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O efeito de subprodutos do café nas alterações induzidas pela frutose no ambiente intestinal e no microbioma em ratos
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Introdução: O consumo excessivo de frutose associa-se ao desenvolvimento de Síndrome Metabólica (SM). O presente estudo avaliou o efeito da suplementação com Polpa de Café (PC) ou com Pele de Prata (SK) nas alterações intestinais morfológicas, metabólicas e microbiológicas induzidas por uma dieta rica em frutose. Métodos: Ratos Sprague-Dawley foram divididos aleatoriamente em seis grupos (n=6): Controlo (alimentação e água ad libitum); Frutose (alimentação e frutose 20% na água, ad libitum), PC (alimentação e água ad libitum e 250 mg/kg peso corporal/dia de PC), PC + Frutose (alimentação e frutose 20% na água, ad libitum e 250 mg/kg peso corporal/dia de PC), SK (alimentação e água ad libitum e 250 mg/kg peso corporal/dia de SK) e SK + Frutose (alimentação e frutose 20% na água, ad libitum e 250 mg/kg peso corporal/dia de SK). Os subprodutos foram administrados por gavagem, utilizando óleo de milho como veículo. Procedeu-se à avaliação de parâmetros biométricos, hemodinâmicos e bioquímicos. A análise intestinal incluiu a análise histológica, da expressão de genes codificadores de transportadores de açúcares e reguladores metabólicos por RT-qPCR, e do perfil da microbiota por sequenciação das zonas V3 e V4 do gene 16S rRNA. Resultados: A ingestão de frutose induziu um fenótipo de SM. A nível intestinal, originou uma sobrexpressão significativa dos transportadores de glicose SGLT1 (co-transportador sódio–glicose 1) e GLUT2 (transportador facilitativo de glicose 2), sem alteração significativa na expressão de GLUT5 (transportador facilitativo de glicose 5) relativamente ao grupo CONT. A suplementação com PC ou SK reverteu a sobrexpressão de SGLT1 e GLUT2 e induziu uma redução significativa da expressão de GLUT5, relativamente ao grupo Frutose. A ingestão de Frutose provocou também uma sobreexpressão muito acentuada dos recetores de sabor doce TAS1R2 e TAS1R3 e dos fatores de transcrição SREBP-1c (Sterol Regulatory Element-Binding Protein-1c) e ChREBP (Carbohydrate Response Element-Binding Protein). Quer a PC quer a SK foram capazes de anular o efeito da Frutose nos TAS1R2 e TAS1R3, e a SK impediu também a sobreexpressão do SREBP-1c e do ChREBP. A análise morfológica do duodeno e do jejuno não revelou efeitos significativos nem da frutose nem dos subprodutos do café (SK e PC), quer isoladamente quer em combinação. Finalmente, a análise da microbiota revelou que quer a PC quer a SK anularam as alterações induzidas pela Frutose na riqueza e diversidade (Shannon-diversidade), e que, adicionalmente, no grupo tratado com frutose + PC mas não no grupo Frutose + SK, ocorreu alteração na diversidade e composição (Beta-diversidade), e uma redução significativa da abundância do género Blautia. Conclusão: A PC e a SK mostraram-se capazes de reverter a maioria das alterações induzidas pela frutose a nível intestinal, através de vias distintas. A PC associa-se a uma maior capacidade de modulação da ecologia intestinal, enquanto a SK parece atuar por regulação da expressão de genes associados ao transporte de açúcares e à lipogénese.
