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4. MAIO AMARELO: INTERVENÇÕES EDUCATIVAS PARA PREVENÇÃO DE ACIDENTES NO TRÂNSITO DE CAMPINAS

Author

FRANCHITO FREIRE, BRUNA, primary, DE TOLEDO PIZA SOARES, JULIANA, additional, PERON GOTHE, JULIANA, additional, IKEHARA DEZOTTI, NAMI, additional, GOMES DE ALMEIDA LACERDA, GUILHERME, additional, MARIA RIBEIRO LESCURA FRANÇA, PALOMA, additional, SHINJI ARASHIRO, MATHEUS, additional, FERRER DE SOUZA, IVANA, additional, BEATRIZ ALISCANTES SILVA BRITO, JULIA, additional, SIMÕES JÚNIOR, JOAQUIM, additional, and SIMÕES NETO, JOAQUIM, additional

Published
2023
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6. Pathogenic Cav3.2 channel mutation in a child with primary generalized epilepsy

Author

Souza, Ivana A, Gandini, Maria A, Zhang, Fang-Xiong, Mitchell, Wendy G, Matsumoto, Joyce, Lerner, Jason, Pierson, Tyler Mark, and Zamponi, Gerald W

Subjects
Epilepsy, Neurodegenerative, Brain Disorders, Neurosciences, Genetics, 2.1 Biological and endogenous factors, Aetiology, Biophysical Phenomena, Calcium Channels, T-Type, Child, Epilepsy, Generalized, Female, Humans, Infant, Infant, Newborn, Mutation, Cav3, 2, T-type, Seizure, Cav3.2, Medical and Health Sciences, Neurology & Neurosurgery
Abstract

Two paternally-inherited missense variants in CACNA1H were identified and characterized in a 6-year-old child with generalized epilepsy. Febrile and unprovoked seizures were present in this child. Both variants were expressed in cis or isolation using human recombinant Cav3.2 calcium channels in tsA-201 cells. Whole-cell patch-clamp recordings indicated that one variant (c.3844C > T; p.R1282W) caused a significant increase in current density consistent with a pathogenic gain-of-function phenotype; while the other cis-related variant (c.5294C > T; p.A1765V) had a benign profile.

Published
2019

8. CaV3.2 T-type calcium channels contribute to CGRP- induced allodynia in a rodent model of experimental migraine.

Author

Baggio, Darciane F., Gambeta, Eder, Souza, Ivana A., Huang, Sun, Zamponi, Gerald W., and Chichorro, Juliana G.

Subjects
IN vitro studies, BIOLOGICAL models, PAIN measurement, RESEARCH funding, PHOTOSENSITIVITY disorders, HEADACHE, IN vivo studies, CELLULAR signal transduction, DESCRIPTIVE statistics, INTRA-articular injections, HYPERALGESIA, MICE, CALCIUM, NEUROPEPTIDES, SENSORY ganglia, ANIMAL experimentation, PAIN management, VOMITING, TRANSFERASES, ION channels, MIGRAINE, BIOMARKERS, NAUSEA, CELL receptors, DISEASE complications
Abstract

Background: Migraine is a painful neurological syndrome characterized by attacks of throbbing headache, of moderate to severe intensity, which is associated with photo- and phono- sensitivity as well as nausea and vomiting. It affects about 15% of the world's population being 2–3 times more prevalent in females. The calcitonin gene-related peptide (CGRP) is a key mediator in the pathophysiology of migraine, and a significant advance in the field has been the development of anti-CGRP therapies. The trigeminal ganglion (TG) is thought to be an important site of action for these drugs. Moreover, experimental migraine can be induced by CGRP injection in the TG. The signaling pathway induced by CGRP in the TG is not fully understood, but studies suggest that voltage-gated calcium channels contribute to CGRP effects relevant to migraine. Objective: We hypothesised that CGRP injection in the TG enhances CaV3.2 T-type calcium channel currents to contribute to the development of periorbital mechanical allodynia. Results: A Co-Immunoprecipitation assay in tsA-201 cells revealed that CaV3.2 channels form a complex with RAMP-1, a component of the CGRP receptor. Constitutive CGRPR activity was able to inhibit CaV3.2 channels and induce a depolarizing shift in both activation and inactivation curves. Incubation of TG neurons with CGRP increased T-type current density by ~ 3.6 fold, an effect that was not observed in TG neurons from CaV3.2 knockout mice. Incubation of TG neurons with Z944, a pan T-type channel blocker, resulted in an approximately 80% inhibition of T-type currents. In vivo, this treatment abolished the development of periorbital mechanical allodynia induced by CGRP in male and female mice. Likewise, CaV3.2 knockout mice did not develop periorbital mechanical allodynia after intraganglionic CGRP injection. Finally, we demonstrated that the CGRP effect depends on the activation of its canonical GPCR, followed by protein kinase A activation. Conclusion: The present study suggests that CGRP modulates CaV3.2 in the TG, an effect possibly mediated by the canonical CGRP receptor and PKA activation. The increase in T-type currents in the TG may represent a contributing factor for the initiation and maintenance of the headache pain during migraine. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Contribution of T‐type calcium channel isoforms to cold and mechanical sensitivity in naïve and oxaliplatin‐treated mice of both sexes.

