Gabriel Forato Anhê

Universidade de São Paulo

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Silvana Bordin

Universidade de São Paulo

Edson Antunes

Universidade Estadual de Campinas (UNICAMP)

Luciana C. Caperuto

Universidade Federal de São Paulo

Carla Roberta de Oliveira Carvalho

Universidade de São Paulo

Rui Curi

Instituto Butantan

Lı́cio A. Velloso

Universidade Estadual de Campinas (UNICAMP)

Caio Jordão Teixeira

Universidade de São Paulo

José Cipolla‐Neto

Universidade de São Paulo

Camilo Lellis‐Santos

Universidade Federal de São Paulo

Dailson Nogueira de Souza

Universidade Estadual de Campinas (UNICAMP)

Cooperative Institutions

Universidade Estadual de Campinas (UNICAMP)

233

Institute of Molecular Biology and Biophysics

201

Universidade de São Paulo

159

Hospital de Clínicas da Unicamp

Universidade Estadual Paulista (Unesp)

Institute of Biomedical Science

Universidade Brasil

Universidade Federal de São Paulo

Harvard University

Pontifícia Universidade Católica de Campinas

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Increased arterial stiffness in resistant hypertension is associated with inflammatory biomarkers

Blood Pressure (2014)

Natália R. Barbaro Vanessa Fontana Rodrigo Modolo Ana Paula de Faria A. Sabbatini

Increased levels of inflammatory biomarkers such as interleukin-6 (IL-6), 10 (IL-10), 1β (IL-1β), tumor necrosis factor-α (TNF-α) high-sensitivity C-reactive protein (hs-CRP) are associated with arterial stiffness in hypertension. Indeed, resistant hypertension (RHTN) leads to unfavorable prognosis attributed to poor blood pressure (BP) control and target organ damage. This study evaluated the potential impact of inflammatory biomarkers on arterial stiffness in RHTN.In this cross-sectional study, 32 RHTN, 20 mild hypertensive (HTN) and 20 normotensive (NT) patients were subjected to office BP and arterial stiffness measurements assessed by pulse wave velocity (PWV). Inflammatory biomarkers were measured in plasma samples.PWV was increased in RHTN compared with HTN and NT (p < 0.05). TNF-α levels were significantly higher in RHTN and HTN than NT patients. No differences in IL-6 levels were observed. RHTN patients had a higher frequency of subjects with increased levels of IL-10 and IL-1β compared with HTN and NT patients. Finally, IL-1β was independently associated with PWV (p < 0.001; R(2) = 0.5; β = 0.077).RHTN subjects have higher levels of inflammatory cytokines (TNF-α, IL-1β and IL-10) as well as increased arterial stiffness, and detectable IL-1β levels are associated arterial stiffness. These findings suggest that inflammation plays a possible role in the pathophysiology of RHTN.

Pathophysiology

10.3109/08037051.2014.940710

Cite

Citations (96)

Investigação do efeito da gestação seguida de lactação na modulação de miRNAs de ilhotas pancreáticas maternas

Revista dos Trabalhos de Iniciação Científica da UNICAMP (2019)

Julia Modesto Vicente Gabriel Forato Anhê Júnia Carolina Rebelo dos Santos Silva Dailson Nogueira de Souza Caio Jordão Teixeira

Uma série de estudos mostra que a duração do período de amamentação tem uma relação inversa com o risco das mães desenvolverem Diabetes Mellitus tipo 2. O presente estudo dividiu fêmeas de camundongo em três grupos: Controle (Virgem), sem lactação após o parto (L0) e 21 dias de lactação após o parto (L21). Esses animais foram submetidos a dois ciclos de gestação e desmame. Dois meses depois do último desmame, as fêmeas foram submetidas ao teste de tolerância à glicose (GTT) e tolerância à insulina (ITT). Após o sacrifício dos animais, foram coletados fígado e pâncreas para rastreamento de lipídeos no tecido hepático, secreção de insulina e investigação de microRNAs (miRNAs) nas ilhotas pancreáticas. As fêmeas do grupo L21 apresentaram maior tolerância à glicose e não houve diferença na tolerância à insulina entre os grupos. No grupo L0, ocorreu maior acúmulo de gordura no fígado. As fêmeas do grupo L21 adquiriram maior capacidade de secretar insulina e o miRNA 7b-3p e 7a-3p estava menos expresso nesses mesmos animais.