Introduction: Excessive fructose consumption is associated with the development of Metabolic Syndrome (MS). The present study evaluated the effect of supplementation with Coffee Pulp (PC) or Silverskin (SK) on intestinal morphological, metabolic, and microbiological alterations induced by a high-fructose diet. Methods: Sprague-Dawley rats were randomly divided into six groups (n=6): Control (food and water ad libitum); Fructose (food and 20% fructose in water, ad libitum); PC (food and water ad libitum and 250 mg/kg body weight/day of PC); PC + Fructose (food and 20% fructose in water, ad libitum and 250 mg/kg body weight/day of PC); SK (food and water ad libitum and 250 mg/kg body weight/day of SK); and SK + Fructose (food and 20% fructose in water, ad libitum and 250 mg/kg body weight/day of SK). The by-products were administered by oral gavage, using corn oil as the vehicle. Biometric, hemodynamic, and biochemical parameters were evaluated. Intestinal analysis included histological assessment, gene expression of sugar transporters and metabolic regulators via RT-qPCR, and microbiota profiling by sequencing the V3 and V4 regions of the 16S rRNA gene. Results: Fructose intake induced a MetS phenotype. At the intestinal level, Fructose induced a significant overexpression of the glucose transporters SGLT1 (sodium-glucose co-transporter 1) and GLUT2 (facilitative glucose transporter 2), with no significant change in GLUT5 (facilitative glucose transporter 5) gene expression compared to the CONT group. PC or SK supplementation reversed SGLT1 and GLUT2 overexpression and induced a significant reduction in GLUT5 expression, compared to the Fructose group. Fructose intake also caused a very marked overexpression of sweet taste receptors TAS1R2 and TAS1R3 and of the transcription factors SREBP-1c (Sterol Regulatory Element-Binding Protein-1c) and ChREBP (Carbohydrate Response Element-Binding Protein). Both PC and SK were able to nullify the effect of Fructose on TAS1R2 and TAS1R3, and SK also prevented the overexpression of SREBP-1c and ChREBP. Morphological analysis of duodenum and jejunum did not reveal significant effects of Fructose and/or PC or SK. Finally, microbiota analysis revealed that both PC and SK were able to abolish the changes in richness and diversity (Shannon-diversity) induced by fructose. Additionally, changes in diversity and composition (Beta-diversity) and a significant reduction in the abundance of the genus Blautia were observed in the Fructose + PC-treated group, but not in the Fructose+ SK group. Conclusion: PC and SK were shown to be capable of reversing most of the fructose-induced changes at the intestinal level through distinct pathways. While PC is associated with a greater capacity to modulate the gut ecology, SK appears to modulate the expression of genes associated with sugar transport and lipogenesis.
Introduction: Excessive fructose consumption is associated with the development of Metabolic Syndrome (MS). The present study evaluated the effect of supplementation with Coffee Pulp (PC) or Silverskin (SK) on intestinal morphological, metabolic, and microbiological alterations induced by a high-fructose diet. Methods: Sprague-Dawley rats were randomly divided into six groups (n=6): Control (food and water ad libitum); Fructose (food and 20% fructose in water, ad libitum); PC (food and water ad libitum and 250 mg/kg body weight/day of PC); PC + Fructose (food and 20% fructose in water, ad libitum and 250 mg/kg body weight/day of PC); SK (food and water ad libitum and 250 mg/kg body weight/day of SK); and SK + Fructose (food and 20% fructose in water, ad libitum and 250 mg/kg body weight/day of SK). The by-products were administered by oral gavage, using corn oil as the vehicle. Biometric, hemodynamic, and biochemical parameters were evaluated. Intestinal analysis included histological assessment, gene expression of sugar transporters and metabolic regulators via RT-qPCR, and microbiota profiling by sequencing the V3 and V4 regions of the 16S rRNA gene. Results: Fructose intake induced a MetS phenotype. At the intestinal level, Fructose induced a significant overexpression of the glucose transporters SGLT1 (sodium-glucose co-transporter 1) and GLUT2 (facilitative glucose transporter 2), with no significant change in GLUT5 (facilitative glucose transporter 5) gene expression compared to the CONT group. PC or SK supplementation reversed SGLT1 and GLUT2 overexpression and induced a significant reduction in GLUT5 expression, compared to the Fructose group. Fructose intake also caused a very marked overexpression of sweet taste receptors TAS1R2 and TAS1R3 and of the transcription factors SREBP-1c (Sterol Regulatory Element-Binding Protein-1c) and ChREBP (Carbohydrate Response Element-Binding Protein). Both PC and SK were able to nullify the effect of Fructose on TAS1R2 and TAS1R3, and SK also prevented the overexpression of SREBP-1c and ChREBP. Morphological analysis of duodenum and jejunum did not reveal significant effects of Fructose and/or PC or SK. Finally, microbiota analysis revealed that both PC and SK were able to abolish the changes in richness and diversity (Shannon-diversity) induced by fructose. Additionally, changes in diversity and composition (Beta-diversity) and a significant reduction in the abundance of the genus Blautia were observed in the Fructose + PC-treated group, but not in the Fructose+ SK group. Conclusion: PC and SK were shown to be capable of reversing most of the fructose-induced changes at the intestinal level through distinct pathways. While PC is associated with a greater capacity to modulate the gut ecology, SK appears to modulate the expression of genes associated with sugar transport and lipogenesis.
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Síndrome metabólica Frutose Intestino Expressão génica Microbiota Polpa de café Pele de prata Metabolic syndrome Fructose Intestine Gene expression Microbiota Coffee pulp Coffee silverskin