Author

Antunes, Flavia T. T., Gandini, Maria A., Gadotti, Vinicius M., Quintão, Nara Lins Meira, Santin, José Roberto, Souza, Ivana A., David, Laurence S., Snutch, Terrance P., Hildebrand, Michael, and Zamponi, Gerald W.

Subjects
CALCIUM channels, SMALL molecules, PERIPHERAL neuropathy, SPINAL cord, ALLERGIES
Abstract

Background and Purpose: The chemotherapy agent oxaliplatin can give rise to oxaliplatin‐induced peripheral neuropathy (OIPN). Here, we investigated whether T‐type calcium channels (Cav3) contribute to OIPN. Experimental Approach: We chronically treated mice with oxaliplatin and assessed pain responses and changes in expression of Cav3.2 calcium channels. We also tested the effects of T‐type channel blockers on cold sensitivity in wild‐type and Cav3.2 null mice. Key Results: Oxaliplatin treatment led to mechanical and cold hypersensitivity in male and female mice. Mechanical hypersensitivity persisted in Cav3.2 null mice of both sexes. Intraperitoneal or intrathecal delivery of pan T‐type channel inhibitors attenuated mechanical hypersensitivity in wild‐type but not Cav3.2 null mice. Remarkably cold hypersensitivity occurred in female but not male Cav3.2 null mice even without oxaliplatin treatment. Unexpectedly, intrathecal, intraplantar or intraperitoneal delivery of T‐type channel inhibitors Z944 or TTA‐P2 transiently induced cold hypersensitivity in both male and female wild‐type mice. Acute knockdown of specific Cav3 isoforms revealed that the depletion of Cav3.1 in males and depletion of either Cav3.1 or Cav3.2 in females triggered cold hypersensitivity. Finally, reducing Cav3.2 expression by disrupting the interactions between Cav3.2 and the deubiquitinase USP5 with the small organic molecule II‐2 reversed oxaliplatin‐induced mechanical and cold hypersensitivity and importantly did not trigger cold allodynia. Conclusion and Implications: Altogether, our data indicate that T‐type channels differentially contribute to the regulation of cold and mechanical hypersensitivity, and raise the possibility that T‐type channel blockers could promote cold allodynia. [ABSTRACT FROM AUTHOR]

Published
2024
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11. De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias

