64 results on '"Viscarra, Jose A."'
Search Results
52. Glut4 is upregulated despite decreased insulin signaling during prolonged fasting in northern elephant seal pups
- Author
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Viscarra, Jose A., primary, Vázquez-Medina, José Pablo, additional, Crocker, Daniel E., additional, and Ortiz, Rudy M., additional
- Published
- 2011
- Full Text
- View/download PDF
53. Blockade of the Renin‐Angiotensin System Improves Glucose Intolerance in Pre‐diabetic Rats on a High Glucose Diet
- Author
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Rodriguez, Ruben, primary, Viscarra, Jose, additional, Nakano, Daisuke, additional, Nishiyama, Akira, additional, and Ortiz, Rudy M., additional
- Published
- 2010
- Full Text
- View/download PDF
54. Prolonged fasting suppresses cellular insulin‐dependent activity in adipose tissue of the northern elephant seal
- Author
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Viscarra, Jose Abraham, primary, Vazquez‐Medina, Jose Pablo, additional, Minas, Jacqueline, additional, Crocker, Daniel E., additional, and Ortiz, Rudy M., additional
- Published
- 2010
- Full Text
- View/download PDF
55. Prolonged food deprivation increases mRNA expression of deiodinase 1 and 2, and thyroid hormone receptor ß-1 in a fasting-adapted mammal.
- Author
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Martinez, Bridget, Soñanez-Organis, José G., Vázquez-Medina, José Pablo, Viscarra, Jose A., MacKenzie, Duncan S., Crocker, Daniel E., and Ortiz, Rudy M.
- Subjects
ANIMAL feeds ,MESSENGER RNA ,GENE expression ,GENE expression in mammals ,IODIDE peroxidase ,THYROID hormone receptors ,MAMMAL metabolism - Abstract
Food deprivation in mammals is typically associated with reduced thyroid hormone (TH) concentrations and deiodinase content and activity to suppress metabolism. However, in prolonged-fasted, metabolically active elephant seal pups, TH levels are maintained, if not elevated. The functional relevance of this apparent paradox is unknown and demonstrates variability in the regulation of TH levels, metabolism and function in food-deprived mammals. To address our hypothesis that cellular TH-mediated activity is upregulated with fasting duration, we quantified the mRNA expression and protein content of adipose and muscle deiodinase type I (DI1) and type II (DI2), and TH receptor beta-1 (THrß-1) after 1, 3 and 7 weeks of fasting in northern elephant seal pups (N=5-7 per week). Fasting did not decrease the concentrations of plasma thyroid stimulating hormone, total triiodothyronine (tT3), free T3, total thyroxine (tT4) or free T4, suggesting that the hypothalamic-pituitary-thyroid axis is not suppressed, but rather maintained during fasting. Mean mRNA expression of adipose DI1 and DI2 increased threefold and fourfold, respectively, and 20- and 30-fold, respectively, in muscle. With the exception of adipose DI1, protein expression of adipose DI2 and muscle DI1 and DI2 increased twofold to fourfold. Fasting also increased adipose (fivefold) and muscle (fourfold) THrß-1 mRNA expression, suggesting that the mechanisms mediating cellular TH activity are upregulated with prolonged fasting. The data demonstrate a unique, atypical mechanism of TH activity and regulation in mammals adapted to prolonged food deprivation in which the potential responsiveness of peripheral tissues and cellular TH activity are increased, which may contribute to their lipid-based metabolism. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
56. Activation of systemic, but not local, renin-angiotensin system is associated with upregulation of TNF-a during prolonged fasting in northern elephant seal pups.
- Author
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Suzuki, Miwa, Vázquez-Medina, José Pablo, Viscarra, Jose A., Soñanez-Organis, José G., Crocker, Daniel E., and Ortiz, Rudy M.
