Obesidade I: Visão geral e mecanismos moleculares e bioquímicos

https://www.sciencedirect.com/science/article/pii/S000629522200106X

Robert H. Lustig, David ^Collier, Christopher ^Kassotis, Troy A. ^Roepke, Min Ji ^Kime ^EtienneBlanc , Robert Barouki , ^{Amita Bansal}, Matthew C. Cave , ^SaurabhChatterjee ^,Mahua Choudhury , Michael ^Gilbertson, ^DominiqueLagadic – ^Gossmann, Sarah ^Howard mLars Lind ⁿCraig R. Tomlinson^oJan Vondracek ^pJerrold J. Heindel ^m

^aDivisão de Endocrinologia, Departamento de Pediatria, Universidade da Califórnia, San Francisco, CA 94143, Estados Unidos;

^bBrody School of Medicine, East Carolina University, Greenville, NC 27834, Estados Unidos;

^cInstituto de Ciências da Saúde Ambiental e Departamento de Farmacologia, Wayne State University, Detroit, MI 48202, Estados Unidos;

^dEscola de Ciências Ambientais e Biológicas, Rutgers University, New Brunswick, NJ 08901, Estados Unidos;

^eUniversidade Sorbonne Paris Nord, Bobigny, INSERM U1124 (T3S), Paris, França;

^fDepartamento de Bioquímica e Toxicologia, Universidade de Paris, INSERM U1224 (T3S), 75006 Paris, França;

^gFaculdade de Saúde e Medicina, Universidade Nacional Australiana, Canberra, Austrália

^hDivisão de Gastroenterologia, Hepatologia e Nutrição, Universidade de Louisville, Louisville, KY 40402, Estados Unidos;

Laboratório de Saúde e Doenças Ambientais, Universidade da Carolina do Sul, Columbia, SC 29208, Estados Unidos;

^jFaculdade de Farmácia, Texas A&M University, College Station, TX 77843, Estados Unidos;

^kGrupo de Pesquisa em Saúde Ocupacional e Ambiental, Universidade de Stirling, Stirling, Escócia, Reino Unido;

^lUniv Rennes, INSERM, EHESP, IRSET – UMR_S 1085, 35000 Rennes, França;

^mAmbiente Saudável e Estratégias de Disrupção Endócrina, Commonweal, Bolinas, CA 92924, Estados Unidos;

ⁿDepartamento de Ciências Médicas, Universidade de Uppsala, Uppsala, Suécia;

^oNorris Cotton Cancer Center, Departamento de Biologia Molecular e de Sistemas, Geisel School of Medicine em Dartmouth, Líbano, NH 03756, Estados Unidos;

^pDepartamento de Citocinética, Instituto de Biofísica da Academia Tcheca de Ciências, Brno, República Tcheca.

Recebido em 8 de dezembro de 2021, revisado em 12 de março de 2022, aceito em 15 de março de 2022, disponível on-line em 5 de abril de 2022, versão do registro em 25 de abril de 2022 .

Destaques

Há uma expansão global da obesidade e da pandemia de doenças não transmissíveis.

A obesidade é uma doença multifatorial, multiorgânica, multihormonal e multimecanística.

Influências genéticas e ambientais controlam a adiposidade e o ganho de peso.

Compreender os tecidos/órgãos, hormônios e mecanismos envolvidos na obesidade prepara o terreno para a compreensão das evidências da hipótese obesogênica.

Resumo

A obesidade é uma condição crônica e recorrente caracterizada pelo excesso de gordura corporal. Sua prevalência aumentou globalmente desde a década de 1970, e o número de pessoas obesas e com sobrepeso é agora maior do que aquelas com baixo peso. A obesidade é uma condição multifatorial e, como tal, muitos componentes contribuem para o seu desenvolvimento e patogênese. Esta é a primeira de três revisões complementares que consideram a obesidade (nt.: estão os fragmentos mais importantes dos textos das três, publicadas neste website. Os textos são longos e complexos, por isso escolhemos os aspectos que possam mais interessar a nós leigos, cidadãos e pais). Esta revisão se concentra na genética, vírus, resistência à insulina, inflamação, microbioma intestinal e ritmos circadianos que promovem a obesidade, juntamente com hormônios, fatores de crescimento e órgãos e tecidos que controlam seu desenvolvimento. Ele mostra que a regulação do balanço energético (ingestão versus gasto) depende da interação de uma variedade de hormônios do tecido adiposo, trato gastrointestinal, pâncreas, fígado e cérebro. Ela detalha como integrar neurotransmissores centrais e sinais metabólicos periféricos (por exemplo, leptina, insulina, grelina, peptídeo YY3-36) é essencial para controlar a homeostase energética e o comportamento alimentar. Descreve os diferentes tipos de adipócitos e como o desenvolvimento das células adiposas é controlado por hormônios e fatores de crescimento que atuam através de uma variedade de receptores, incluindo o receptor-gama ativado pelo proliferador de peroxissoma, retinóide X, insulina, estrogênio, andrógeno, glicocorticóide, hormônio da tireóide, fígado X, androstano constitutivo, pregnano X, farnesóide e receptores de hidrocarboneto aril. Finalmente, demonstra que a obesidade provavelmente tem origens no útero (nt.: aspecto importantíssimo porque estamos agredindo com as moléculas modernas sintéticas os que ainda nem nasceram. ESTAMOS DETERMINANDO A EXISTÊNCIA DESTA SÍNDROME NOS QUE PODERIAM NASCER SAUDÁVEIS). Compreender esses fatores bioquímicos de adiposidade e disfunção metabólica ao longo do ciclo de vida confere plausibilidade e credibilidade à “hipótese obesogênica” (ou seja, a importância de substâncias químicas ambientais que interrompem esses receptores para promover adiposidade ou alterar o metabolismo), elucidada mais detalhadamente na avaliações destas duas situações.