Author

Helbig, Katherine L, Lauerer, Robert J, Bahr, Jacqueline C, Souza, Ivana A, Myers, Candace T, Uysal, Betül, Schwarz, Niklas, Gandini, Maria A, Huang, Sun, Keren, Boris, Mignot, Cyril, Afenjar, Alexandra, de Villemeur, Thierry Billette, Héron, Delphine, Nava, Caroline, Valence, Stéphanie, Buratti, Julien, Fagerberg, Christina R, Soerensen, Kristina P, Kibaek, Maria, Kamsteeg, Erik-Jan, Koolen, David A, Gunning, Boudewijn, Schelhaas, H Jurgen, Kruer, Michael C, Fox, Jordana, Bakhtiari, Somayeh, Jarrar, Randa, Padilla-Lopez, Sergio, Lindstrom, Kristin, Jin, Sheng Chih, Zeng, Xue, Bilguvar, Kaya, Papavasileiou, Antigone, Xing, Qinghe, Zhu, Changlian, Boysen, Katja, Vairo, Filippo, Lanpher, Brendan C, Klee, Eric W, Tillema, Jan-Mendelt, Payne, Eric T, Cousin, Margot A, Kruisselbrink, Teresa M, Wick, Myra J, Baker, Joshua, Haan, Eric, Smith, Nicholas, Sadeghpour, Azita, Davis, Erica E, Katsanis, Nicholas, Genomics, Task Force for Neonatal, Allori, Alexander, Angrist, Misha, Ashley, Patricia, Bidegain, Margarita, Boyd, Brita, Chambers, Eileen, Cope, Heidi, Cotten, C Michael, Curington, Theresa, Ellestad, Sarah, Fisher, Kimberley, French, Amanda, Gallentine, William, Goldberg, Ronald, Hill, Kevin, Kansagra, Sujay, Katsanis, Sara, Kurtzberg, Joanne, Marcus, Jeffrey, McDonald, Marie, Mikati, Mohammed, Miller, Stephen, Murtha, Amy, Perilla, Yezmin, Pizoli, Carolyn, Purves, Todd, Ross, Sherry, Smith, Edward, Wiener, John, Corbett, Mark A, MacLennan, Alastair H, Gecz, Jozef, Biskup, Saskia, Goldmann, Eva, Rodan, Lance H, Kichula, Elizabeth, Segal, Eric, Jackson, Kelly E, Asamoah, Alexander, Dimmock, David, McCarrier, Julie, Botto, Lorenzo D, Filloux, Francis, Tvrdik, Tatiana, and Cascino, Gregory D

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Neurodegenerative, Brain Disorders, Neurosciences, Epilepsy, Pediatric, 2.1 Biological and endogenous factors, Aetiology, Neurological, Adolescent, Adult, Calcium Channels, R-Type, Cation Transport Proteins, Child, Child, Preschool, Contracture, Dyskinesias, Female, Genetic Variation, Humans, Infant, Male, Megalencephaly, Neurodevelopmental Disorders, Spasms, Infantile, Task Force for Neonatal Genomics, Deciphering Developmental Disorders Study, CACNA1E, ion channel, arthrogryposis, calcium channel, epilepsy, Biological Sciences, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Developmental and epileptic encephalopathies (DEEs) are severe neurodevelopmental disorders often beginning in infancy or early childhood that are characterized by intractable seizures, abundant epileptiform activity on EEG, and developmental impairment or regression. CACNA1E is highly expressed in the central nervous system and encodes the α1-subunit of the voltage-gated CaV2.3 channel, which conducts high voltage-activated R-type calcium currents that initiate synaptic transmission. Using next-generation sequencing techniques, we identified de novo CACNA1E variants in 30 individuals with DEE, characterized by refractory infantile-onset seizures, severe hypotonia, and profound developmental impairment, often with congenital contractures, macrocephaly, hyperkinetic movement disorders, and early death. Most of the 14, partially recurring, variants cluster within the cytoplasmic ends of all four S6 segments, which form the presumed CaV2.3 channel activation gate. Functional analysis of several S6 variants revealed consistent gain-of-function effects comprising facilitated voltage-dependent activation and slowed inactivation. Another variant located in the domain II S4-S5 linker results in facilitated activation and increased current density. Five participants achieved seizure freedom on the anti-epileptic drug topiramate, which blocks R-type calcium channels. We establish pathogenic variants in CACNA1E as a cause of DEEs and suggest facilitated R-type calcium currents as a disease mechanism for human epilepsy and developmental disorders.

Published
2018

14. ODONTOLOGIA NO SERVIÇO HOSPITALAR

Author

Silva, Daniele Cabral da, primary, Souza, Ivana da Silva, additional, Queiroz, Gabrielle de Souza, additional, Andrade, Bruna Fernandes, additional, Castro, Cristiane Ribeiro da Silva, additional, and Casais, Paula Milena Melo, additional

Published
2022
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19. Maize

Author

Marucci, Rosangela C., Mendes, Simone Martins, Souza, Ivana Lemos, Souza, Brígida, editor, Vázquez, Luis L., editor, and Marucci, Rosangela C., editor

Published
2019
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20. Parasitoid Insects

Author

Silveira, Luis Cláudio Paterno, Souza, Ivana Lemos, Tomazella, Vitor Barrile, Mendez, Heisler Alexsander Gomez, Souza, Brígida, editor, Vázquez, Luis L., editor, and Marucci, Rosangela C., editor

