Heat processing of food has been well validated as the trigger to generate heat-processing side product of advanced lipoxidation end products(ALEs),which potentially engenders the threat on systemic health or progress...Heat processing of food has been well validated as the trigger to generate heat-processing side product of advanced lipoxidation end products(ALEs),which potentially engenders the threat on systemic health or progression of diseases,especially the accumulated effect after long-term intake.Thus,the study was proposed to evaluate the effect of dietary ALEs on health after long-term ingestion,specifically through simulating the intake of dietary ALE in mice within 9 months to investigate the intervention effect and underlying mechanism.The unexpected observation of renal insufficiency or impairment after long-term intake of dietary ALEs indicated the negative impact on renal health,which has been verified by the pathological analysis.Further studies revealed that a high-ALEs diet disrupted the intestinal barrier,with enhanced impact after disturbing the gut microbiota to potentially lower the abundance of beneficial microbiome through producing nephrotoxic metabolites.Correlation analysis showed that the proliferation of harmful bacteria and the reduction of beneficial bacteria were strongly correlated with intestinal barrier damage and the development of renal insufficiency.Furthermore,the underlying mechanism was unveiled as that ALEs could inhibit AMPK/SIRT1 signaling to fundamentally induce renal inflammation and oxidative stress.Thus,it was revealed that long-term intake of dietary ALE could result in renal impairment,and the results emphasized the control or intervention on dietary ALE to decrease to accumulated impairment on systemic health.展开更多
Advanced lipoxidation end products(ALEs)are formed by modifying proteins with lipid oxidation products.ALEs formed in the body have been linked to diabetes and hepatic disease.However,it is not known whether ALEs form...Advanced lipoxidation end products(ALEs)are formed by modifying proteins with lipid oxidation products.ALEs formed in the body have been linked to diabetes and hepatic disease.However,it is not known whether ALEs formed in heat-processed foods can induce metabolic diseases.Our results indicate that dietary ALEs induce lipid accumulation in the liver of mice at an early stage and continuous feeding of ALEs induces inflammation,oxidative stress and hepatic insulin resistance.The core reason for these adverse reactions is the damage to the intestinal barrier caused by ALEs.Due to the damage to the intestinal barrier,there is an increase in lipopolysaccharides(LPS)in the liver that induces hepatic lipid accumulation by modulating hepatic lipid metabolism.Furthermore,ALEs plays a major role in the regulation of metabolic diseases by directly or indirectly inhibiting AMP activated protein kinase(AMPK)/Sirtuin 1(SIRT1)signaling through LPS.展开更多
The oxidative modification of myofibrillar proteins(MPs)has been identified as a crucial factor affecting meat quality during processing.We compared the effects of 4-hydroxy-2-nonenal(HNE)and lipoxygenase(LOX)-catalyz...The oxidative modification of myofibrillar proteins(MPs)has been identified as a crucial factor affecting meat quality during processing.We compared the effects of 4-hydroxy-2-nonenal(HNE)and lipoxygenase(LOX)-catalyzed linoleic acid(LA)oxidation products on the digestibility and gel properties in MPs from bighead carp.Both treatments resulted in decreased free amino acid content,reduced digestibility,and loss of amino acids in MPs.The HNE treatment enhanced gel strength by increasing hydrophobic interactions within the gel matrix.Conversely,the LOX-catalyzed LA oxidation enhanced disulfide bonds,leading to an agglomerated microstructure.Reduced myofibrillar protein(MP)solubility,primarily due to protein aggregation,was observed in the LA group but not in the HNE group.This distinction suggests that the impact on MP functionality is predominantly influenced by the protein aggregation induced by LOX-catalyzed LA oxidation rather than by HNE alone.展开更多
基金supported by grants from the National Natural Science Foundation of China(32030083)。
文摘Heat processing of food has been well validated as the trigger to generate heat-processing side product of advanced lipoxidation end products(ALEs),which potentially engenders the threat on systemic health or progression of diseases,especially the accumulated effect after long-term intake.Thus,the study was proposed to evaluate the effect of dietary ALEs on health after long-term ingestion,specifically through simulating the intake of dietary ALE in mice within 9 months to investigate the intervention effect and underlying mechanism.The unexpected observation of renal insufficiency or impairment after long-term intake of dietary ALEs indicated the negative impact on renal health,which has been verified by the pathological analysis.Further studies revealed that a high-ALEs diet disrupted the intestinal barrier,with enhanced impact after disturbing the gut microbiota to potentially lower the abundance of beneficial microbiome through producing nephrotoxic metabolites.Correlation analysis showed that the proliferation of harmful bacteria and the reduction of beneficial bacteria were strongly correlated with intestinal barrier damage and the development of renal insufficiency.Furthermore,the underlying mechanism was unveiled as that ALEs could inhibit AMPK/SIRT1 signaling to fundamentally induce renal inflammation and oxidative stress.Thus,it was revealed that long-term intake of dietary ALE could result in renal impairment,and the results emphasized the control or intervention on dietary ALE to decrease to accumulated impairment on systemic health.
基金supported by grants from the National Natural Science Foundation of China(32030083)。
文摘Advanced lipoxidation end products(ALEs)are formed by modifying proteins with lipid oxidation products.ALEs formed in the body have been linked to diabetes and hepatic disease.However,it is not known whether ALEs formed in heat-processed foods can induce metabolic diseases.Our results indicate that dietary ALEs induce lipid accumulation in the liver of mice at an early stage and continuous feeding of ALEs induces inflammation,oxidative stress and hepatic insulin resistance.The core reason for these adverse reactions is the damage to the intestinal barrier caused by ALEs.Due to the damage to the intestinal barrier,there is an increase in lipopolysaccharides(LPS)in the liver that induces hepatic lipid accumulation by modulating hepatic lipid metabolism.Furthermore,ALEs plays a major role in the regulation of metabolic diseases by directly or indirectly inhibiting AMP activated protein kinase(AMPK)/Sirtuin 1(SIRT1)signaling through LPS.
基金supported by the National Key R&D Program of China(2022YFD2100902)the National Natural Science Foundation of China(32172133)+1 种基金the earmarked fund forCARS(CARS-45)funded by Chiang Mai University.
文摘The oxidative modification of myofibrillar proteins(MPs)has been identified as a crucial factor affecting meat quality during processing.We compared the effects of 4-hydroxy-2-nonenal(HNE)and lipoxygenase(LOX)-catalyzed linoleic acid(LA)oxidation products on the digestibility and gel properties in MPs from bighead carp.Both treatments resulted in decreased free amino acid content,reduced digestibility,and loss of amino acids in MPs.The HNE treatment enhanced gel strength by increasing hydrophobic interactions within the gel matrix.Conversely,the LOX-catalyzed LA oxidation enhanced disulfide bonds,leading to an agglomerated microstructure.Reduced myofibrillar protein(MP)solubility,primarily due to protein aggregation,was observed in the LA group but not in the HNE group.This distinction suggests that the impact on MP functionality is predominantly influenced by the protein aggregation induced by LOX-catalyzed LA oxidation rather than by HNE alone.