- Subjects
RENIN-angiotensin system ,FASTING ,NORTHERN elephant seal ,ADIPONECTIN ,INSULIN resistance ,ANGIOTENSIN II - Abstract
Northern elephant seal pups naturally endure a 2-3?month post-weaning fast that is associated with activation of systemic renin-angiotensin system (RAS), a decrease in plasma adiponectin (Acrp30), and insulin resistance (IR)-like conditions. Angiotensin II (Ang II) and tumor necrosis factor-alpha (TNF-a) are potential causal factors of IR, while Acrp30 may improve insulin signaling. However, the effects of fasting-induced activation of RAS on IR-like conditions in seals are not well described. To assess the effects of prolonged food deprivation on systemic and local RAS, and their potential contribution to TNF-a as they relate to an IR condition, the mRNA expressions of adipose and muscle RAS components and immuno-relevant molecules were measured along with plasma RAS components. Mean plasma renin activity and Ang II concentrations increased by 89 and 1658%, respectively, while plasma angiotensinogen (AGT) decreased by 49% over the fast, indicative of systemic RAS activation. Prolonged fasting was associated with decreases in adipose and muscle AGT mRNA expressions of 69 and 68%, respectively, corresponding with decreases in tissue protein content, suggesting suppression of local AGT production. Muscle TNF-a mRNA and protein increased by 239 and 314%, whereas those of adipose Acrp30 decreased by 32 and 98%, respectively. Collectively, this study suggests that prolonged fasting activates a systemic RAS, which contributes to an increase in muscle TNF-a and suppression of adipose Acrp30. This targeted and tissue-specific regulation of TNF-a and Acrp30 is likely coordinated to synergistically contribute to the development of an IR-like condition, independent of local RAS activity. These data enhance our understanding of the adaptive mechanisms evolved by elephant seals to tolerate potentially detrimental conditions. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
57. Innovative Methods for Using Census Data to Study Poverty, Labor Markets, and Policy
- Author
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Pacas Viscarra, Jose
- Subjects
- Labor economics, Labor unions, Policy analysis, Poverty
- Abstract
This dissertation studies poverty, labor markets, and policy. Integral to this effort are innovative methods for using Census data to study these topics. The dissertation consists of three chapters. The first chapter studies year-to-year poverty transitions in the United States. The second chapter measures the extent to which individuals’ union membership status affects the levels of taxes they pay and the cost of public benefits they receive. The third chapter analyzes how the electronic employment verification system, known as E-Verify, affects the labor market outcomes of unauthorized immigrants.
- Published
- 2017
58. Transcriptional regulation of hepatic lipogenesis
- Author
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Wang, Yuhui, Viscarra, Jose, Kim, Sun-Joong, and Sul, Hei Sook
- Published
- 2016
- Full Text
- View/download PDF
59. Exogenous GLP-1 stimulates TCA cycle and suppresses gluconeogenesis and ketogenesis in late-fasted northern elephant seals pups.
- Author
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Dhillon J, Viscarra JA, Newman JW, Fiehn O, Crocker DE, and Ortiz RM
- Subjects
- Animals, Biomarkers blood, Blood Glucose metabolism, Dose-Response Relationship, Drug, Fasting blood, Infusions, Intravenous, Male, Metabolome, Metabolomics, Seals, Earless blood, Time Factors, Weaning, Blood Glucose drug effects, Citric Acid Cycle drug effects, Glucagon-Like Peptide 1 administration & dosage, Gluconeogenesis drug effects, Ketone Bodies metabolism, Seals, Earless metabolism
- Abstract
The postweaning fast of northern elephant seal pups is characterized by a lipid-dependent metabolism and associated with a decrease in plasma glucagon-like peptide-1 (GLP-1), insulin, and glucose and increased gluconeogenesis (GNG) and ketogenesis. We have also demonstrated that exogenous GLP-1 infusion increased plasma insulin despite simultaneous increases in cortisol and glucagon, which collectively present contradictory regulatory stimuli of GNG, ketogenesis, and glycolysis. To assess the effects of GLP-1 on metabolism using primary carbon metabolite profiles in late-fasted seal pups, we dose-dependently infused late-fasted seals with low (LDG; 10 pM/kg; n = 3) or high (HDG; 100 pM/kg; n = 4) GLP-1 immediately following a glucose bolus (0.5 g/kg), using glucose without GLP-1 as control ( n = 5). Infusions were performed in similarly aged animals 6-8 wk into their postweaning fast. The plasma metabolome was measured from samples collected at five time points just prior to and during the infusions, and network maps constructed to robustly evaluate the effects of GLP-1 on primary carbon metabolism. HDG increased key tricarboxylic acid (TCA) cycle metabolites, and decreased phosphoenolpyruvate and acetoacetate ( P < 0.05) suggesting that elevated levels of GLP-1 promote glycolysis and suppress GNG and ketogenesis, which collectively increase glucose clearance. These GLP-1-mediated effects on cellular metabolism help to explain why plasma GLP-1 concentrations decrease naturally in fasting pups as an evolved mechanism to help conserve glucose during the late-fasting period.