Published
2019
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27. De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias

Author

Allori, Alexander, Angrist, Misha, Ashley, Patricia, Bidegain, Margarita, Boyd, Brita, Chambers, Eileen, Cope, Heidi, Cotten, C. Michael, Curington, Theresa, Davis, Erica E., Ellestad, Sarah, Fisher, Kimberley, French, Amanda, Gallentine, William, Goldberg, Ronald, Hill, Kevin, Kansagra, Sujay, Katsanis, Nicholas, Katsanis, Sara, Kurtzberg, Joanne, Marcus, Jeffrey, McDonald, Marie, Mikati, Mohammed, Miller, Stephen, Murtha, Amy, Perilla, Yezmin, Pizoli, Carolyn, Purves, Todd, Ross, Sherry, Sadeghpour, Azita, Smith, Edward, Wiener, John, Helbig, Katherine L., Lauerer, Robert J., Bahr, Jacqueline C., Souza, Ivana A., Myers, Candace T., Uysal, Betül, Schwarz, Niklas, Gandini, Maria A., Huang, Sun, Keren, Boris, Mignot, Cyril, Afenjar, Alexandra, Billette de Villemeur, Thierry, Héron, Delphine, Nava, Caroline, Valence, Stéphanie, Buratti, Julien, Fagerberg, Christina R., Soerensen, Kristina P., Kibaek, Maria, Kamsteeg, Erik-Jan, Koolen, David A., Gunning, Boudewijn, Schelhaas, H. Jurgen, Kruer, Michael C., Fox, Jordana, Bakhtiari, Somayeh, Jarrar, Randa, Padilla-Lopez, Sergio, Lindstrom, Kristin, Jin, Sheng Chih, Zeng, Xue, Bilguvar, Kaya, Papavasileiou, Antigone, Xing, Qinghe, Zhu, Changlian, Boysen, Katja, Vairo, Filippo, Lanpher, Brendan C., Klee, Eric W., Tillema, Jan-Mendelt, Payne, Eric T., Cousin, Margot A., Kruisselbrink, Teresa M., Wick, Myra J., Baker, Joshua, Haan, Eric, Smith, Nicholas, Corbett, Mark A., MacLennan, Alastair H., Gecz, Jozef, Biskup, Saskia, Goldmann, Eva, Rodan, Lance H., Kichula, Elizabeth, Segal, Eric, Jackson, Kelly E., Asamoah, Alexander, Dimmock, David, McCarrier, Julie, Botto, Lorenzo D., Filloux, Francis, Tvrdik, Tatiana, Cascino, Gregory D., Klingerman, Sherry, Neumann, Catherine, Wang, Raymond, Jacobsen, Jessie C., Nolan, Melinda A., Snell, Russell G., Lehnert, Klaus, Sadleir, Lynette G., Anderlid, Britt-Marie, Kvarnung, Malin, Guerrini, Renzo, Friez, Michael J., Lyons, Michael J., Leonhard, Jennifer, Kringlen, Gabriel, Casas, Kari, El Achkar, Christelle M., Smith, Lacey A., Rotenberg, Alexander, Poduri, Annapurna, Sanchis-Juan, Alba, Carss, Keren J., Rankin, Julia, Zeman, Adam, Raymond, F. Lucy, Blyth, Moira, Kerr, Bronwyn, Ruiz, Karla, Urquhart, Jill, Hughes, Imelda, Banka, Siddharth, Hedrich, Ulrike B.S., Scheffer, Ingrid E., Helbig, Ingo, Zamponi, Gerald W., Lerche, Holger, and Mefford, Heather C.

Published
2018
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44. Differential regulation of Cav3.2 and Cav2.2 calcium channels by CB1 receptors and cannabidiol.

Author

Harding, Erika K., Souza, Ivana A., Gandini, Maria A., Gadotti, Vinícius M., Ali, Md Yousof, Huang, Sun, Antunes, Flavia T. T., Trang, Tuan, and Zamponi, Gerald W.

