, Won Kim, Suhkneung Pyo, Eun-Yi Moon, Sung Hee Um
Impaired nutrient sensing and dysregulated glucose homeostasis are common in diabetes. However, how nutrient-sensitive signaling components control glucose homeostasis and β cell survival under diabetic stress is not well understood. Here, we show that mice lacking the core nutrient-sensitive signaling component mammalian target of rapamycin (mTOR) in β cells exhibit reduced β cell mass and smaller islets. mTOR deficiency leads to a severe reduction in β cell survival and increased mitochondrial oxidative stress in chemical-induced diabetes...
June 12, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28605280/the-gut-a-key-to-the-pathogenesis-of-type-2-diabetes
#17
Jens Juul Holst, Jens Pedersen, Nicolai Jacob Wewer Albrechtsen, Filip Krag Knop
In this communication we discuss the role of the gut for the development of type 2 diabetes mellitus (T2DM). Gastric emptying rates importantly determine postprandial glucose excursions and regulate postprandial secretion of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). It thereby also determines their powerful, amplifying effect on glucose-induced insulin secretion and thus the ability of the body to regulate glucose disposal. Although disturbances in gastric emptying are not consistent findings in type 2 diabetes, the incretin system is seriously impaired, probably associated with insulin resistance and obesity...
June 12, 2017: Metabolic Syndrome and related Disorders
https://www.readbyqxmd.com/read/28604389/a-cullin-4b-ring-e3-ligase-complex-fine-tunes-pancreatic-%C3%AE-cell-paracrine-interactions
#18
Qing Li, Min Cui, Fan Yang, Na Li, Baichun Jiang, Zhen Yu, Daolai Zhang, Yijing Wang, Xibin Zhu, Huili Hu, Pei-Shan Li, Shang-Lei Ning, Si Wang, Haibo Qi, Hechen Song, Dongfang He, Amy Lin, Jingjing Zhang, Feng Liu, Jiajun Zhao, Ling Gao, Fan Yi, Tian Xue, Jin-Peng Sun, Yaoqin Gong, Xiao Yu
Somatostatin secreted by pancreatic δ cells mediates important paracrine interactions in Langerhans islets, including maintenance of glucose metabolism through the control of reciprocal insulin and glucagon secretion. Disruption of this circuit contributes to the development of diabetes. However, the precise mechanisms that control somatostatin secretion from islets remain elusive. Here, we found that a super-complex comprising the cullin 4B-RING E3 ligase (CRL4B) and polycomb repressive complex 2 (PRC2) epigenetically regulates somatostatin secretion in islets...
June 12, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28600551/epe1-contributes-to-activation-of-ampk-by-promoting-phosphorylation-of-ampk-alpha-subunit-ssp2
#19
Yongyi Chen, Xiaoyue Hu, Chao Guo, Yao Yu, Hong Lu
AMP-activated protein kinase (AMPK) is a pivotal cellular energy sensor. It is activated by stresses that cause depletion of energy and initiates adaptive responses by regulating metabolism balance. AMPK forms αβγ heterotrimer. In fission yeast, activation of AMPK mainly depends on the phosphorylation of AMPKα subunit Ssp2 at Thr(189) by upstream kinase Ssp1. However, not much is known about the regulation of this process. In this study, we identified Epe1 as a novel positive regulator of AMPK. Epe1, a jmjC-domain-containing protein, is best-known as a negative regulator of heterochromatin spreading...
June 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28596682/diabetes-recurrence-after-metabolic-surgeries-correlates-with-re-impaired-insulin-sensitivity-rather-than-beta-cell-function
#20
Teng Liu, Ming-Wei Zhong, Yi Liu, Dong Sun, Meng Wei, Xin Huang, Yu-Gang Cheng, Qun-Zheng Wu, Dong Wu, Xiao-Qian Zhang, Ke-Xin Wang, San-Yuan Hu, Shao-Zhuang Liu
AIM: To investigate factors causing diabetes recurrence after sleeve gastrectomy (SG) and duodenal-jejunal bypass (DJB). METHODS: SG and DJB were performed on rats with diabetes induced by high-fat diet (HFD) and streptozotocin (STZ). HFD was used to induce diabetes recurrence at 4 wk postoperatively. Body weight, oral glucose tolerance test, homeostatic model assessment of insulin resistance (HOMA-IR), insulin signaling [IR, insulin receptor substrate (IRS)1, IRS2, phosphatidylinositol 3-kinase and AKT in liver and skeletal muscle], oral glucose stimulated insulin secretion, beta-cell morphology (mass, apoptosis and insulin secretion), glucagon-like peptide (GLP)-1, PYY and ghrelin were compared among SG rats with common low-fat diet (SG-LFD), SG with HFD (SG-HFD), DJB rats with LFD (DJB-LFD), DJB with HFD (DJB-HFD) and sham-operation with LFD (Sham) at targeted postoperative times...
May 21, 2017: World Journal of Gastroenterology: WJG
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