- Published
- 2021
- Full Text
- View/download PDF
60. Glucose delays the insulin-induced increase in thyroid hormone-mediated signaling in adipose of prolong-fasted elephant seal pups.
- Author
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Martinez B, Soñanez-Organis JG, Viscarra JA, Jaques JT, MacKenzie DS, Crocker DE, and Ortiz RM
- Subjects
- Animals, Gene Expression drug effects, Hypothalamo-Hypophyseal System drug effects, Infusions, Intravenous, Iodide Peroxidase biosynthesis, RNA, Messenger biosynthesis, RNA, Messenger genetics, Thyroid Gland drug effects, Thyroid Hormone Receptors beta biosynthesis, Thyroid Hormones blood, Thyroid Hormones genetics, Adipose Tissue drug effects, Adipose Tissue metabolism, Fasting metabolism, Glucose pharmacology, Insulin pharmacology, Seals, Earless, Signal Transduction drug effects, Thyroid Hormones biosynthesis
- Abstract
Prolonged food deprivation in mammals typically reduces glucose, insulin, and thyroid hormone (TH) concentrations, as well as tissue deiodinase (DI) content and activity, which, collectively, suppress metabolism. However, in elephant seal pups, prolonged fasting does not suppress TH levels; it is associated with upregulation of adipose TH-mediated cellular mechanisms and adipose-specific insulin resistance. The functional relevance of this apparent paradox and the effects of glucose and insulin on TH-mediated signaling in an insulin-resistant tissue are not well defined. To address our hypothesis that insulin increases adipose TH signaling in pups during extended fasting, we assessed the changes in TH-associated genes in response to an insulin infusion in early- and late-fasted pups. In late fasting, insulin increased DI1, DI2, and THrβ-1 mRNA expression by 566%, 44%, and 267% at 60 min postinfusion, respectively, with levels decreasing by 120 min. Additionally, we performed a glucose challenge in late-fasted pups to differentiate between insulin- and glucose-mediated effects on TH signaling. In contrast to the insulin-induced effects, glucose infusion did not increase the expressions of DI1, DI2, and THrβ-1 until 120 min, suggesting that glucose delays the onset of the insulin-induced effects. The data also suggest that fasting duration increases the sensitivity of adipose TH-mediated mechanisms to insulin, some of which may be mediated by increased glucose. These responses appear to be unique among mammals and to have evolved in elephant seals to facilitate their adaptation to tolerate an extreme physiological condition., (Copyright © 2016 the American Physiological Society.)
- Published
- 2016
- Full Text
- View/download PDF
61. Activation of systemic, but not local, renin-angiotensin system is associated with upregulation of TNF-α during prolonged fasting in northern elephant seal pups.
- Author
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Suzuki M, Vázquez-Medina JP, Viscarra JA, Soñanez-Organis JG, Crocker DE, and Ortiz RM
- Subjects
- Adiponectin metabolism, Adipose Tissue metabolism, Animals, California, Chemokine CCL2 metabolism, DNA, Complementary genetics, DNA, Complementary metabolism, Insulin Resistance, Molecular Sequence Data, RNA, Messenger genetics, RNA, Messenger metabolism, Real-Time Polymerase Chain Reaction, Seals, Earless genetics, Seals, Earless growth & development, Sequence Analysis, DNA, Time Factors, Tumor Necrosis Factor-alpha metabolism, Up-Regulation, Adiponectin genetics, Chemokine CCL2 genetics, Food Deprivation physiology, Renin-Angiotensin System, Seals, Earless physiology, Tumor Necrosis Factor-alpha genetics
- Abstract
Northern elephant seal pups naturally endure a 2-3 month post-weaning fast that is associated with activation of systemic renin-angiotensin system (RAS), a decrease in plasma adiponectin (Acrp30), and insulin resistance (IR)-like conditions. Angiotensin II (Ang II) and tumor necrosis factor-alpha (TNF-α) are potential causal factors of IR, while Acrp30 may improve insulin signaling. However, the effects of fasting-induced activation of RAS on IR-like conditions in seals are not well described. To assess the effects of prolonged food deprivation on systemic and local RAS, and their potential contribution to TNF-α as they relate to an IR condition, the mRNA expressions of adipose and muscle RAS components and immuno-relevant molecules were measured along with plasma RAS components. Mean plasma renin activity and Ang II concentrations increased by 89 and 1658%, respectively, while plasma angiotensinogen (AGT) decreased by 49% over the fast, indicative of systemic RAS activation. Prolonged fasting was associated with decreases in adipose and muscle AGT mRNA expressions of 69 and 68%, respectively, corresponding with decreases in tissue protein content, suggesting suppression of local AGT production. Muscle TNF-α mRNA and protein increased by 239 and 314%, whereas those of adipose Acrp30 decreased by 32 and 98%, respectively. Collectively, this study suggests that prolonged fasting activates a systemic RAS, which contributes to an increase in muscle TNF-α and suppression of adipose Acrp30. This targeted and tissue-specific regulation of TNF-α and Acrp30 is likely coordinated to synergistically contribute to the development of an IR-like condition, independent of local RAS activity. These data enhance our understanding of the adaptive mechanisms evolved by elephant seals to tolerate potentially detrimental conditions.