Resumo gráfico

1 . Introdução e tendências seculares

A obesidade é uma condição crônica e recidivante caracterizada pelo excesso de gordura corporal [1], [2]. Está entre os problemas de saúde globais mais críticos e uma pandemia crescente que afeta adultos, crianças e bebês [3], [4], [5]. As taxas de obesidade triplicaram desde a década de 1970, e a prevalência de obesidade em adultos nos EUA aumentou de 30,5% em 2000 para 42,4% em 2018, um aumento de 40% na frequência em menos de duas décadas [6]. Atualmente, existem mais indivíduos obesos globalmente do que aqueles que estão abaixo do peso [7], [8], [9]. (nt.: destaque dado pela tradução).

No entanto, esse aumento na prevalência da obesidade não se restringe aos humanos. Em 2011, Klimentidis e colegas [10] relataram pesos corporais médios na meia-idade de muitos animais, incluindo cães e gatos domésticos, primatas não humanos e roedores, independentemente das condições de vida (tanto selvagens quanto vivendo em colônias de pesquisa) também aumentou. Essas mudanças no peso dos animais em várias espécies sugerem que mudanças ambientais semelhantes impactaram tanto animais quanto humanos para promover a obesidade. Embora as mudanças no comportamento humano, sem dúvida, desempenhem um papel na manifestação da obesidade, mecanismos hormonais e bioquímicos específicos, fora de seu controle imediato, provavelmente contribuem.

Esta é a primeira de três revisões complementares com foco em obesidade e obesogênios. Esta primeira revisão delineia os órgãos e mecanismos responsáveis pela regulação do metabolismo e seu rígido controle por hormônios e seus respectivos receptores. A interrupção dessa regulação por hormônios ou outros estímulos ambientais pode levar à obesidade em qualquer momento do ciclo de vida, inclusive no pré-natal. A revisão complementar elucidará a química e a ação fisiopatológica dos obesogênicos – produtos químicos ambientais projetados para um propósito específico, como agrotóxicos, retardadores de chama ou plastificantes, mas que têm efeitos colaterais que interferem na ação hormonal – o que pode levar a alterações no metabolismo e, finalmente, à obesidade. A segunda revisão também estabelecerá o nexo causal entre os obesógenos e a obesidade, fornecendo explicitamente evidências que apoiam a “hipótese dos obesógenos” e discutirá as lacunas de pesquisa que devem ser exploradas. A terceira se concentrará em ensaios diretos e indiretos para detectar obesogênios.

2 . Obesidade e doença

[nota do website: não iremos transcrever todos os textos por serem técnicos e específicos, podendo tornar a leitura muito difícil e longa. Iremos somente colocar os aspectos que considerados relevantes para nós, os leigos.]

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3 . Desenvolvimento e função do tecido adiposo

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4 . Receptores envolvidos no controle do metabolismo energético

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5 . Neuroendocrinologia da obesidade

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6 . Natureza heterogênea do controle de peso e adiposidade

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7 . Mecanismos fisiopatológicos que promovem obesidade

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8 . Origens fetais da obesidade

