xMonitorace glukózy pomocí kontinuálních monitorů u pacientů s diabetem je v současné době běžným standardem v managementu kompenzace a léčby diabetu. Senzory se staly běžnou součástí života pacientů. Kromě záznamů běžných dní našich pacientů se diabetolog může setkat i se zcela nestandardním záznamem. Takový záznam analyzuje i následující kazuistika, která popisuje případ mladého muže s diabetes mellitus 1. typu, který měl v době tragické události aplikovaný glukózový senzor.
Glucose monitoring using continuous monitors in patients with diabetes is currently a common standard in the management of diabetes control and treatment. Sensors have become a common part of patients’ lives. In addition to the recorded data of the patients’ ordinary days, a diabetologist may also encounter a completely non-standard data record. Such a record is analysed in the following case report, which describes the case of a young man with type 1 diabetes mellitus who had a glucose sensor applied at the time of the tragic event.
Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing global health problem closely linked to dietary habits, particularly high fructose consumption. This study investigates the combined effects of fructose and common food preservatives (sodium benzoate, sodium nitrite, and potassium sorbate) on the development and progression of MASLD. Methods: We utilized a human microbiota-associated mouse model, administering 10% fructose with or without preservatives for 11 weeks. Liver histology, hepatic gene expression (microarray analysis), biochemical markers, cytokine profiles, intestinal permeability, and gut microbiome composition (16S rRNA and Internal Transcribed Spacer (ITS) sequencing) were evaluated. Results: Fructose and potassium sorbate synergistically induced liver pathology characterized by increased steatosis, inflammation and fibrosis. These histological changes were associated with elevated liver function markers and altered lipid profiles. The treatments also induced significant changes in both the bacterial and fungal communities and disrupted intestinal barrier function, leading to increased pro-inflammatory responses in the mesenteric lymph nodes. Liver gene expression analysis revealed a wide range of transcriptional changes induced by fructose and modulated by the preservative. Key genes involved in lipid metabolism, oxidative stress, and inflammatory responses were affected. Conclusions: Our findings highlight the complex interactions between dietary components, gut microbiota, and host metabolism in the development of MASLD. The study identifies potential risks associated with the combined consumption of fructose and preservatives, particularly potassium sorbate. Our data reveal new mechanisms that are involved in the development of MASLD and open up a new avenue for the prevention and treatment of MASLD through dietary interventions and the modulation of the microbiome.
- MeSH
- exprese genu účinky léků MeSH
- fruktosa * škodlivé účinky MeSH
- játra * metabolismus účinky léků MeSH
- kyselina sorbová farmakologie MeSH
- modely nemocí na zvířatech MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- potravinářské konzervační látky * farmakologie škodlivé účinky MeSH
- střevní mikroflóra * účinky léků MeSH
- synergismus léků MeSH
- ztučnělá játra MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
V následující kazuistice prezentuji případ 79leté pacientky s diabetes mellitus 2. typu s délkou trvání 16 let. Případ demonstruje, že ani selhání dlouhodobě dobře fungujícího konvenčního režimu nemusí pro pacienta automaticky znamenat převod na režim intenzifikovaný. Zvlášť u geriatrické populace může být navýšení počtu aplikací inzulínu zátěží nejen pro pacienty samotné, ale i pro okolí pacienta. Vhodnou změnou preparátu (z tradičních premixovaných inzulínů na Ryzodeg) bylo docíleno zlepšení kompenzace pacientky, aniž by došlo ke změně schématu léčby. Dalším benefitem bylo snížení hypoglykemií, které dovolilo ve spolupráci s pacientkou postupně navýšit celkovou denní dávku inzulínu, což vedlo ke zlepšení kompenzace.
The following case report presents a case of a 79-year-old female patient with type 2 diabetes mellitus with duration of 16 years. The case demonstrates that even the failure of a long-term well-functioning conventional regimen may not automatically mean a transfer to an intensified regimen for the patient. An appropriate change of the preparation (from traditional premixed insulins to Ryzodeg) improved the patient’s diabetes control without changing the treatment regimen. Another benefit was the reduction of hypoglycaemia, which allowed the patient to gradually increase the total daily dose of insulin, which led to further improvement in diabetes control.