- Published
- 2013
- Full Text
- View/download PDF
62. Angiotensin receptor-mediated oxidative stress is associated with impaired cardiac redox signaling and mitochondrial function in insulin-resistant rats.
- Author
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Vázquez-Medina JP, Popovich I, Thorwald MA, Viscarra JA, Rodriguez R, Sonanez-Organis JG, Lam L, Peti-Peterdi J, Nakano D, Nishiyama A, and Ortiz RM
- Subjects
- Aldehydes metabolism, Angiotensin II Type 1 Receptor Blockers pharmacology, Animals, Catalase metabolism, Citrate (si)-Synthase metabolism, Disease Models, Animal, Gene Expression Regulation, Enzymologic, Glutathione Peroxidase metabolism, Imidazoles pharmacology, Male, Membrane Glycoproteins genetics, Membrane Glycoproteins metabolism, NADPH Oxidase 2, NADPH Oxidase 4, NADPH Oxidases genetics, NADPH Oxidases metabolism, NF-E2-Related Factor 2 metabolism, Obesity genetics, Obesity physiopathology, Oxidation-Reduction, RNA, Messenger metabolism, Rats, Rats, Inbred OLETF, Receptor, Angiotensin, Type 1 drug effects, Succinate Dehydrogenase metabolism, Superoxide Dismutase metabolism, Tetrazoles pharmacology, Time Factors, Tyrosine analogs & derivatives, Tyrosine metabolism, Insulin Resistance, Mitochondria, Heart metabolism, Myocardium metabolism, Obesity metabolism, Oxidative Stress drug effects, Receptor, Angiotensin, Type 1 metabolism, Signal Transduction drug effects
- Abstract
Activation of angiotensin receptor type 1 (AT1) contributes to NADPH oxidase (Nox)-derived oxidative stress during metabolic syndrome. However, the specific role of AT1 in modulating redox signaling, mitochondrial function, and oxidative stress in the heart remains more elusive. To test the hypothesis that AT1 activation increases oxidative stress while impairing redox signaling and mitochondrial function in the heart during diet-induced insulin resistance in obese animals, Otsuka Long Evans Tokushima Fatty (OLETF) rats (n = 8/group) were treated with the AT1 blocker (ARB) olmesartan for 6 wk. Cardiac Nox2 protein expression increased 40% in OLETF compared with age-matched, lean, strain-control Long Evans Tokushima Otsuka (LETO) rats, while mRNA and protein expression of the H₂O₂-producing Nox4 increased 40-100%. ARB treatment prevented the increase in Nox2 without altering Nox4. ARB treatment also normalized the increased levels of protein and lipid oxidation (nitrotyrosine, 4-hydroxynonenal) and increased the redox-sensitive transcription factor Nrf2 by 30% and the activity of antioxidant enzymes (SOD, catalase, GPx) by 50-70%. Citrate synthase (CS) and succinate dehydrogenase (SDH) activities decreased 60-70%, whereas cardiac succinate levels decreased 35% in OLETF compared with LETO, suggesting that mitochondrial function in the heart is impaired during obesity-induced insulin resistance. ARB treatment normalized CS and SDH activities, as well as succinate levels, while increasing AMPK and normalizing Akt, suggesting that AT1 activation also impairs cellular metabolism in the diabetic heart. These data suggest that the cardiovascular complications associated with metabolic syndrome may result from AT1 receptor-mediated Nox2 activation leading to impaired redox signaling, mitochondrial activity, and dysregulation of cellular metabolism in the heart.