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9 . Conclusões

Esta revisão concentrou-se nos tecidos/órgãos, hormônios, vias e mecanismos que desempenham papéis-chave no metabolismo para induzir o tecido adiposo, resultando em obesidade. A obesidade é uma doença multifuncional, multi-tecidos, multi-hormônio, multirreceptor e multimecanismo. Quando a obesidade resulta do aumento do VAT ou da gordura do fígado com grandes células de gordura, inflamação e resistência à insulina e à leptina, também está associada a vários distúrbios metabólicos, incluindo DM2 (nt.: diabetes tipo 2), DHGNA (nt.: doença hepática gordurosa não alcoólica), DCV (nt.: doença cardiovascular) e alguns tipos de câncer. Por outro lado, quando a obesidade resulta do aumento da TAS com pequenos adipócitos, inflamação limitada e atividade normal de insulina e leptina, há, em alguns casos, falta de perturbação metabólica correspondente, pelo menos inicialmente. A natureza multifuncional da obesidade resulta de muitos fatores de interação altamente coordenados que desempenham um papel na obesidade, incluindo fatores genéticos e ambientais. O ambiente inclui nutrição, exercício, vírus, microbioma, ritmos circadianos (esta revisão) e produtos químicos ambientais (discutidos na revisão complementar). Os fatores ambientais atuam nos complexos sistemas de órgãos interativos que controlam o metabolismo, incluindo tecido adiposo, trato gastrointestinal, músculo, pâncreas, fígado e várias partes do cérebro, que integram o controle do comportamento alimentar, incluindo a alimentação hedônica homeostática. O controle do desenvolvimento do tecido adiposo, bem como o número e tamanho dos adipócitos, depende da atividade e interação de uma variedade de fatores de transcrição, incluindo os dois reguladores mestres da adipogênese: PPARγ; e RXR , que pode ativar a adipogênese sozinho ou como um heterodímero com PPARγ. Os hormônios insulina, estrogênio, andrógeno, glicocorticóide e hormônio tireoidiano também desempenham papéis importantes no metabolismo e na adipogênese, ligando-se aos seus receptores. Outros fatores de transcrição do fígado modulam sinais metabólicos específicos, que podem levar à doença quando disfuncionais. O LXR, embora não seja ativado por hormônios específicos, regula a diferenciação dos adipócitos, o transporte de colesterol e o acúmulo de triglicerídeos. O PXR e o CAR parecem atuar em conjunto com o PPARγ e regulam a homeostase da glicose e energia e o metabolismo imunológico e lipídico. O FXR regula a síntese de ácidos biliares e o metabolismo lipídico, e o AhR pode resultar em resistência à insulina hepática. A ativação desses receptores pode resultar em hiperinsulinemia, resistência à leptina e ganho de peso.

Os tecidos e órgãos que controlam o metabolismo e, portanto, o ganho de peso, se comunicam por meio de uma rede de hormônios e neurotransmissores. Por exemplo, leptina, resistina e adiponectina são induzidas a partir de adipócitos; grelina e GIP do estômago; CCK, GLP-1, OXM e PYY_3-36 do trato gastrointestinal; insulina e glucagon do pâncreas; NPY-AgRP e POMC de neurônios hipotalâmicos; dopamina do VTA e NA; bem como estrogênio, andrógeno, hormônio tireoidiano e cortisol de suas respectivas glândulas endócrinas.

Embora a obesidade possa ocorrer ao longo da vida, ela pode ter suas origens durante o desenvolvimento fetal e a infância e, portanto, é regulada por mudanças na regulação epigenética ou na programação de desenvolvimento da expressão gênica. Essas perturbações são particularmente suscetíveis a influências ambientais.

Esta revisão do metabolismo destaca os órgãos e mecanismos responsáveis pela regulação da adiposidade. Também estabelece a hipótese de que substâncias químicas ambientais capazes de interromper esses mecanismos, denominadas obesogênicos, podem levar à obesidade. Numerosos compostos, alguns nutricionais e alguns disruptores endócrinos (EDCs/endocrine disruptors chemicals), podem afetar o controle hormonal da diferenciação, desenvolvimento, crescimento e/ou manutenção do tecido adiposo. Essas alterações subsequentemente resultam em efeitos diferenciais nos depósitos de gordura que podem afetar a disfunção metabólica. Assim, propomos que a mudança na prevalência e gravidade da obesidade é, pelo menos em parte, devido à ocorrência e acúmulo de várias alterações ambientais – na forma de má nutrição ou EDCs obesogênicos – em uma população geneticamente suscetível, o mais suscetível é o feto. O segundo artigo complementar revisará a plausibilidade, mecanismo e evidência para esses obesogênicos –in vitro , animais e humanos.

Financiamento

Christopher Kassotis, NIH, R00ES030405.

Dominique Lagadic-Gossman, European Union Horizon 2020 Research and Innovation Program, Oberon #825712.

Vesna Munic Kos, Swedish Research Council for Sustainable Development (FORMAS) #2019-00375.

Troy Roepke, NIH, R01MH12 3544, P30ES005022, USDA/NIFA NJ6195.

Jan Vondracek, Czech Science Foundation #21-005335, Institute of Biophysics of the Czech Academy of Science, RVO-68081707.

Robert Barouki, European Union Horizon 2020 Research and Innovation Program, Oberon #825712.

Amita Bansal, Diabetes Australia #S5610040.

Mathew Cave, NIH, R35ES028373, R01ES032189, T32ES011564, P42ES023716, P30ES030283, R21ES031510.

Saurabh Chatterjee, NIH, P20GM103641, P01ES028942, P01AT003961, DoD-IIRFA W81XWH1810374.

Mahua Choudhury, Morris L Lichtenstein Jr Medical Research Foundation.

David Collier, NIH, P30ES025128.

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