10.20396/revpibic262018717

Cite

Citations (1)

Tumor necrosis factor alpha has a crucial role in increased reactive oxygen species production in platelets of mice injected with lipopolysaccharide

Platelets (2019)

Ana Carolina Antunes Naime Pedro Henrique Leite Bonfitto Carolina Solon Maria Elisa Lopes Pires Gabriel Forato Anhê

Increased reactive oxygen species (ROS) production leads to tissue damage observed in sepsis and lipopolysaccharide (LPS)-exposed animals. LPS stimulates cytokines releasing, including tumor necrosis factor alpha (TNF-α), that is important to ROS production. Platelets, considered inflammatory cells, generate ROS when exposed to LPS in vivo, but not when they are incubated in vitro with this compound. Therefore, we investigated the role of TNF-α on the increased intraplatelet ROS levels after LPS treatment. Mice were injected with LPS (1 mg/kg) or TNF-α (10 ng/kg), and blood was collected to prepare the washed platelets. Animals were treated with infliximab (anti-TNF-α antibody), R-7050 (non-selective TNF-α receptor antagonist) or apocynin (NADPH oxidase inhibitor). At 48 h after LPS or TNF-α injection, the ROS levels in ADP (25 µM)-activated platelets were evaluated by flow cytometry. Our data showed that injection of mice with LPS increased by 4-fold the ROS production (p < 0.05), which was significantly reduced by the treatments with infliximab, R-7050 or apocynin. Injection of mice with TNF-α markedly elevated the ROS formation in platelets (p < 0.05) that was reduced by infliximab, R-7050 or apocynin treatments. In separate experiments, platelets from saline-injected mice were incubated with TNF-α (30 to 3000 pg/mL) in absence or presence of infliximab, R-7050, apocynin or GKT137831 (NOX1/NOX4 inhibitor) before ROS measurements. TNF-α in vitro markedly increased the ROS levels, an effect significantly reduced by all treatments. Therefore, platelets are involved in the oxidative stress induced by LPS through TNF-α action, and NADPH oxidase takes part in this effect.

Apocynin

NOX4

10.1080/09537104.2019.1588241

Cite

Citations (19)

Additional file 1: Figure S1. of MALDI-MSI: a fast and reliable method for direct melatonin quantification in biological fluids

Mônica Spadafora-Ferreira Diogo Noin de Oliveira Caroline Costa Mesquita Ana Claudia Honório Barbosa Gabriel Forato Anhê

Fragment structures of (A) MS2 of precursor ion m/z 233 and (B) MS3 of its secondary ion m/z 174 by MALDI-MSI. (PDF 16 kb)

10.6084/m9.figshare.c.3697606_d1

Cite

Citations (0)

Investigating the role of the gut in fructose induced glucose intolerance

Physiology (2024)

Eya Sellami Fernando Forato-Anhe Gabriel Forato Anhê Caio Teixeira Francielton Da Silva Lima

