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NAD+ AND Insulin

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https://www.readbyqxmd.com/read/28193789/enriching-islet-phospholipids-with-eicosapentaenoic-acid-reduces-prostaglandin-e2-signaling-and-enhances-diabetic-%C3%AE-cell-function
#1
Joshua C Neuman, Michael D Schaid, Allison L Brill, Rachel J Fenske, Carly R Kibbe, Danielle A Fontaine, Sophia M Sdao, Harpreet K Brar, Kelsey M Connors, Haley N Wienkes, Kevin W Eliceiri, Matthew J Merrins, Dawn B Davis, Michelle E Kimple
Prostaglandin E2 (PGE2) is derived from arachidonic acid, while PGE3 is derived from eicosapentaenoic acid (EPA) using the same downstream metabolic enzymes. Little is known about the impact of EPA and PGE3 on β-cell function, particularly in the diabetic state. In this work, we determined PGE3 elicits a 10-fold weaker reduction in glucose-stimulated insulin secretion through the EP3 receptor as compared to PGE2 We tested the hypothesis that enriching pancreatic islet cell membranes with EPA, thereby reducing arachidonic acid abundance, would positively impact β-cell function in the diabetic state...
February 13, 2017: Diabetes
https://www.readbyqxmd.com/read/28178612/dietary-soy-protein-improves-adipose-tissue-dysfunction-by-modulating-parameters-related-with-oxidative-stress-in-dyslipidemic-insulin-resistant-rats
#2
Paola G Illesca, Silvina M Álvarez, Dante A Selenscig, María Del R Ferreira, María S Giménez, Yolanda B Lombardo, María E D'Alessandro
The present study investigates the benefits of the dietary intake of soy protein on adipose tissue dysfunction in a rat model that mimics several aspects of the human metabolic syndrome. Wistar rats were fed a sucrose-rich diet (SRD) for 4 months. After that, half of the animals continued with SRD until month 8 while in the other half, casein protein was replaced by isolated soy protein for 4 months (SRD-S). A reference group consumed a control diet all the time. In adipose tissue we determined: i) the activities of antioxidant enzymes, gene expression of Mn-superoxide dismutase (SOD) and glutathione peroxidase (GPx), and glutathione redox state ii) the activity of xanthine oxidase (XO), ROS levels and the gene expression of NAD(P)H oxidase iii) the expression of the nuclear factor erythroid-2 related factor-2 (Nrf2)...
February 5, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28122227/protection-against-high-fat-diet-induced-obesity-in-mdm2-c305f-mice-due-to-reduced-p53-activity-and-enhanced-energy-expenditure
#3
Shijie Liu, Tae-Hyung Kim, Derek A Franklin, Yanping Zhang
The RPL11-MDM2 interaction constitutes a p53 signaling pathway activated by deregulated ribosomal biosynthesis in response to stress. Mice bearing an MDM2(C305F) mutation that disrupts RPL11-MDM2 binding were analyzed on a high-fat diet (HFD). The Mdm2(C305F/C305F) mice, although phenotypically indistinguishable from wild-type (WT) mice when fed normal chow, demonstrated decreased fat accumulation along with improved insulin sensitivity and glucose tolerance after prolonged HFD feeding. We found that HFD increases expression of c-MYC and RPL11 in both WT and Mdm2(C305F/C305F) mice; however, p53 was induced in WT but not in Mdm2(C305F/C305F) mice...
January 24, 2017: Cell Reports
https://www.readbyqxmd.com/read/28068222/long-term-administration-of-nicotinamide-mononucleotide-mitigates-age-associated-physiological-decline-in-mice
#4
Kathryn F Mills, Shohei Yoshida, Liana R Stein, Alessia Grozio, Shunsuke Kubota, Yo Sasaki, Philip Redpath, Marie E Migaud, Rajendra S Apte, Koji Uchida, Jun Yoshino, Shin-Ichiro Imai
NAD(+) availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD(+) intermediate, has been shown to enhance NAD(+) biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD(+) in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice...
December 13, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/28003588/effectiveness-of-medium-chain-triglyceride-oil-therapy-in-two-japanese-citrin-deficient-siblings-evaluation-using-oral-glucose-tolerance-tests
#5
Hiroki Otsuka, Hideo Sasai, Elsayed Abdelkreem, Norio Kawamoto, Minako Kawamoto, Toshiya Kamiya, Yasuo Tanimoto, Atsuo Kikuchi, Shigeo Kure, Chikahiko Numakura, Kiyoshi Hayasaka, Toshiyuki Fukao
Citrin deficiency, an inherited defect of the liver-type mitochondrial aspartate/glutamate carrier isoform (citrin), may cause impairment of glycolysis because of an increase in the cytosolic NADH/NAD(+) ratio. We report a Japanese boy whose main complaint was recurrent hypoglycemic episodes. He was suspected as having citrin deficiency because of his peculiar preference for protein- and fat-rich food. His young sister also had a similar food preference. Both siblings were diagnosed with citrin deficiency by genetic analysis...