Subjects
*CALCIUM channels, *CANNABINOID receptors, *CANNABIDIOL, *CANNABINOIDS, *CHRONIC pain, *NEURALGIA, *PAIN management
Abstract

Background and Purpose: Cannabinoids are a promising therapeutic avenue for chronic pain. However, clinical trials often fail to report analgesic efficacy of cannabinoids. Inhibition of voltage gate calcium (Cav) channels is one mechanism through which cannabinoids may produce analgesia. We hypothesized that cannabinoids and cannabinoid receptor agonists target different types of Cav channels through distinct mechanisms. Experimental Approach: Electrophysiological recordings from tsA‐201 cells expressing either Cav3.2 or Cav2.2 were used to assess inhibition by HU‐210 or cannabidiol (CBD) in the absence and presence of the CB1 receptor. Homology modelling assessed potential interaction sites for CBD in both Cav2.2 and Cav3.2. Analgesic effects of CBD were assessed in mouse models of inflammatory and neuropathic pain. Key Results: HU‐210 (1 μM) inhibited Cav2.2 function in the presence of CB1 receptor but had no effect on Cav3.2 regardless of co‐expression of CB1 receptor. By contrast, CBD (3 μM) produced no inhibition of Cav2.2 and instead inhibited Cav3.2 independently of CB1 receptors. Homology modelling supported these findings, indicating that CBD binds to and occludes the pore of Cav3.2, but not Cav2.2. Intrathecal CBD alleviated thermal and mechanical hypersensitivity in both male and female mice, and this effect was absent in Cav3.2 null mice. Conclusion and Implications: Our findings reveal differential modulation of Cav2.2 and Cav3.2 channels by CB1 receptors and CBD. This advances our understanding of how different cannabinoids produce analgesia through action at different voltage‐gated calcium channels and could influence the development of novel cannabinoid‐based therapeutics for treatment of chronic pain. [ABSTRACT FROM AUTHOR]

Published
2023
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47. Impact of perigestational exposure to a high sucrose diet on the early development of metabolic dysfunctions in the offspring of Wistar rats

Author

SOUZA, Ivana Letícia Santos, PAES, Antonio Marcus de Andrade, GASPAR, Renato Simões, NASCIMENTO, Joelma Ximenes Prado Teixeira, and FRANÇA, Lucas Martins

Subjects
Ciências da Saúde, Dieta materna rica em sacarose, DOHaD, Metabolic programming, Metabolic syndrome, highsugar diet, Síndrome metabólica, Programação metabólica
Abstract

