Gut microbiota dysbiosis -associated obesity and its involvement in cardiovascular diseases and type 2 diabetes. A systematic review

Hamjane, Nadia; Mechita, Mohcine Bennani; Nourouti, Naima Ghailani; Barakat, Amina

doi:10.1016/j.mvr.2023.104601

Cited by 12 publications

(10 citation statements)

References 139 publications

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“…Gut microbiota dysbiosis has serious consequences for the host’s health, including obesity, T2D, and cardiovascular diseases, which represent major health problems in several countries around the world [ 99 ]. There are other diseases associated with microbiota dysbiosis, such as chronic obstructive pulmonary disease [ 100 ], Huntington’s disease [ 101 ], immune-mediated necrotizing myopathy [ 102 ], neuroinflammation and neurodegeneration [ 103 ], Alzheimer’s disease [ 104 ], Parkinson´s disease [ 105 ], and even increased susceptibility to COVID-19, as recently observed [ 106 ].…”

Section: Gut Microbiota Dysbiosis Arises From Sleep Deprivationmentioning

confidence: 99%

Chronodisruption and Gut Microbiota: Triggering Glycemic Imbalance in People with Type 2 Diabetes

Moreno-Cortés,

Meza-Alvarado,

García-Mena

et al. 2024

Nutrients

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The desynchronization of physiological and behavioral mechanisms influences the gut microbiota and eating behavior in mammals, as shown in both rodents and humans, leading to the development of pathologies such as Type 2 diabetes (T2D), obesity, and metabolic syndrome. Recent studies propose resynchronization as a key input controlling metabolic cycles and contributing to reducing the risk of suffering some chronic diseases such as diabetes, obesity, or metabolic syndrome. In this analytical review, we present an overview of how desynchronization and its implications for the gut microbiome make people vulnerable to intestinal dysbiosis and consequent chronic diseases. In particular, we explore the eubiosis–dysbiosis phenomenon and, finally, propose some topics aimed at addressing chronotherapy as a key strategy in the prevention of chronic diseases.

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Section: Gut Microbiota Dysbiosis Arises From Sleep Deprivationmentioning

confidence: 99%

Chronodisruption and Gut Microbiota: Triggering Glycemic Imbalance in People with Type 2 Diabetes

Moreno-Cortés,

Meza-Alvarado,

García-Mena

et al. 2024

Nutrients

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“…The liver has a dual blood supply, the hepatic arterial system and the portal vein system, with approximately 70% of the blood supply coming from the portal vein, a direct outflow from the intestine. , In 1998, Marshall first proposed the gut–liver axis hypothesis, suggesting that a disrupted intestinal barrier leads to the transport of gut-derived bacteria and bacterial metabolites (such as LPS) into the liver, thereby activating inflammatory pathways and causing irrecoverable metabolic disorders. ,− Therefore, the development of glucose homeostatic imbalance by exogenous stimulation via the gut–liver axis deserves further investigation. Some nanoparticles in food (<100 nm) may contribute to metabolic disease development by altering the gut microbiota.…”

Section: Introductionmentioning

confidence: 99%

Foodborne Carbon Dots Aggravate High-Fat-Diet-Induced Glucose Homeostasis Imbalance by Disrupting the Gut-Liver Axis