2016: Tohoku Journal of Experimental Medicine
https://www.readbyqxmd.com/read/27882448/sirtuins-and-their-roles-in-brain-aging-and-neurodegenerative-disorders
#6
Henryk Jęśko, Przemysław Wencel, Robert P Strosznajder, Joanna B Strosznajder
Sirtuins (SIRT1-SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD(+) levels and thus on the cellular metabolic status. SIRTs regulate energy metabolism and mitochondrial function. They orchestrate the stress response and damage repair. Through these functions sirtuins modulate the course of aging and affect neurodegenerative diseases. SIRTSs interact with multiple signaling proteins, transcription factors (TFs) and poly(ADP-ribose) polymerases (PARPs) another class of NAD(+)-dependent post-translational protein modifiers...
November 24, 2016: Neurochemical Research
https://www.readbyqxmd.com/read/27856259/potential-suppression-of-the-high-glucose-and-insulin-induced-retinal-neovascularization-by-sirtuin-3-in-the-human-retinal-endothelial-cells
#7
Xin-Bang Mao, Zhi-Peng You, Chen Wu, Jun Huang
Retinal neovascularization generally play roles in the formation of various severe eye diseases, such as age-related macular degeneration and diabetic retinopathy. The regulation of neovascularization-related pathways by Sirtuin 3 (Sirt3), a major mitochondrial NAD(+)-dependent deacetylase, give us a cue that Sirt3 may participate in the retinal neovascularization. However, the mechanism remains unclear. Here, we established a retinal neovascularization model by using human retinal endothelial cells (HRECs) under the induction of high glucose and insulin (HGI)...
January 8, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27735893/-neurological-complications-in-patients-with-diabetes-mellitus-type-1-treated-with-different-methods-of-insulinotherapy
#8
N F Shimkina, Yu G Nad', E R Barantsevich
: The study aims to examine the neurological complications of patients with type 1 diabetes treated with different methods of insulin therapy. MATERIAL AND METHODS: Thirty-four patients, aged from 18 to 40 years, with diabetes mellitus type 1 receiving insulinotherapy, with a duration of the disease 14.25±9.25 years, have been examined. By the time of the study the patients of the first group have been treated with continuous subcutaneous insulin infusion therapy (CSII) for 4...
2016: Zhurnal Nevrologii i Psikhiatrii Imeni S.S. Korsakova
https://www.readbyqxmd.com/read/27664519/nadph-oxidase-2-does-not-contribute-to-%C3%AE-cell-glucotoxicity-in-cultured-pancreatic-islets-from-c57bl-6j-mice
#9
Arnaldo H de Souza, Laila R B Santos, Leticia P Roma, Mohammed Bensellam, Angelo R Carpinelli, Jean-Christophe Jonas
High glucose-induced oxidative stress and increased NADPH oxidase-2 (NOX2) activity may contribute to the progressive decline of the functional β-cell mass in type 2 diabetes. To test that hypothesis, we characterized, in islets from male NOX2 knockout (NOX2-KO) and wild-type (WT) C57BL/6J mice cultured for up to 3 weeks at 10 or 30 mmol/l glucose (G10 or G30), the in vitro effects of glucose on cytosolic oxidative stress using probes sensing glutathione oxidation (GRX1-roGFP2), thiol oxidation (roGFP1) or H2O2 (roGFP2-Orp1), on β-cell stimulus-secretion coupling events and on β-cell apoptosis...
September 22, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/27634872/mitochondrial-aldehyde-dehydrogenase-obliterates-insulin-resistance-induced-cardiac-dysfunction-through-deacetylation-of-pgc-1%C3%AE
#10
Nan Hu, Jun Ren, Yingmei Zhang
Insulin resistance contributes to the high prevalence of type 2 diabetes mellitus, leading to cardiac anomalies. Emerging evidence depicts a pivotal role for mitochondrial injury in oxidative metabolism and insulin resistance. Mitochondrial aldehyde dehydrogenase (ALDH2) is one of metabolic enzymes detoxifying aldehydes although its role in insulin resistance remains elusive. This study was designed to evaluate the impact of ALDH2 overexpression on insulin resistance-induced myocardial damage and mechanisms involved with a focus on autophagy...