- MeSH
- diabetes mellitus 2. typu * farmakoterapie MeSH
- fixní kombinace léků MeSH
- glykovaný hemoglobin analýza MeSH
- hypoglykemika terapeutické užití MeSH
- inzuliny * aplikace a dávkování MeSH
- lidé MeSH
- náhrada léků MeSH
- progrese nemoci MeSH
- senioři MeSH
- výsledek terapie MeSH
- Check Tag
- lidé MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- kazuistiky MeSH
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. Its worldwide prevalence is rapidly increasing and is currently estimated at 24%. NAFLD is highly associated with many features of the metabolic syndrome, including obesity, insulin resistance, hyperlipidaemia, and hypertension. The pathogenesis of NAFLD is complex and not fully understood, but there is increasing evidence that the gut microbiota is strongly implicated in the development of NAFLD. In this review, we discuss the major factors that induce dysbiosis of the gut microbiota and disrupt intestinal permeability, as well as possible mechanisms leading to the development of NAFLD. We also discuss the most consistent NAFLD-associated gut microbiota signatures and immunological mechanisms involved in maintaining the gut barrier and liver tolerance to gut-derived factors. Gut-derived factors, including microbial, dietary, and host-derived factors involved in NAFLD pathogenesis, are discussed in detail. Finally, we review currently available diagnostic and prognostic methods, summarise latest knowledge on promising microbiota-based biomarkers, and discuss therapeutic strategies to manipulate the microbiota, including faecal microbiota transplantation, probiotics and prebiotics, deletions of individual strains with bacteriophages, and blocking the production of harmful metabolites.
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
The worldwide incidence of many immune-mediated and metabolic diseases, initially affecting only the wealthy Western countries, is increasing rapidly. Many of these diseases are associated with the compositional and functional alterations of gut microbiota, i.e., dysbiosis. The most consistent markers of the dysbiosis are a decrease in microbiota diversity and an expansion of Proteobacteria. The role of food preservatives as potential triggers of gut microbiota dysbiosis has been long overlooked. Using a human microbiota-associated mouse model, we demonstrate that a mixture of common antimicrobial food additives induces dysbiosis characterised by an overgrowth of Proteobacteria phylum and a decrease in the Clostridiales order. Remarkably, human gut microbiota in a Nod2-deficient genetic background is even more susceptible to the induction of Proteobacteria dysbiosis by additives than the microbiota in a wild-type background. To conclude, our data demonstrate that antimicrobial food additives trigger gut microbiota dysbiosis in both wild-type and Nod2-deficient backgrounds and at the exposure levels reached in European populations. Whether this additive-modified gut microbiota plays a significant role in the pathogenesis of immune-mediated and metabolic diseases remains to be elucidated.
- Publikační typ
- časopisecké články MeSH
The aim of this work was to test the hypothesis that antimicrobial food additives may alter the composition of human gut microbiota by selectively suppressing the growth of susceptible gut microbes. To explore the influence of antimicrobial food additives on the composition of the human gut microbiota, we examined the susceptibility of both aerobic and anaerobic gut bacteria to sodium benzoate, sodium nitrite, and potassium sorbate, and their combinations, using a broth microdilution method. The tested bacteria exhibited a wide range of susceptibilities to food additives. For example, the most susceptible strain, Bacteroides coprocola, was almost 580 times more susceptible to sodium nitrite than the most resistant strain, Enterococcus faecalis. However, most importantly, we found that gut microbes with known anti-inflammatory properties, such as Clostridium tyrobutyricum or Lactobacillus paracasei, were significantly more susceptible to additives than microbes with known proinflammatory or colitogenic properties, such as Bacteroides thetaiotaomicron or Enterococcus faecalis. Our data show that some human gut microbes are highly susceptible to antimicrobial food additives. We speculate that permanent exposure of human gut microbiota to even low levels of additives may modify the composition and function of gut microbiota and thus influence the host's immune system. Whether the effect of additive-modified gut microbiota on the human immune system could explain, at least in part, the increasing incidence of allergies and autoimmune diseases remains to be shown.