Submitted by Jonathan Sousa de Almeida (jonathan.sousa@ufma.br) on 2022-05-24T15:27:48Z No. of bitstreams: 1 IVANALETÍCIASANTOSSOUZA.pdf: 2988199 bytes, checksum: 3dd83d2ad7342895f6e1cf64afda92c7 (MD5) Made available in DSpace on 2022-05-24T15:27:48Z (GMT). No. of bitstreams: 1 IVANALETÍCIASANTOSSOUZA.pdf: 2988199 bytes, checksum: 3dd83d2ad7342895f6e1cf64afda92c7 (MD5) Previous issue date: 2022-03-30 FAPEMA The prevalence of metabolic diseases in children and adolescents is increasing rapidly and significantly, being pointed out by the World Health Organization as one of the biggest public health problems in the world. The expressive growth of these pathologies is mainly related to changes in the behavior of society in general, which started to consume diets with a high content of added sugars (sucrose) and ultra processed foods, in addition to the increase in sedentary lifestyle. In this context, the DOHaD concept aims to elucidate how punctual changes that occur early in developing organisms can result in late metabolic alterations and an increased risk of chronic diseases in adult life. Taking these aspects into account, the aim of this study is to investigate the impact of excessive exposure to added sugars during pregnancy and lactation on the onset and early progression of metabolic syndrome in offspring. For this purpose, adult Wistar female rats (n = 15), with approximately 75-90 days of life, were divided into two groups: those exposed to nutritional stress (n = 7) and those that were not exposed (n = 8). This nutritional stress was through a diet containing 25% sucrose (DRS) compared to a control diet, which contained 10% sucrose (CTR). After the 7-week induction period the rats were mated with age-matched rats (n=15) and pregnancy confirmed from the morning vaginal smear. The rats continued with their respective diets (CTR or DRS) throughout pregnancy and lactation. At the birth of the pups, the offspring was adjusted to 8 pups per rat, due to the mother's breastfeeding contribution. At 21 days of age, the pups were weaned and separated from their mothers and divided into two experimental groups: the CTR group (offspring of males and females of the mothers fed with CTR diet during pregnancy and lactation) and the DRS group (offspring of males and females of the mothers fed with DRS diet during pregnancy and lactation). All offspring animals were fed with a CTR diet ad libitum from weaning and were equally followed up to 30 days of life, when euthanasia occurred. The calculation of the Lee Index and glucose tolerance test were performed, in addition to blood collection for biochemical analysis and key-organs for morphometry and histology. From these procedures, it can be stated that the main result obtained was the significant impairment in the DRS offspring's glycolipid homeostasis, through glucose intolerance, hypertriglyceridemia, hypercholesterolemia and the significant increase in TyG, which indicates the beginning of the development of type 2 diabetes mellitus and the consequent establishment of the metabolic syndrome as early as during the late childhood of these animals. In addition, there was the significant increase in steatosis, inflation and ballooning in the liver of experimental animals, which culminated in steatohepatitis, the predecessor stage of hepatocellular cancer. Finally, it is concluded that the period of pregnancy and lactation are a metabolic window susceptible to nutritional stresses and metabolic reprogramming of offspring, and that this reprogramming occurs differently between sex. A prevalência de doenças metabólicas em crianças e adolescentes está aumentando de maneira rápida e significativa, sendo apontado pela Organização Mundial de Saúde como um dos maiores problemas de saúde pública no mundo. O crescimento expressivo destas patologias está relacionado, principalmente, às mudanças ocorridas no comportamento da sociedade em geral, que passou a consumir dietas com elevado teor de açucares de adição (sacarose) e alimentos ultraprocessados, além do aumento do sedentarismo. Nessa conjuntura, o conceito DOHaD tem como propósito elucidar como mudanças pontuais ocorridas precocemente em organismos em desenvolvimento podem resultar em alterações metabólicas tardias e um risco aumentado de doenças crônicas na vida adulta. Levando esses aspectos em consideração, o objetivo deste trabalho é investigar o impacto da exposição excessiva a açúcares de adição durante as fases pré-gestacional, de gestação e de lactação sobre a instalação e progressão precoce da síndrome metabólica na prole. Para tanto, ratas Wistar adultas (n = 15), com aproximadamente 75-90 dias de vida, foram divididas em dois grupos: as que foram expostas ao estresse nutricional (n = 7) e as que não foram expostas (n = 8). Esse estresse nutricional se deu através de uma dieta contendo 25% de sacarose (DRS), em comparação a uma dieta controle, que continha 10% de sacarose (CTR). Após o período de indução de 7 semanas, as ratas foram acasaladas com ratos da mesma idade (n = 15), com confirmação da prenhez a partir do esfregaço vaginal matinal. As ratas continuaram com suas respectivas dietas (CTR ou DRS) durante toda a gestação e lactação. Ao nascimento dos filhotes, a ninhada foi ajustada para 8 filhotes por rata, devido ao aporte de aleitamento materno. Aos 21 dias de vida, os filhotes foram desmamados e separados das mães e divididos em dois grupos experimentais: o grupo CTR (prole de machos e fêmeas das mães alimentadas com ração CTR durante a gestação e lactação) e o grupo DRS (prole de machos e fêmeas das mães alimentadas com ração DRS durante a gestação e lactação). Todas as proles foram alimentadas com dieta CTR ad libitum desde o desmame e foram igualmente acompanhados até os 30 dias de vida, quando ocorreu a eutanásia. Foi realizado o cálculo do Índice de Lee e teste de tolerância à glicose, além da coleta de sangue para as análises bioquímicas e órgãos-chave para a morfometria e histologia. A partir desses procedimentos, pode-se afirmar que os principais resultados obtidos foram o prejuízo significativo na homeostase glicolipídica das proles DRS, através da intolerância à glicose, hipertrigliceridemia, hipercolesterolemia e aumento significativo do TyG, que indica o início do desenvolvimento do diabetes mellitus tipo 2 e consequente instauração da síndrome metabólica tão logo durante a infância tardia desses animais. Além disso, houve aumento significativo da esteatose, inflamação e ballooning no fígado dos animais experimentais, o que culmina na esteato-hepatite, estágio antecessor do câncer hepatocelular. Por fim, conclui-se que o período da gestação e lactação são uma janela metabólica suscetível aos estresses nutricionais e à reprogramação metabólica dos descendestes, e que essa reprogramação ocorre de forma diferente entre os sexos.

Published
2022

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