Indicaxanthin is a betalain that is abundant in Opuntia ficus-indica orange fruit and has antioxidative and anti-inflammatory effects. Nevertheless, very little is known about the neuroprotective potential of indicaxa...Indicaxanthin is a betalain that is abundant in Opuntia ficus-indica orange fruit and has antioxidative and anti-inflammatory effects. Nevertheless, very little is known about the neuroprotective potential of indicaxanthin. This study investigated the impact of indicaxanthin on neuronal damage and gut microbiota dysbiosis induced by a high-fat diet in mice. The mice were divided into three groups according to different diets: the negative control group was fed a standard diet;the high-fat diet group was fed a high-fat diet;and the high-fat diet + indicaxanthin group was fed a high-fat diet and received indicaxanthin orally(0.86 mg/kg per day) for 4 weeks. Brain apoptosis, redox status, inflammation, and the gut microbiota composition were compared among the different animal groups. The results demonstrated that indicaxanthin treatment reduced neuronal apoptosis by downregulating the expression of proapoptotic genes and increasing the expression of antiapoptotic genes. Indicaxanthin also markedly decreased the expression of neuroinflammatory proteins and genes and inhibited high-fat diet–induced neuronal oxidative stress by reducing reactive oxygen and nitrogen species, malondialdehyde, and nitric oxide levels. In addition, indicaxanthin treatment improved the microflora composition by increasing the abundance of healthy bacterial genera, known as producers of short-chain fatty acids(Lachnospiraceae, Alloprovetella, and Lactobacillus), and by reducing bacteria related to unhealthy profiles(Blautia, Faecalibaculum, Romboutsia and Bilophila). In conclusion, indicaxanthin has a positive effect on high-fat diet–induced neuronal damage and on the gut microbiota composition in obese mice.展开更多
Obesity is widely recognized as a global epidemic,primarily driven by an imbalance between energy expenditure and caloric intake associated with a sedentary lifestyle.Diets high in carbohydrates and saturated fats,par...Obesity is widely recognized as a global epidemic,primarily driven by an imbalance between energy expenditure and caloric intake associated with a sedentary lifestyle.Diets high in carbohydrates and saturated fats,particularly palmitic acid,are potent inducers of chronic low-grade inflammation,largely due to disruptions in glucose metabolism and the onset of insulin resistance(Qiu et al.,2022).While many organs are affected,the brain,specifically the hypothalamus,is among the first to exhibit inflammation in response to an unhealthy diet,suggesting that obesity may,in fact,be a brain-centered disease with neuroinflammation as a central factor(Thaler et al., 2012).展开更多
Overweight and obesity has been a major public health problem globally.It was estimated that more than 2.1 billion adults were affected by overweight or obese in 2021 worldwide,about one fifth of whom lived in China^(...Overweight and obesity has been a major public health problem globally.It was estimated that more than 2.1 billion adults were affected by overweight or obese in 2021 worldwide,about one fifth of whom lived in China^([1]).By 2050,the country is forecast to remain the one with the largest population of overweight and obese globally^([1]),if no effective strategies were applied on overweight/obesity control.展开更多
With the industrialization of agriculture and the advancement of medical care,human life expectancy has increased considerably and continues to rise steadily.This results in novel and unprecedented challenges,namely o...With the industrialization of agriculture and the advancement of medical care,human life expectancy has increased considerably and continues to rise steadily.This results in novel and unprecedented challenges,namely obesity and neurodegeneration.展开更多
BACKGROUND Major depressive disorder(MDD)and obesity(OB)are bidirectionally comorbid conditions with common neurobiological underpinnings.However,the neurocognitive mechanisms of their comorbidity remain poorly unders...BACKGROUND Major depressive disorder(MDD)and obesity(OB)are bidirectionally comorbid conditions with common neurobiological underpinnings.However,the neurocognitive mechanisms of their comorbidity remain poorly understood.AIM To examine regional abnormalities in spontaneous brain activity among patients with MDD-OB comorbidity.METHODS This study adopted a regional homogeneity(ReHo)analysis of resting-state functional magnetic resonance imaging.The study included 149 hospital patients divided into four groups:Patients experiencing their first episode of drug-naive MDD with OB,patients with MDD without OB,and age-and sex-matched healthy individuals with and without OB.Whole-brain ReHo analysis was conducted using SPM12 software and RESTplus toolkits,with group comparisons via ANOVA and post-hoc tests.Correlations between ReHo values and behavioral measures were examined.RESULTS ANOVA revealed significant whole-brain ReHo differences among the four groups in four key regions:The left middle temporal gyrus(MTG.L),right cuneus,left precuneus,and left thalamus.Post-hoc analyses confirmed pairwise differences between all groups across these regions(P<0.05).OB was associated with ReHo alterations in the MTG.L,right cuneus,and left thalamus,whereas abnormalities in the precuneus suggested synergistic pathological mechanisms between MDD and OB.Statistically significant correlations were found between the drive and fun-seeking dimensions of the behavioral activation system,as well as behavioral inhibition and the corresponding ReHo values.CONCLUSION Our findings provide novel evidence for the neuroadaptive mechanisms underlying the MDD-OB comorbidity.Further validation could lead to personalized interventions targeting MTG.L hyperactivity and targeting healthy food cues.展开更多
