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1.
Nutrients ; 15(15)2023 Jul 28.
Article in English | MEDLINE | ID: mdl-37571301

ABSTRACT

Obesity is a multifactorial disease that continues to increase in prevalence worldwide. Emerging evidence has shown that the development of obesity may be influenced by taxonomic shifts in gut microbiota in response to the consumption of dietary fats. Further, these alterations in gut microbiota have been shown to promote important changes in satiation signals including gut hormones (leptin, ghrelin, GLP-1, peptide YY and CCK) and orexigenic and anorexigenic neuropeptides (AgRP, NPY, POMC, CART) that influence hyperphagia and therefore obesity. In this review, we highlight mechanisms by which gut microbiota can influence these satiation signals both locally in the gastrointestinal tract and via microbiota-gut-brain communication. Then, we describe the effects of dietary interventions and associated changes in gut microbiota on satiety signals through microbiota-dependent mechanisms. Lastly, we present microbiota optimizing therapies including prebiotics, probiotics, synbiotics and weight loss surgery that can help restore beneficial gut microbiota by enhancing satiety signals to reduce hyperphagia and subsequent obesity. Overall, a better understanding of the mechanisms by which dietary fats induce taxonomical shifts in gut microbiota and their impact on satiation signaling pathways will help develop more targeted therapeutic interventions in delaying the onset of obesity and in furthering its treatment.


Subject(s)
Gastrointestinal Microbiome , Probiotics , Humans , Dietary Fats/therapeutic use , Obesity/metabolism , Prebiotics , Eating , Hyperphagia
2.
Int J Mol Sci ; 23(16)2022 Aug 18.
Article in English | MEDLINE | ID: mdl-36012562

ABSTRACT

Coronaviruses represent a diverse family of enveloped positive-sense single stranded RNA viruses. COVID-19, caused by Severe Acute Respiratory Syndrome Coronavirus-2, is a highly contagious respiratory disease transmissible mainly via close contact and respiratory droplets which can result in severe, life-threatening respiratory pathologies. It is understood that glutathione, a naturally occurring antioxidant known for its role in immune response and cellular detoxification, is the target of various proinflammatory cytokines and transcription factors resulting in the infection, replication, and production of reactive oxygen species. This leads to more severe symptoms of COVID-19 and increased susceptibility to other illnesses such as tuberculosis. The emergence of vaccines against COVID-19, usage of monoclonal antibodies as treatments for infection, and implementation of pharmaceutical drugs have been effective methods for preventing and treating symptoms. However, with the mutating nature of the virus, other treatment modalities have been in research. With its role in antiviral defense and immune response, glutathione has been heavily explored in regard to COVID-19. Glutathione has demonstrated protective effects on inflammation and downregulation of reactive oxygen species, thereby resulting in less severe symptoms of COVID-19 infection and warranting the discussion of glutathione as a treatment mechanism.


Subject(s)
COVID-19 , COVID-19/therapy , COVID-19 Vaccines , Glutathione , Humans , Reactive Oxygen Species , SARS-CoV-2
3.
Infect Dis Rep ; 13(4): 1018-1035, 2021 Dec 04.
Article in English | MEDLINE | ID: mdl-34940403

ABSTRACT

COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has infected over 200 million people, causing over 4 million deaths. COVID-19 infection has been shown to lead to hypoxia, immunosuppression, host iron depletion, hyperglycemia secondary to diabetes mellitus, as well as prolonged hospitalizations. These clinical manifestations provide favorable conditions for opportunistic fungal pathogens to infect hosts with COVID-19. Interventions such as treatment with corticosteroids and mechanical ventilation may further predispose COVID-19 patients to acquiring fungal coinfections. Our literature review found that fungal coinfections in COVID-19 infected patients were most commonly caused by Aspergillus, Candida species, Cryptococcus neoformans, and fungi of the Mucorales order. The distribution of these infections, particularly Mucormycosis, was found to be markedly skewed towards low- and middle-income countries. The purpose of this review is to identify possible explanations for the increase in fungal coinfections seen in COVID-19 infected patients so that physicians and healthcare providers can be conscious of factors that may predispose these patients to fungal coinfections in order to provide more favorable patient outcomes. After identifying risk factors for coinfections, measures should be taken to minimize the dosage and duration of drugs such as corticosteroids, immunosuppressants, and antibiotics.

4.
Infect Dis Rep ; 13(3): 821-834, 2021 Sep 06.
Article in English | MEDLINE | ID: mdl-34562999

ABSTRACT

Tuberculosis disease is caused by the bacterium Mycobacterium tuberculosis. It is estimated that 10 million people have developed tuberculosis disease globally, leading to 1.4 million deaths in 2019. Treatment of tuberculosis has been especially challenging due to the rise of multidrug-resistant (MDR-TB) and extensive drug-resistant (XDR-TB) tuberculosis. In addition to drug-resistant genotypes, the standard treatment of tuberculosis by first-line agents is also challenging due to toxicity and costs. In the last four decades, there have only been two new anti-tuberculosis agents-bedaquiline and delamanid. Therefore, shorter, safer, and more cost-effective therapies are needed to adequately treat tuberculosis. In this review, we explore various adjuvants such as glutathione, everolimus, vitamin D, steroid, aspirin, statin, and metformin and their usefulness in reducing the burden of tuberculosis. Glutathione, everolimus, aspirin, and metformin showed the most promise in alleviating the burden of tuberculosis. Despite their potential, more clinical trials are needed to unequivocally establish the effectiveness of these adjuvants as future clinical therapies. Methods: The journals for this review were selected by conducting a search via PubMed, Google Scholar, and The Lancet. Our first search included keywords such as "tuberculosis" and "adjuvant therapy." From the search, we made a list of adjuvants associated with tuberculosis, and this helped guide us with our second online database search. Using the same three online databases, we searched "tuberculosis" and "respective therapy." The adjuvants included in the paper were selected based on the availability of sufficient research and support between the therapy and tuberculosis. Adjuvants with minimal research support were excluded. There were no specific search criteria regarding the timing of publication, with our citations ranging between 1979 to 2021.

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