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1. Metabolic reprogramming of macrophages in the context of type 2 diabetes

Author

Leonel Witcoski Junior, Jordana Dinorá de Lima, Amanda Girardi Somensi, Lucas Brito de Souza Santos, Giulia Leonel Paschoal, Thalita Suemy Uada, Thais Sibioni Berti Bastos, André Guilherme Portela de Paula, Rebeca Bosso Dos Santos Luz, Andressa Pacheco Czaikovski, Mariana Rodrigues Davanso, and Tarcio Teodoro Braga

Subjects
Immunometabolism, T2D, Macrophage, Epigenetic modifications, Medicine
Abstract

Abstract Type 2 diabetes (T2D) is associated with insulin resistance and progressive dysfunction of β-pancreatic cells, leading to persistent hyperglycemia. Macrophages play a crucial role in this context, influencing both the development and progression of insulin resistance. These innate immune cells respond to inflammatory stimuli and reprogram their metabolism, directly impacting the pathophysiology of T2D. Macrophages are highly plastic and can adopt either pro-inflammatory or pro-resolutive phenotypic profiles. In T2D, pro-inflammatory macrophages, which rely on glycolysis, exacerbate insulin resistance through increased production of pro-inflammatory cytokines and nitric oxide. In contrast, pro-resolutive macrophages, which prioritize fatty acid metabolism, have different effects on glucose homeostasis. Metaflammation, a chronic low-grade inflammation, is induced by pro-inflammatory macrophages and significantly contributes to the progression of T2D, creating an environment conducive to metabolic dysfunction. This review aims to clarify the contribution of macrophages to the progression of T2D by detailing how their inflammatory responses and metabolic reprogramming influence insulin resistance and the disease’s pathophysiology. The review seeks to deepen the understanding of the biochemical and metabolic mechanisms involved, offering broader insights into the impact on the quality of life for millions of patients worldwide.

Published
2024
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2. Sensing soluble uric acid by Naip1-Nlrp3 platform

Author

Tarcio Teodoro Braga, Mariana Rodrigues Davanso, Davi Mendes, Tiago Antonio de Souza, Anderson Fernandes de Brito, Mario Costa Cruz, Meire Ioshie Hiyane, Dhemerson Souza de Lima, Vinicius Nunes, Juliana de Fátima Giarola, Denio Emanuel Pires Souto, Tomasz Próchnicki, Mario Lauterbach, Stellee Marcela Petris Biscaia, Rilton Alves de Freitas, Rui Curi, Alessandra Pontillo, Eicke Latz, and Niels Olsen Saraiva Camara

Subjects
Cytology, QH573-671
Abstract

Abstract Uric acid (UA), a product of purine nucleotide degradation able to initiate an immune response, represents a breakpoint in the evolutionary history of humans, when uricase, the enzyme required for UA cleavage, was lost. Despite being inert in human cells, UA in its soluble form (sUA) can increase the level of interleukin-1β (IL-1β) in murine macrophages. We, therefore, hypothesized that the recognition of sUA is achieved by the Naip1-Nlrp3 inflammasome platform. Through structural modelling predictions and transcriptome and functional analyses, we found that murine Naip1 expression in human macrophages induces IL-1β expression, fatty acid production and an inflammation-related response upon sUA stimulation, a process reversed by the pharmacological and genetic inhibition of Nlrp3. Moreover, molecular interaction experiments showed that Naip1 directly recognizes sUA. Accordingly, Naip may be the sUA receptor lost through the human evolutionary process, and a better understanding of its recognition may lead to novel anti-hyperuricaemia therapies.

Published
2021
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3. Combination of a high-fat diet with sweetened condensed milk exacerbates inflammation and insulin resistance induced by each separately in mice

Author

Laureane Nunes Masi, Amanda Roque Martins, Amanda Rabello Crisma, Cátia Lira do Amaral, Mariana Rodrigues Davanso, Tamires Duarte Afonso Serdan, Roberta Dourado Cavalcante da Cunha de Sá, Maysa Mariana Cruz, Maria Isabel Cardoso Alonso-Vale, Rosângela Pavan Torres, Jorge Mancini-Filho, Joice Naiara Bertaglia Pereira, Marta Maria da Silva Righetti, Edson Aparecido Liberti, Sandro Massao Hirabara, and Rui Curi