Zhang,

Yu,

Zhao

et al. 2024

ACS Appl. Mater. Interfaces

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Foodborne carbon dots (CDs) are generally produced during cooking and exist in food items. Generally, CDs are regarded as nontoxic materials, but several studies have gradually confirmed the cytotoxicity of CDs, such as oxidative stress, reduced cellular activity, apoptosis, etc. However, studies focusing on the health effects of long-term intake of food-borne CDs are scarce, especially in populations susceptible to metabolic disease. In this study, we reported that CDs in self-brewing beer had no effect on glucose metabolism in CHOW-fed mice but exacerbated high-fat-diet (HFD)-induced glucose metabolism disorders via the gut-liver axis. Chronic exposure to foodborne CDs increased fasting glucose levels and exacerbated liver and intestinal barrier damage in HFD-fed mice. The 16s rRNA sequencing analysis revealed that CDs significantly altered the gut microbiota composition and promoted lipopolysaccharide (LPS) synthesis-related KEGG pathways (superpathway of (Kdo)2-lipid A, Kdo transfer to lipid IVA Ill (Chlamydia), lipid IVA biosynthesis, and so on) in HFD-fed mice. Mechanically, CD exposure increased the abundance of Gram-negative bacteria (Proteobacteria and Desulfovibrionaceae), thus producing excessive endotoxin-LPS, and then LPS was transferred by the blood circulation to the liver due to the damaged intestinal barrier. In the liver, LPS promoted TLR4/NF-κB/P38 MAPK signaling, thus enhancing systemic inflammation and exacerbating HFD-induced insulin resistance. However, pretreating mice with antibiotics eliminated these effects, indicating a key role for gut microbiota in CDs exacerbating glucose metabolism disorders in HFD-fed mice. The finding herein provides new insight into the potential health risk of foodborne nanoparticles in susceptible populations by disturbing the gut-liver axis.

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“…Importantly, we have recently discovered differences in biodiversity and composition of intestinal microbes in a cohort of Italian patients affected by CDD (16). Disturbances in the composition or equilibrium of the gut microbiota, termed dysbiosis, have been associated with inflammatory bowel disease (IBD), metabolic disturbances, and even neuropsychiatric conditions (17–20). Nevertheless, the composition of the intestinal microbiota in widely used CDD models, and the impact of alterations in microbiota composition on neurologically relevant outcomes has not been explored.…”

Section: Introductionmentioning

confidence: 99%

Multi-Site Investigation of Gut Microbiota in CDKL5 Deficiency Disorder Mouse Models: Targeting Dysbiosis to Improve Neurological Outcomes

Damiani,

Giuliano,

Cornuti

et al. 2024

Preprint

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BackgroundCyclin-Dependent Kinase-Like 5 (CDKL5) deficiency disorder (CDD) is a rare X-linked developmental encephalopathy caused by pathogenic variants of the CDKL5 gene. In addition to a diverse range of neurological symptoms, CDD patients frequently manifest gastrointestinal (GI) issues and subclinical immune dysregulation. This comorbidity suggests a potential association with the intestinal microbiota, prompting an investigation into whether gut dysbiosis contributes to the severity of both GI and neurological symptoms.MethodsWe examined the gut microbiota composition in two CDKL5 null (KO) mouse models in males at three different developmental stages: postnatal day (P) 25 and P32 during youth, and P70 during adulthood.ResultsChanges in diversity and composition were observed, particularly during juvenile ages, suggesting a potential gut microbiota dysbiosis in the CDD mouse models. To further understand the role of the gut microbiota in CDD, we administered an antibiotic cocktail to the mice and conducted functional and behavioral assessments. Remarkably, significant improvement in visual cortical responses and reductions in hyperactive behavior were observed. To shed light on the cellular mechanisms we focused on microglia. Alterations in specific aspects of microglia morphology, indicative of activation state and surveillance of the microenvironment, were observed in the CDKL5 KO mice and ameliorated by antibiotic administration.ConclusionsOur findings highlight the potential impact of modifications in the intestinal microbiota on the severity of CDD symptoms, expanding our understanding beyond GI disturbances to encompass influences on neurological outcomes. This cross-border study provides valuable insights into the intricate interplay between gut microbiota and neurodevelopmental disorders.

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Gut microbiota dysbiosis -associated obesity and its involvement in cardiovascular diseases and type 2 diabetes. A systematic review

Cited by 12 publications

References 139 publications

Chronodisruption and Gut Microbiota: Triggering Glycemic Imbalance in People with Type 2 Diabetes

Chronodisruption and Gut Microbiota: Triggering Glycemic Imbalance in People with Type 2 Diabetes

Foodborne Carbon Dots Aggravate High-Fat-Diet-Induced Glucose Homeostasis Imbalance by Disrupting the Gut-Liver Axis

Multi-Site Investigation of Gut Microbiota in CDKL5 Deficiency Disorder Mouse Models: Targeting Dysbiosis to Improve Neurological Outcomes

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