BACKGROUND Organ transplantation has emerged as a globally prevalent therapeutic modality for end-stage organ failure,yet the post-transplantation trajectory is increasingly complicated by a spectrum of metabolic sequ...BACKGROUND Organ transplantation has emerged as a globally prevalent therapeutic modality for end-stage organ failure,yet the post-transplantation trajectory is increasingly complicated by a spectrum of metabolic sequelae,with obesity emerging as a critical clinical challenge.AIM To systematically review the multifactorial mechanisms underlying obesity following organ transplantation and to integrate evidence from pharmacological,behavioral,and molecular perspectives,thereby providing a foundation for targeted interventions.METHODS We conducted a systematic search in PubMed and Web of Science for literature published from 2020 to 15 July 2025.The search strategy incorporated terms including“obesity”,“overweight”and“post organ transplantation”.Only randomized controlled trials,meta-analyses,and systematic reviews were included.Non-empirical publications and irrelevant studies were excluded.Data extraction and quality assessment were performed by two independent reviewers,with disagreements resolved by a third researcher.RESULTS A total of 1457 articles were initially identified,of which 146 met the inclusion criteria.These studies encompassed liver,kidney,heart,and lung transplant recipients.Key findings indicate that immunosuppressive drugs-especially corticosteroids and calcineurin inhibitors-promote hyperphagia,insulin resistance,and dyslipidemia.Post-transplant sedentary behavior and hypercaloric diets further contribute to positive energy balance.At the molecular level,immunosuppressants disrupt adipokine signaling(e.g.,leptin and adiponectin),induce inflammatory and oxidative stress responses,and activate adipogenic pathways leading to lipid accumulation.CONCLUSION Post-transplant obesity arises from a complex interplay of pharmacological,behavioral,and molecular factors.A multidisciplinary approach-incorporating pharmacological modification,nutritional management,physical activity,and molecular-targeted therapies-is essential to mitigate obesity and improve transplant outcomes.Further large-scale and mechanistic studies are warranted to establish evidence-based preventive and treatment strategies.展开更多
基金funding from the European Union -NextGenerationEU through the Italian Ministry of University and Research under PRIN PNRR REG D.R.1718-2022– Project number PRJ-1575 INDICA。
文摘Indicaxanthin is a betalain that is abundant in Opuntia ficus-indica orange fruit and has antioxidative and anti-inflammatory effects. Nevertheless, very little is known about the neuroprotective potential of indicaxanthin. This study investigated the impact of indicaxanthin on neuronal damage and gut microbiota dysbiosis induced by a high-fat diet in mice. The mice were divided into three groups according to different diets: the negative control group was fed a standard diet;the high-fat diet group was fed a high-fat diet;and the high-fat diet + indicaxanthin group was fed a high-fat diet and received indicaxanthin orally(0.86 mg/kg per day) for 4 weeks. Brain apoptosis, redox status, inflammation, and the gut microbiota composition were compared among the different animal groups. The results demonstrated that indicaxanthin treatment reduced neuronal apoptosis by downregulating the expression of proapoptotic genes and increasing the expression of antiapoptotic genes. Indicaxanthin also markedly decreased the expression of neuroinflammatory proteins and genes and inhibited high-fat diet–induced neuronal oxidative stress by reducing reactive oxygen and nitrogen species, malondialdehyde, and nitric oxide levels. In addition, indicaxanthin treatment improved the microflora composition by increasing the abundance of healthy bacterial genera, known as producers of short-chain fatty acids(Lachnospiraceae, Alloprovetella, and Lactobacillus), and by reducing bacteria related to unhealthy profiles(Blautia, Faecalibaculum, Romboutsia and Bilophila). In conclusion, indicaxanthin has a positive effect on high-fat diet–induced neuronal damage and on the gut microbiota composition in obese mice.
文摘Obesity is widely recognized as a global epidemic,primarily driven by an imbalance between energy expenditure and caloric intake associated with a sedentary lifestyle.Diets high in carbohydrates and saturated fats,particularly palmitic acid,are potent inducers of chronic low-grade inflammation,largely due to disruptions in glucose metabolism and the onset of insulin resistance(Qiu et al.,2022).While many organs are affected,the brain,specifically the hypothalamus,is among the first to exhibit inflammation in response to an unhealthy diet,suggesting that obesity may,in fact,be a brain-centered disease with neuroinflammation as a central factor(Thaler et al., 2012).
