Viviane Delghingaro‐Augusto

ORCID: 0000-0002-5107-2384
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About
Contact & Profiles
Research Areas
  • Pancreatic function and diabetes
  • Adipose Tissue and Metabolism
  • Diet, Metabolism, and Disease
  • Diabetes and associated disorders
  • Metabolism, Diabetes, and Cancer
  • Birth, Development, and Health
  • Respiratory Support and Mechanisms
  • Diet and metabolism studies
  • Cardiac and Coronary Surgery Techniques
  • Diabetes Treatment and Management
  • Diabetes Management and Research
  • Optical Coherence Tomography Applications
  • Gestational Diabetes Research and Management
  • Nitric Oxide and Endothelin Effects
  • Advanced Fluorescence Microscopy Techniques
  • Airway Management and Intubation Techniques
  • Cellular Mechanics and Interactions
  • Pregnancy and preeclampsia studies
  • Regulation of Appetite and Obesity
  • Cardiac Ischemia and Reperfusion
  • Nutrition and Health in Aging
  • Asthma and respiratory diseases
  • Circadian rhythm and melatonin
  • Peroxisome Proliferator-Activated Receptors
  • Hemodynamic Monitoring and Therapy

Australian National University
2011-2025

Université de Montréal
2004-2014

Canberra Hospital
2011-2013

Universidade de Ribeirão Preto
2009-2012

Universidade de São Paulo
2008-2012

Clinics Hospital of Ribeirão Preto
2011

Diabetes Research Center
2010

Centre Hospitalier de l’Université de Montréal
2004-2009

Universidade Estadual de Campinas (UNICAMP)
2001-2004

University of Lausanne
2004

The malonyl-CoA/long-chain acyl-CoA (LC-CoA) model of glucose-induced insulin secretion (GIIS) predicts that malonyl-CoA derived from glucose metabolism inhibits fatty acid oxidation, thereby increasing the availability LC-CoA for lipid signaling to cellular processes involved in exocytosis. For directly testing model, INSr3 cell clones overexpressing decarboxylase cytosol (MCDc) a tetracycline regulatable manner were generated, and INS(832/13) rat islets infected with MCDc-expressing...

10.2337/diabetes.53.4.1007 article EN Diabetes 2004-04-01

The failure of pancreatic β cells to adapt an increasing demand for insulin is the major mechanism by which patients progress from resistance type 2 diabetes (T2D) and thought be related dysfunctional lipid homeostasis within those cells. In multiple animal models diabetes, females demonstrate relative protection cell failure. We previously found that hormone 17β-estradiol (E2) in part mediates this benefit. Here, we show treating male Zucker diabetic fatty (ZDF) rats with E2 suppressed...

10.1172/jci44564 article EN Journal of Clinical Investigation 2011-07-11

Abstract Aims/hypothesis Pancreatic beta cell dedifferentiation, transdifferentiation into other islet cells and apoptosis have been implicated in failure type 2 diabetes, although the mechanisms are poorly defined. The endoplasmic reticulum stress response factor X-box binding protein 1 (XBP1) is a major regulator of unfolded response. XBP1 expression reduced islets people with but its role adult differentiated unclear. Here, we assessed effects Xbp1 deletion tested whether XBP1-mediated...

10.1007/s00125-022-05669-7 article EN cc-by Diabetologia 2022-03-22

Obese Alms1 mutant (foz/foz) NOD.B10 mice develop diabetes and fibrotic NASH when fed high-fat(HF) diet. To establish whether or obesity is more closely associated with fibrosis, we compared diabetic foz/foz C57BL6/J non-diabetic BALB/c mice. We also determined hepatic cytokines, growth factors related profibrotic pathways.Male female were HF chow for 24 weeks before determining metabolic indices, liver injury, factors, pathology/fibrosis matrix deposition pathways.All obese. Hepatomegaly,...