Background: Obesity and type 2 diabetes (T2D) are global health challenges linked to the consumption of ultra processed foods high in sucrose. The latter sugar is one key source of excess dietary fructose. Although evidence indicates that excess fructose can negatively impact metabolic health and blood glucose regulation, the mechanisms are ill-defined. Excess dietary fructose overwhelms enterocyte absorption in the small intestine and spills over the distal gut. Interestingly, excess fructose has been linked to an expansion of the gut's absorptive surface and increased fat absorption. However, it remains uncertain whether excess dietary fructose impairs glucose tolerance by increasing gut absorptive surface and gut glucose absorption (GGA). Aims and Hypothesis: We hypothesized that dietary fructose impairs glucose tolerance by expanding gut surface and upregulating glucose transport machinery, which promotes increased GGA and glucose intolerance. We aim to (i) map the onset of altered glucose tolerance, plasma insulin, and altered GGA in mice fed a high-fructose diet, and (ii) investigate whether fructose driven increase in GGA correlates with an expansion of absorptive surface. Methodology: C57BL6J male mice were fed a high-sucrose (HS, with 8.5 %Kcal fructose) or a sucrose-free (CTL) diet. Oral glucose tolerance tests (OGTT) and 3-O-methyl-glucose (3-OMG) tests were conducted at weeks 1, 4, and 7 weeks after introduction of diets. Results: We found that 4 weeks, but not 1 week, on HS diet is suffcient to cause glucose intolerance, which persists, but is not aggravated, at week 7. Interestingly, HS-mice did not become insulin resistant, as revealed by plasma insulin levels, homa-ir, and insulin resistance index comparable to that of CTL-mice. HS-fed mice had longer small intestines than CTL-fed counterparts, which is indicative of increased absorptive surface. Furthermore, HS-fed mice presented higher plasma 3-OMG than CTL-mice at weeks 4 and 7, but not at week 1, indicating higher GGA that parallels the trajectory of deteriorated glucose tolerance. Conclusion: Changes in GGA and gut surface are early fructose-induced manifestations relevant to blood glucose control. We will next assess the expression of glucose transporters and perform morphometric analysis in the small intestine of these mice. We will also analyze how gut microbial populations correlate with fructose-induced changes to gut homeostasis. This study uncovers novel mechanisms by which dietary fructose contributes to impaired blood glucose control and elevates the risk of T2D. The findings from this work will lay the groundwork for novel approaches to address the growing burden of metabolic disorders worldwide. Laval university, CRIUCPQ, Fonds de recherche santé Québec. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

10.1152/physiol.2024.39.s1.2308

Cite

Citations (0)

Body Mass Variability in Age-Matched Outbred Swiss Mice is Associated to Differential Control of Food Intake by Ghrelin

SSRN Electronic Journal (2021)

Joseane Morari Roberta Haddad-Tóvolli Rafael Maróstica Natália Tobar Celso Darío Ramos

Swiss mice belong to an outbred strain of mice largely used as a model for experimental obesity induced by high fat diet (HFD). We have previously demonstrated that a given cohort of age-matched Swiss mice is hallmarked by heterogeneous changes in body weight when exposed to HFD. The reasons underlying such variability, however, are not completely understood. Therefore we aimed to clarify the mechanisms underlying the variability in spontaneous weight gain in age-matched male swiss mice. To achieve that, individuals in a cohort of age-matched male Swiss mice were categorized as prone to body mass gain (PBMG) and resistant to body mass gain (RBMG). PBMG animals had higher caloric intake and body mass gain. PBMG also showed increased midbrain levels of Tyrosine Hydroxilase (Th ) and ghrelin receptor ( Ghsr) mRNAs. The ratio of activated ghrelin normalized by total ghrelin exhibited a transitory increase 1h after refeeding exclusively in RBMG mice. Pharmacological blockade of Ghsr-1a failed to reduce food intake in PMBG mice. Accordingly, RBMG mice, but not PBMG mice, exhibited a reduction in the hypothalamic expression of the orexigenic gene AgRP when treated with the Ghsr-1a antagonist. Thus, the present data shows that RBMG mice have a hypothalamic homeostatic control of food intake that is sensitive to GHS-R1a/ghrelin signaling and controls AgRP1. Individuals classified as PBMG display increased midbrain expression of Th , Drd1 and Drd2 and increased food intake that is not sensitive to GHS-R1a inhibition.

