Publications by authors named "Taghreed Fadhul"

Background/objectives: Numerous studies have implicated high intake of sugar, particularly fructose, with the development of obesity and metabolic complications. On the other hand, fructose from fruits and vegetables has undisputed benefits for metabolic health. This paradox questions how the same fructose molecule can be associated with detrimental health effects in some studies and beneficial in others.

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Excessive fructose intake is a risk factor for the development of obesity and its complications. Targeting ketohexokinase (KHK), the first enzyme of fructose metabolism, has been investigated for the management of metabolic dysfunction-associated steatotic liver disease (MASLD). We compared the effects of systemic, small molecule inhibitor of KHK enzymatic activity with hepatocyte-specific, N-acetylgalactosamine siRNA-mediated knockdown of KHK in mice on an HFD.

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Non-alcoholic fatty liver disease (NAFLD) is a liver manifestation of metabolic syndrome, and is estimated to affect one billion individuals worldwide. An increased intake of a high-fat diet (HFD) and sugar-sweetened beverages are risk-factors for NAFLD development, but how their combined intake promotes progression to a more severe form of liver injury is unknown. Here we show that fructose metabolism via ketohexokinase (KHK) C isoform leads to unresolved endoplasmic reticulum (ER) stress when coupled with a HFD intake.

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Article Synopsis
  • Non-alcoholic fatty liver disease (NAFLD) affects around one billion people globally and is linked to a high-fat diet and sugar intake, but the precise mechanism of how these factors interact to worsen liver injury is not well understood.
  • The study identifies that the ketohexokinase (KHK) C isoform plays a crucial role in increasing endoplasmic reticulum (ER) stress when fructose intake is combined with a high-fat diet, leading to more severe liver damage.
  • By reducing KHK levels in certain mouse models, researchers found improvements in liver health, suggesting that targeting KHK could be a potential strategy for managing NAFLD and its metabolic effects.
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