文摘Overweight and obesity has been a major public health problem globally.It was estimated that more than 2.1 billion adults were affected by overweight or obese in 2021 worldwide,about one fifth of whom lived in China^([1]).By 2050,the country is forecast to remain the one with the largest population of overweight and obese globally^([1]),if no effective strategies were applied on overweight/obesity control.
文摘With the industrialization of agriculture and the advancement of medical care,human life expectancy has increased considerably and continues to rise steadily.This results in novel and unprecedented challenges,namely obesity and neurodegeneration.
基金Supported by Provincial Key Research Project of Henan Province,No.232102310081.
文摘BACKGROUND Major depressive disorder(MDD)and obesity(OB)are bidirectionally comorbid conditions with common neurobiological underpinnings.However,the neurocognitive mechanisms of their comorbidity remain poorly understood.AIM To examine regional abnormalities in spontaneous brain activity among patients with MDD-OB comorbidity.METHODS This study adopted a regional homogeneity(ReHo)analysis of resting-state functional magnetic resonance imaging.The study included 149 hospital patients divided into four groups:Patients experiencing their first episode of drug-naive MDD with OB,patients with MDD without OB,and age-and sex-matched healthy individuals with and without OB.Whole-brain ReHo analysis was conducted using SPM12 software and RESTplus toolkits,with group comparisons via ANOVA and post-hoc tests.Correlations between ReHo values and behavioral measures were examined.RESULTS ANOVA revealed significant whole-brain ReHo differences among the four groups in four key regions:The left middle temporal gyrus(MTG.L),right cuneus,left precuneus,and left thalamus.Post-hoc analyses confirmed pairwise differences between all groups across these regions(P<0.05).OB was associated with ReHo alterations in the MTG.L,right cuneus,and left thalamus,whereas abnormalities in the precuneus suggested synergistic pathological mechanisms between MDD and OB.Statistically significant correlations were found between the drive and fun-seeking dimensions of the behavioral activation system,as well as behavioral inhibition and the corresponding ReHo values.CONCLUSION Our findings provide novel evidence for the neuroadaptive mechanisms underlying the MDD-OB comorbidity.Further validation could lead to personalized interventions targeting MTG.L hyperactivity and targeting healthy food cues.
基金Supported by the National Natural Science Foundation of China,No.82305376the Youth Talent Support Project of the China Acupuncture and Moxibustion Association,No.2024-2026ZGZJXH-QNRC005+2 种基金the 2024 Jiangsu Province Youth Science and Technology Talent Support Project,No.JSTJ-2024-3802025 Jiangsu Provincial Science and Technology Think Tank Program Project,No.JSKX0125035and 2025 College Student Innovation Training Program Project,No.X202510315373。
文摘BACKGROUND Organ transplantation has emerged as a globally prevalent therapeutic modality for end-stage organ failure,yet the post-transplantation trajectory is increasingly complicated by a spectrum of metabolic sequelae,with obesity emerging as a critical clinical challenge.AIM To systematically review the multifactorial mechanisms underlying obesity following organ transplantation and to integrate evidence from pharmacological,behavioral,and molecular perspectives,thereby providing a foundation for targeted interventions.METHODS We conducted a systematic search in PubMed and Web of Science for literature published from 2020 to 15 July 2025.The search strategy incorporated terms including“obesity”,“overweight”and“post organ transplantation”.Only randomized controlled trials,meta-analyses,and systematic reviews were included.Non-empirical publications and irrelevant studies were excluded.Data extraction and quality assessment were performed by two independent reviewers,with disagreements resolved by a third researcher.RESULTS A total of 1457 articles were initially identified,of which 146 met the inclusion criteria.These studies encompassed liver,kidney,heart,and lung transplant recipients.Key findings indicate that immunosuppressive drugs-especially corticosteroids and calcineurin inhibitors-promote hyperphagia,insulin resistance,and dyslipidemia.Post-transplant sedentary behavior and hypercaloric diets further contribute to positive energy balance.At the molecular level,immunosuppressants disrupt adipokine signaling(e.g.,leptin and adiponectin),induce inflammatory and oxidative stress responses,and activate adipogenic pathways leading to lipid accumulation.CONCLUSION Post-transplant obesity arises from a complex interplay of pharmacological,behavioral,and molecular factors.A multidisciplinary approach-incorporating pharmacological modification,nutritional management,physical activity,and molecular-targeted therapies-is essential to mitigate obesity and improve transplant outcomes.Further large-scale and mechanistic studies are warranted to establish evidence-based preventive and treatment strategies.