Subjects
Medicine, Science
Abstract

Abstract Obesogenic diets increase body weight and cause insulin resistance (IR), however, the association of these changes with the main macronutrient in the diet remains to be elucidated. Male C57BL/6 mice were fed with: control (CD), CD and sweetened condensed milk (HS), high-fat (HF), and HF and condensed milk (HSHF). After 2 months, increased body weight, glucose intolerance, adipocyte size and cholesterol levels were observed. As compared with CD, HS ingested the same amount of calories whereas HF and HSHF ingested less. HS had increased plasma AST activity and liver type I collagen. HF caused mild liver steatosis and hepatocellular damage. HF and HSHF increased LDL-cholesterol, hepatocyte and adipocyte hypertrophy, TNF-α by macrophages and decreased lipogenesis and adiponectin in adipose tissue (AT). HSHF exacerbated these effects, increasing IR, lipolysis, mRNA expression of F4/80 and leptin in AT, Tlr-4 in soleus muscle and IL-6, IL-1β, VCAM-1, and ICAM-1 protein in AT. The three obesogenic diets induced obesity and metabolic dysfunction. HS was more proinflammatory than the HF and induced hepatic fibrosis. The HF was more detrimental in terms of insulin sensitivity, and it caused liver steatosis. The combination HSHF exacerbated the effects of each separately on insulin resistance and AT inflammatory state.

Published
2017
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4. Soluble Uric Acid Activates the NLRP3 Inflammasome

Author

Mariana Rodrigues Davanso, Maria Fernanda Forni, Bernardo S. Franklin, Tarcio Teodoro Braga, Alicia J. Kowaltowski, Niels Olsen Saraiva Camara, José Alexandre Marzagão Barbuto, Meire Ioshie Hiyane, Rodrigo Nalio Ramos, Angela Castoldi, Matheus Correa-Costa, Eicke Latz, and Paola Cristina Branco

Subjects
0301 basic medicine, Damp, Mitochondrial ROS, Male, Inflammasomes, genetics [Myeloid Differentiation Factor 88], metabolism [NLR Family, Pyrin Domain-Containing 3 Protein], Interleukin-1beta, metabolism [Voltage-Dependent Anion Channels], Kidney, chemistry.chemical_compound, Mice, 0302 clinical medicine, Fibrosis, pathology [Kidney], Voltage-Dependent Anion Channels, metabolism [Reactive Oxygen Species], Respiratory system, metabolism [Kidney Diseases], Cells, Cultured, Mice, Knockout, Multidisciplinary, biology, Caspase 1, Inflammasome, Cell biology, metabolism [Myeloid Differentiation Factor 88], Biochemistry, 030220 oncology & carcinogenesis, Kidney Diseases, Oxidation-Reduction, medicine.drug, Voltage-dependent anion channel, Article, metabolism [Uric Acid], 03 medical and health sciences, metabolism [Interleukin-1beta], NLR Family, Pyrin Domain-Containing 3 Protein, medicine, Renal fibrosis, Animals, genetics [NLR Family, Pyrin Domain-Containing 3 Protein], Macrophages, metabolism [Caspase 1], physiology [Macrophages], medicine.disease, Uric Acid, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, chemistry, Myeloid Differentiation Factor 88, biology.protein, Uric acid, Reactive Oxygen Species, ddc:600, metabolism [Inflammasomes]
Abstract

Uric acid is a damage-associated molecular pattern (DAMP), released from ischemic tissues and dying cells which, when crystalized, is able to activate the NLRP3 inflammasome. Soluble uric acid (sUA) is found in high concentrations in the serum of great apes, and even higher in some diseases, before the appearance of crystals. In the present study, we sought to investigate whether uric acid, in the soluble form, could also activate the NLRP3 inflammasome and induce the production of IL-1β. We monitored ROS, mitochondrial area and respiratory parameters from macrophages following sUA stimulus. We observed that sUA is released in a hypoxic environment and is able to induce IL-1β release. This process is followed by production of mitochondrial ROS, ASC speck formation and caspase-1 activation. Nlrp3−/− macrophages presented a protected redox state, increased maximum and reserve oxygen consumption ratio (OCR) and higher VDAC protein levels when compared to WT and Myd88−/− cells. Using a disease model characterized by increased sUA levels, we observed a correlation between sUA, inflammasome activation and fibrosis. These findings suggest sUA activates the NLRP3 inflammasome. We propose that future therapeutic strategies for renal fibrosis should include strategies that block sUA or inhibit its recognition by phagocytes. © The Author(s) 2017. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Published
2017
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5. Macadamia Oil Supplementation Attenuates Inflammation and Adipocyte Hypertrophy in Obese Mice