September 12, 2016: Oncotarget
https://www.readbyqxmd.com/read/27622707/benzylglucosinolate-derived-isothiocyanate-from-tropaeolum-majus-reduces-gluconeogenic-gene-and-protein-expression-in-human-cells
#11
Valentina Guzmán-Pérez, Christiane Bumke-Vogt, Monika Schreiner, Inga Mewis, Andrea Borchert, Andreas F H Pfeiffer
Nasturtium (Tropaeolum majus L.) contains high concentrations of benzylglcosinolate. We found that a hydrolysis product of benzyl glucosinolate-the benzyl isothiocyanate (BITC)-modulates the intracellular localization of the transcription factor Forkhead box O 1 (FOXO1). FoxO transcription factors can antagonize insulin effects and trigger a variety of cellular processes involved in tumor suppression, longevity, development and metabolism. The current study evaluated the ability of BITC-extracted as intact glucosinolate from nasturtium and hydrolyzed with myrosinase-to modulate i) the insulin-signaling pathway, ii) the intracellular localization of FOXO1 and, iii) the expression of proteins involved in gluconeogenesis, antioxidant response and detoxification...
2016: PloS One
https://www.readbyqxmd.com/read/27594836/head-to-head-comparison-of-short-term-treatment-with-the-nad-precursor-nicotinamide-mononucleotide-nmn-and-6-weeks-of-exercise-in-obese-female-mice
#12
Golam M Uddin, Neil A Youngson, David A Sinclair, Margaret J Morris
Obesity is well known to be a major cause of several chronic metabolic diseases, which can be partially counteracted by exercise. This is due, in part, to an upregulation of mitochondrial activity through increased nicotinamide adenine dinucleotide (NAD(+)). Recent studies have shown that NAD(+) levels can be increased by using the NAD(+) precursor, nicotinamide mononucleotide (NMN) leading to the suggestion that NMN could be a useful intervention in diet related metabolic disorders. In this study we compared the metabolic, and especially mitochondrial-associated, effects of exercise and NMN in ameliorating the consequences of high-fat diet (HFD) induced obesity in mice...
2016: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/27541013/monomeric-enampt-in-the-development-of-experimental-diabetes-in-mice-a-potential-target-for-type-2-diabetes-treatment
#13
Julius Kieswich, Sophie R Sayers, Marta F Silvestre, Steven M Harwood, Muhammad M Yaqoob, Paul W Caton
AIMS/HYPOTHESIS: Serum extracellular nicotinamide phosphoribosyltransferase (eNAMPT) concentrations are elevated in type 2 diabetes. However, the relationship between abnormally elevated serum eNAMPT and type 2 diabetes pathophysiology is unclear. eNAMPT circulates in functionally and structurally distinct monomeric and dimeric forms. Dimeric eNAMPT promotes NAD biosynthesis. The role of eNAMPT-monomer is unclear but it may have NAD-independent proinflammatory effects. However, studies of eNAMPT in type 2 diabetes have not distinguished between monomeric and dimeric forms...
November 2016: Diabetologia
https://www.readbyqxmd.com/read/27498863/nampt-mediated-nad-biosynthesis-in-adipocytes-regulates-adipose-tissue-function-and-multi-organ-insulin-sensitivity-in-mice
#14
Kelly L Stromsdorfer, Shintaro Yamaguchi, Myeong Jin Yoon, Anna C Moseley, Michael P Franczyk, Shannon C Kelly, Nathan Qi, Shin-Ichiro Imai, Jun Yoshino
Obesity is associated with adipose tissue dysfunction and multi-organ insulin resistance. However, the mechanisms of such obesity-associated systemic metabolic complications are not clear. Here, we characterized mice with adipocyte-specific deletion of nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting NAD(+) biosynthetic enzyme known to decrease in adipose tissue of obese and aged rodents and people. We found that adipocyte-specific Nampt knockout mice had severe insulin resistance in adipose tissue, liver, and skeletal muscle and adipose tissue dysfunction, manifested by increased plasma free fatty acid concentrations and decreased plasma concentrations of a major insulin-sensitizing adipokine, adiponectin...
August 16, 2016: Cell Reports
https://www.readbyqxmd.com/read/27479696/acetylation-control-of-cardiac-fatty-acid-%C3%AE-oxidation-and-energy-metabolism-in-obesity-diabetes-and-heart-failure
#15
REVIEW
Arata Fukushima, Gary D Lopaschuk
Alterations in cardiac energy metabolism are an important contributor to the cardiac pathology associated with obesity, diabetes, and heart failure. High rates of fatty acid β-oxidation with cardiac insulin resistance represent a cardiac metabolic hallmark of diabetes and obesity, while a marginal decrease in fatty acid oxidation and a prominent decrease in insulin-stimulated glucose oxidation are commonly seen in the early stages of heart failure. Alterations in post-translational control of energy metabolic processes have recently been identified as an important contributor to these metabolic changes...