10.1111/liv.12335 article EN Liver International 2013-10-12

Type 2 diabetes is a metabolic disorder characterized by the inability of beta-cells to secrete enough insulin maintain glucose homeostasis. MIN6 cells in response and other secretagogues, but high passage (HP) lose their ability glucose. We hypothesized that metabolism lipids were defective HP causing impaired stimulated secretion (GSIS). had no first phase second GSIS indicative global functional impairment. This was coupled with markedly reduced ATP content at basal states. Glucose uptake...

10.1371/journal.pone.0040868 article EN cc-by PLoS ONE 2012-07-13

Abstract Context The obesity epidemic parallels an increasing type 1 diabetes incidence, such that westernized diets, containing high fat, sugar and/or protein, through inducing nutrient-induced islet beta-cell stress, have been proposed as contributing factors. broad-spectrum neutral amino acid transporter (B0AT1), encoded by Slc6a19, is the major acids in intestine and kidney. B0AT1 deficiency C567Bl/6J mice, causes aminoaciduria, lowers insulinemia improves glucose tolerance. Objective We...

10.1210/endocr/bqaf016 article EN cc-by-nc-nd Endocrinology 2025-01-23

The cellular response to fasting and starvation in tissues such as heart, skeletal muscle, liver requires peroxisome proliferator-activated receptor-alpha (PPARalpha)-dependent up-regulation of energy metabolism toward fatty acid oxidation (FAO). PPARalpha null (PPARalphaKO) mice develop hyperinsulinemic hypoglycemia the state, we previously showed that expression is increased islets at low glucose. On this basis, hypothesized enhanced FAO, via depletion lipid-signaling molecule(s) for...

10.1210/en.2004-0667 article EN Endocrinology 2004-12-15

Short-term cold exposure of homeothermic animals leads to higher thermogenesis and food consumption accompanied by weight loss. An analysis cDNA-macroarray was employed identify candidate mRNA species that encode proteins involved in thermogenic adaptation cold. A analysis, confirmed RT-PCR, immunoblot, RIA, revealed the hypothalamic expression melanin-concentrating hormone (MCH) is enhanced rats environment. The blockade MCH antisense oligonucleotide cold-exposed promoted no changes feeding...

10.1210/en.2003-0243 article EN Endocrinology 2003-07-29

Physical activity improves glycemic control in type 2 diabetes (T2D), but its contribution to preserving β-cell function is uncertain. We evaluated the role of physical on secretory and glycerolipid/fatty acid (GL/FA) cycling male Zucker diabetic fatty (ZDF) rats. Six-week-old ZDF rats engaged voluntary running for 6 wk (ZDF-A). Inactive lean (ZDF-I) served as controls. ZDF-I displayed progressive hyperglycemia with failure evidenced by falling insulinemia reduced insulin secretion oral...

10.1152/ajpendo.00360.2011 article EN AJP Endocrinology and Metabolism 2011-11-02

Hyperinsulinemia associated with non-ketotic hypoglycemia is observed in patients mutated β-oxidation enzyme short-chain 3-hydroxyacyl-CoA dehydrogenase (HADHSC). In the present study, we investigated mechanism underlying HADHSC-mediated regulation of insulin secretion.Knockdown HADHSC expression by RNA interference INS832/13 β-cells was achieved using short hairpin and RNA.Knockdown increased both fuel- (glucose or leucine plus glutamine) non-fuel (high KCl)-induced secretion. Enhanced...

10.1111/j.1753-0407.2010.00076.x article EN Journal of Diabetes 2010-04-23

In this study, we examined glucose homeostasis and insulin secretion in transgenic mice overexpressing the human apolipoprotein CIII gene (apo tg). These have elevated plasma levels of triglycerides, FFA cholesterol compared to control mice. The body weight, glucose, levels, disappearance rates, areas under ipGTT curve for adult (4 - 8 mo. old) aged (20 24 apo tg determination during were not different from those However, an additional elevation by treatment with heparin 2 4 h impaired...

10.1055/s-2002-19962 article EN Hormone and Metabolic Research 2002-01-01
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