10.2139/ssrn.3945548

Cite

Citations (0)

Agomelatine reduces circulating triacylglycerides and hepatic steatosis in fructose-treated rats

Biomedicine & Pharmacotherapy (2021)

Vanessa Barbosa Veronesi Mariana Rodrigues Pioli Dailson Nogueira de Souza Caio Jordão Teixeira Gilson Masahiro Murata

Agomelatine (AGO) is an antidepressant drug with agonistic activity at melatonin receptor 1 (MT1) and MT2 and with neutral antagonistic activity at serotonin receptor 5-HT2C. Although experimental studies show that melatonin reduces hypertriglyceridemia and hepatic steatosis induced by excessive fructose intake, no studies have tested if AGO exerts similar actions. To address this issue we have treated male Wistar rats with fructose (15% in the drinking water) and/or AGO (40 mg/kg/day) for two weeks. AGO reduced body weight gain, feeding efficiency and hepatic lipid levels without affecting caloric intake in fructose-treated rats. AGO has also decreased very low-density lipoprotein (VLDL) production and circulating TAG levels after an oral load with olive oil. Accordingly, treatment with AGO reduced the hepatic expression of fatty acid synthase (Fasn), a limiting step for hepatic de novo lipogenesis (DNLG). The expression of apolipoprotein B (Apob) and microsomal triglyceride transfer protein (Mttp) in the ileum, two crucial proteins for intestinal lipoprotein production, were also downregulated by treatment with AGO. Altogether, the present data show that AGO mimics the metabolic benefits of melatonin when used in fructose-treated rats. This study also suggests that it is relevant to evaluate the potential of AGO to treat metabolic disorders in future clinical trials.

Steatosis

Lipogenesis

10.1016/j.biopha.2021.111807

Cite

Citations (9)

Interleucina-6 não protege célula-'beta' pancreática da apoptose por estresse de retículo endoplasmático induzido pelo palmitato

Arquivos Brasileiros de Endocrinologia & Metabologia (2008)

José E Nicoletti-Carvalho Gabriel Forato Anhê Renata Gorjão Luciana C. Caperuto José Cipolla‐Neto

Source

Cite

Citations (0)

Exposure to PM_2.5 during pregnancy or lactation increases methylation while reducing the expression of Pdx1 and NEUROG3 in mouse pancreatic islets

bioRxiv (Cold Spring Harbor Laboratory) (2019)

Raquel Patrícia Ataíde Lima Vitor Ferreira Boico Guilherme Francisco Peruca Kellen Cristina da Cruz Rodrigues Victor Yuji Yariwake

ABSTRACT Air pollution is comprised of several substances, including particulate matter (PM). Exposure to air pollution may trigger alterations in DNA methylation thus modifying gene expression patterns. This phenomenon is likely to mediate the relationship between exposure to air pollution and adverse health effects. The purpose of this study was analyzing the effects of exposure to PM 2.5 during pregnancy or lactation and whether it would cause multigenerational epigenetic alterations in the promoter region of the genes Pdx1 and NEUROG3 within mouse pancreatic islets. Our results show that maternal exposure to PM 2.5 led to an elevation in blood glucose levels within the two following generations (F1 and F2). There was also an increase in DNA methylation in the aforementioned promoter regions accompanied by reduced gene expression in generations F1 and F2 upon F0 exposure to PM 2.5 during pregnancy. These data suggest that maternal exposure to PM 2.5 from air pollution, particularly during pregnancy, may lead to a multigenerational and lifelong negative impact on glucose homeostasis mediated by an increase in DNA methylation within the promoter region of the genes Pdx1 and NEUROG3 in pancreatic islets.

PDX1

Pancreatic Islets

10.1101/852509

Cite

Citations (0)

Melatonina induz fosforilação do irs-1 na região pré-optica hipotalâmica anterior de ratas pré-puberes

Resumos (2001)

Gabriel Forato Anhê Luciana Capureto L C. Souza Carmen Sílvia Grubert Campbell José Cipolla‐Neto

Source

Cite

Citations (0)