December 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27456392/activation-of-the-ampk-sirt1-pathway-by-a-leucine-metformin-combination-increases-insulin-sensitivity-in-skeletal-muscle-and-stimulates-glucose-and-lipid-metabolism-and-increases-life-span-in-caenorhabditis-elegans
#16
Jheelam Banerjee, Antje Bruckbauer, Michael B Zemel
BACKGROUND: We have previously shown leucine (Leu) to activate Sirt1 by lowering its KM for NAD(+), thereby amplifying the effects of other sirtuin activators and improving insulin sensitivity. Metformin (Met) converges on this pathway both indirectly (via AMPK) and by direct activation of Sirt1, and we recently found Leu to synergize with Met to improve insulin sensitivity and glycemic control while achieving ~80% dose-reduction in diet-induced obese mice. Accordingly, we sought here to define the mechanism of this interaction...
November 2016: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/27449933/sirtuin-3-sirt3-protects-pancreatic-%C3%AE-cells-from-endoplasmic-reticulum-er-stress-induced-apoptosis-and-dysfunction
#17
Hao-Hao Zhang, Xiao-Jun Ma, Li-Na Wu, Yan-Yan Zhao, Peng-Yu Zhang, Ying-Hui Zhang, Ming-Wei Shao, Fei Liu, Fei Li, Gui-Jun Qin
Insufficient insulin produced by pancreatic β-cells in the control of blood sugar is a central feature of the etiology of diabetes. Reports have shown that endoplasmic reticulum (ER) stress is fundamentally involved in β-cell dysfunction. In this study, we hypothesized that NAD-dependent deacetylase sirtuin-3 (SIRT3), an important regulator of cell metabolism, protects pancreatic β-cells from ER stress-mediated apoptosis. To validate our hypothesis, a rat diabetic model was established by a high-fat diet (HFD)...
September 2016: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/27284112/pancreatic-%C3%AE-cells-from-mice-offset-age-associated-mitochondrial-deficiency-with-reduced-katp-channel-activity
#18
Trillian Gregg, Chetan Poudel, Brian A Schmidt, Rashpal S Dhillon, Sophia M Sdao, Nathan A Truchan, Emma L Baar, Luis A Fernandez, John M Denu, Kevin W Eliceiri, Jeremy D Rogers, Michelle E Kimple, Dudley W Lamming, Matthew J Merrins
Aging is accompanied by impaired glucose homeostasis and an increased risk of type 2 diabetes, culminating in the failure of insulin secretion from pancreatic β-cells. To investigate the effects of age on β-cell metabolism, we established a novel assay to directly image islet metabolism with NAD(P)H fluorescence lifetime imaging (FLIM). We determined that impaired mitochondrial activity underlies an age-dependent loss of insulin secretion in human islets. NAD(P)H FLIM revealed a comparable decline in mitochondrial function in the pancreatic islets of aged mice (≥24 months), the result of 52% and 57% defects in flux through complex I and II, respectively, of the electron transport chain...
September 2016: Diabetes
https://www.readbyqxmd.com/read/27255381/mechanisms-of-doxorubicin-toxicity-in-pancreatic-%C3%AE-cells
#19
Emma A Heart, Shpetim Karandrea, Xiaomei Liang, Maren E Balke, Patrick A Beringer, Elyse M Bobczynski, Delaine Zayas-Bazán Burgos, Tiffany Richardson, Joshua P Gray
Exposure to chemotherapeutic agents has been linked to an increased risk of type 2 diabetes (T2D), a disease characterized by both the peripheral insulin resistance and impaired glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells. Using the rat β-cell line INS-1 832/13 and isolated mouse pancreatic islets, we investigated the effect of the chemotherapeutic drug doxorubicin (Adriamycin) on pancreatic β-cell survival and function. Exposure of INS-1 832/13 cells to doxorubicin caused impairment of GSIS, cellular viability, an increase in cellular toxicity, as soon as 6 h post-exposure...
August 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/27230286/nicotinamide-riboside-opposes-type-2-diabetes-and-neuropathy-in-mice
#20
Samuel A J Trammell, Benjamin J Weidemann, Ankita Chadda, Matthew S Yorek, Amey Holmes, Lawrence J Coppey, Alexander Obrosov, Randy H Kardon, Mark A Yorek, Charles Brenner
Male C57BL/6J mice raised on high fat diet (HFD) become prediabetic and develop insulin resistance and sensory neuropathy. The same mice given low doses of streptozotocin are a model of type 2 diabetes (T2D), developing hyperglycemia, severe insulin resistance and diabetic peripheral neuropathy involving sensory and motor neurons. Because of suggestions that increased NAD(+) metabolism might address glycemic control and be neuroprotective, we treated prediabetic and T2D mice with nicotinamide riboside (NR) added to HFD...
May 27, 2016: Scientific Reports
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