- Published
- 2013
- Full Text
- View/download PDF
63. Prolonged fasting activates Nrf2 in post-weaned elephant seals.
- Author
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Vázquez-Medina JP, Soñanez-Organis JG, Rodriguez R, Viscarra JA, Nishiyama A, Crocker DE, and Ortiz RM
- Subjects
- Amino Acid Sequence, Angiotensin II blood, Animals, Conserved Sequence, Fasting blood, Female, Male, Mice, Models, Biological, Molecular Sequence Data, NADPH Oxidases chemistry, NADPH Oxidases metabolism, Rats, Seals, Earless blood, Signal Transduction, Smad Proteins metabolism, Transforming Growth Factor beta blood, Fasting physiology, NF-E2-Related Factor 2 metabolism, Seals, Earless metabolism, Weaning
- Abstract
Elephant seals naturally experience prolonged periods of absolute food and water deprivation (fasting). In humans, rats and mice, prolonged food deprivation activates the renin-angiotensin system (RAS) and increases oxidative damage. In elephant seals, prolonged fasting activates RAS without increasing oxidative damage likely due to an increase in antioxidant defenses. The mechanism leading to the upregulation of antioxidant defenses during prolonged fasting remains elusive. Therefore, we investigated whether prolonged fasting activates the redox-sensitive transcription factor Nrf2, which controls the expression of antioxidant genes, and if such activation is potentially mediated by systemic increases in RAS. Blood and skeletal muscle samples were collected from seals fasting for 1, 3, 5 and 7 weeks. Nrf2 activity and nuclear content increased by 76% and 167% at week 7. Plasma angiotensin II (Ang II) and transforming growth factor β (TGF-β) were 5000% and 250% higher at week 7 than at week 1. Phosphorylation of Smad2, an effector of Ang II and TGF signaling, increased by 120% at week 7 and by 84% in response to intravenously infused Ang II. NADPH oxidase 4 (Nox4) mRNA expression, which is controlled by smad proteins, increased 430% at week 7, while Nox4 protein expression, which can activate Nrf2, was 170% higher at week 7 than at week 1. These results demonstrate that prolonged fasting activates Nrf2 in elephant seals and that RAS stimulation can potentially result in increased Nox4 through Smad phosphorylation. The results also suggest that Nox4 is essential to sustain the hormetic adaptive response to oxidative stress in fasting seals.
- Published
- 2013
- Full Text
- View/download PDF
64. Glut4 is upregulated despite decreased insulin signaling during prolonged fasting in northern elephant seal pups.
- Author
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Viscarra JA, Vázquez-Medina JP, Crocker DE, and Ortiz RM
- Subjects
- Adiponectin blood, Adipose Tissue metabolism, Animals, Animals, Newborn metabolism, Blood Glucose metabolism, Hydrocortisone blood, Insulin Resistance physiology, Models, Animal, Muscle, Skeletal metabolism, Fasting metabolism, Glucose Transporter Type 4 metabolism, Insulin metabolism, Seals, Earless metabolism, Signal Transduction physiology, Up-Regulation physiology
- Abstract
Postprandial cellular glucose uptake is dependent on an insulin-signaling cascade in muscle and adipose tissue, resulting in the translocation of the insulin-dependent glucose transporter 4 (Glut4) into the plasma membrane. Additionally, extended food deprivation is characterized by suppressed insulin signaling and decreased Glut4 expression. Northern elephant seals are adapted to prolonged fasts characterized by high levels of plasma glucose. To address the hypothesis that the fasting-induced decrease in insulin is associated with reduced insulin signaling in prolonged fasted seals, we compared the adipose protein levels of the cellular insulin-signaling pathway, Glut4 and plasma glucose, insulin, cortisol, and adiponectin concentrations between Early (n = 9; 2-3 wks postweaning) and Late (n = 8; 6-8 wks postweaning) fasted seals. Plasma adiponectin (230 ± 13 vs. 177 ± 11 ng/ml), insulin (2.7 ± 0.4 vs. 1.0 ± 0.1 μU/ml), and glucose (9.8 ± 0.5 vs. 8.0 ± 0.3 mM) decreased, while cortisol (124 ± 6 vs. 257 ± 30 nM) doubled with fasting. Glut4 increased (31%) with fasting despite the significant decreases in the cellular content of phosphatidylinositol 3-kinase as well as phosphorylated insulin receptor, insulin receptor substrate-1, and Akt2. Increased Glut4 may have contributed to the decrease in plasma glucose, but the decrease in insulin and insulin signaling suggests that Glut4 is not insulin-dependent in adipose tissue during prolonged fasting in elephant seals. The reduction of plasma glucose independent of insulin may make these animals an ideal model for the study of insulin resistance.
- Published
- 2011
- Full Text
- View/download PDF
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