Author

Laureane Nunes Masi, Renata Guimarães Moreira, Mariana Rodrigues Davanso, Edson A. Lima, Sandro M. Hirabara, José Cesar Rosa Neto, Gabriel I. G Souza, Amanda R. Martins, Amanda Rabello Crisma, Loreana Sanches Silveira, Luís G O de Sousa, Aline Boveto Santamarina, Universidade de São Paulo (USP), Universidade Estadual Paulista (Unesp), Univ Sao Judas Tadeu, Universidade Federal de São Paulo (UNIFESP), and Univ Cruzeiro Sul

Subjects
Male, medicine.medical_specialty, Article Subject, Immunology, Adipose tissue, Inflammation, Biology, Macadamia oil, Cell Enlargement, Diet, High-Fat, Nitric Oxide, Muscle hypertrophy, chemistry.chemical_compound, Mice, Insulin resistance, ÁCIDOS GRAXOS, Adipocyte, Internal medicine, medicine, lcsh:Pathology, Adipocytes, Animals, Plant Oils, Obesity, medicine.diagnostic_test, Cell Biology, medicine.disease, Mice, Inbred C57BL, Endocrinology, Cholesterol, chemistry, Macadamia, Macrophages, Peritoneal, Cytokines, medicine.symptom, Adipocyte hypertrophy, Insulin Resistance, Lipid profile, lcsh:RB1-214, Research Article
Abstract

Made available in DSpace on 2015-03-18T15:55:38Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-01-01Bitstream added on 2015-03-18T16:28:36Z : No. of bitstreams: 1 WOS000344673400001.epub: 1369846 bytes, checksum: bc6efb2183924a71e7fb2e30828cb77c (MD5)Bitstream added on 2015-03-18T16:28:36Z : No. of bitstreams: 2 WOS000344673400001.epub: 1369846 bytes, checksum: bc6efb2183924a71e7fb2e30828cb77c (MD5) WOS000344673400001.pdf: 2000918 bytes, checksum: 799fc4c459de9af835594951c96f9c0d (MD5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Excess of saturated fatty acids in the diet has been associated with obesity, leading to systemic disruption of insulin signaling, glucose intolerance, and inflammation. Macadamia oil administration has been shown to improve lipid profile in humans. We evaluated the effect of macadamia oil supplementation on insulin sensitivity, inflammation, lipid profile, and adipocyte size in high-fat diet (HF) induced obesity in mice. C57BL/6 male mice (8 weeks) were divided into four groups: (a) control diet (CD), (b) HF, (c) CD supplemented with macadamia oil by gavage at 2g/Kg of body weight, three times per week, for 12 weeks (CD + MO), and (d) HF diet supplemented with macadamia oil (HF + MO). CD and HF mice were supplemented with water. HF mice showed hypercholesterolemia and decreased insulin sensitivity as also previously shown. HF induced inflammation in adipose tissue and peritoneal macrophages, as well as adipocyte hypertrophy. Macadamia oil supplementation attenuated hypertrophy of adipocytes and inflammation in the adipose tissue and macrophages. Univ Sao Paulo, Dept Biol Celular & Desenvolvimento, BR-05508000 Sao Paulo, Brazil Univ Estadual Paulista, UNESP, Dept Educ Fis, Programa Posgrad Ciencia Motricidad, BR-13506900 Rio Claro, SP, Brazil Univ Sao Paulo, Inst Ciencias Biomed, Dept Fisiol & Biofis, BR-05508000 Sao Paulo, Brazil Univ Sao Judas Tadeu, Dept Ciencias Biol, Lab Movimento Humano, BR-05503001 Sao Paulo, Brazil Univ Fed Sao Paulo, Dept Fisiol, Disciplina Fisiol Nutr, BR-04023901 Sao Paulo, Brazil Univ Sao Paulo, Inst Biociencias, Dept Fisiol Geral, BR-05508090 Sao Paulo, Brazil Univ Cruzeiro Sul, Inst Ciencias Atividade Fis & Esporte, Programa Posgrad Ciencia Movimento Humano, BR-01506000 Sao Paulo, Brazil Univ Estadual Paulista, UNESP, Dept Educ Fis, Programa Posgrad Ciencia Motricidad, BR-13506900 Rio Claro, SP, Brazil

Published
2014

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