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Obesity is a pandemic currently affecting the world's population that decreases the quality of life and promotes the development of chronic non-communicable diseases. Lactobacillus rhamnosus is recognized for multiple positive effects on obesity and overall health. In fact, such effects may occur even when the microorganisms do not remain alive (paraprobiotic effects). This raises the need to elucidate the mechanisms by which obesity-associated factors can be modulated. This narrative review explores recent findings on the effects of L. rhamnosus , particularly, its postbiotic and paraprobiotic effects, on the modulation of adiposity, weight gain, oxidative stress, inflammation, adipokines, satiety, and maintenance of intestinal integrity, with the aim of providing a better understanding of its mechanisms of action in order to contribute to streamlining its clinical and therapeutic applications. The literature shows that L. rhamnosus can modulate obesity-associated factors when analyzed in vitro and in vivo. Moreover, its postbiotic and paraprobiotic effects may be comparable to the more studied probiotic actions. Some mechanisms involve regulation of gene expression, intracellular signaling, and enteroendocrine communication, among others. We conclude that the evidence is promising, although there are still multiple knowledge gaps that require further study in order to fully utilize L. rhamnosus to improve human health.

The nutritional status is a determinant of the immune response that promotes a cellular homeostasis. In particular, adequate selenium levels lead to a better antioxidant and immune response. The aim of this work is to assess whether blood selenium levels, at time of SARS-CoV-2 infection, have an impact on the development and severity of COVID-19. A systematic review and meta-analysis of comparative and descriptive studies using MeSH terms, selenium and COVID-19 was performed. We searched bibliographic databases up to 17 July 2022 in PubMed and ScienceDirect. Studies that reported data on blood selenium levels were considered. A total of 629 articles were examined by abstract and title, of which 595 abstracts were read, of which 38 were included in the systematic review and 11 in the meta-analysis. Meta-analysis was conducted to mean difference (MD) with a 95 % confidence interval (CI), and heterogeneity was tested by I 2 with random factors with a MD between selenium levels, mortality, morbidity and healthy subjects with a P -value of 0⋅05. Selenium levels were higher in healthy people compared to those in patients with COVID-19 disease (six studies, random effects MD: test for overall effect Z = 3⋅28 ( P = 0⋅001), 97 % CI 28⋅36 (11⋅41-45⋅31), P < 0⋅00001), but without difference when compared with the degree of severity in mild, moderate or severe cases. In conclusion, the patients with active SARS-CoV-2 infection had lower selenium levels than the healthy population. More studies are needed to evaluate its impact on clinical severity through randomised clinical trials., (© The Author(s) 2023.)

Obesity is a serious health problem worldwide, since it is associated with multiple metabolic disorders and complications such as cardiovascular disease, type 2 diabetes, fatty liver disease and overall metabolic dysfunction. Dysregulation of the hunger-satiety pathway, which includes alterations of central and peripheral signaling, explains some forms of obesity by favoring hyperphagia and weight gain. The present work comprehensively summarizes the mechanisms by which naringenin (NAR), a predominant flavanone in citrus fruits, could modulate the main pathways associated with the development of obesity and some of its comorbidities, such as oxidative stress (OS), inflammation, insulin resistance (IR) and dyslipidemia, as well as the role of NAR in modulating the secretion of enterohormones of the satiety pathway and its possible antiobesogenic effect. The results of multiple in vitro and in vivo studies have shown that NAR has various potentially modulatory biological effects against obesity by countering IR, inflammation, OS, macrophage infiltration, dyslipidemia, hepatic steatosis, and adipose deposition. Likewise, NAR is capable of modulating peptides or peripheral hormones directly associated with the hunger-satiety pathway, such as ghrelin, cholecystokinin, insulin, adiponectin and leptin. The evidence supports the use of NAR as a promising alternative to prevent overweight and obesity., Competing Interests: The authors declare no conflicts of interest.

Infectious agents such as viruses, bacteria, and parasites can lead to cancer development. Infection with the helminthic parasite Schistosoma haematobium can cause cancer of the urinary bladder in humans, and infection with the parasites Clonorchis sinensis and Opisthorchis viverrini can promote cholangiocarcinoma. These three pathogens have been categorized as "group 1: carcinogenic to humans" by the International Agency for Research on Cancer (IARC). Additionally, the parasite Schistosoma japonicum has been associated with liver and colorectal cancer and classified as "group 2B: possibly carcinogenic to humans". These parasites express regulatory non-coding RNAs as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), which modulate genic expression in different biological processes. In this review, we discuss the potential roles of miRNAS and lncRNAs encoded by helminthic parasites that are classified by the IARC as carcinogenic and possibly carcinogenic to humans. The miRNAs of these parasites may be involved in carcinogenesis by modulating the biological functions of the pathogen and the host and by altering microenvironments prone to tumor growth. miRNAs were identified in different host fluids. Additionally, some miRNAs showed direct antitumoral effects. Together, these miRNAs show potential for use in future therapeutic and diagnostic applications. LncRNAs have been less studied in these parasites, and their biological effects in the parasite-host interaction are largely unknown.

Background: Patients with celiac disease (CD) require a gluten-free (GF) diet, including industrialized products containing ≤ 20 mg gluten/kg. The market status of GF food products is almost unknown in Mexico. Therefore, we studied the GF-labeled products on the northwestern Mexican market and analyzed their gluten content. Methods: We searched for GF type of foods in three different supermarkets of each chain in Mexicali Baja California and Hermosillo Sonora and corroborated the price, origin, and GF certification of each item using internet sites. We quantified the gluten in the foods using the sandwich R5-enzyme-linked immunosorbent assay (ELISA) and detected their immune-reactivity for IgA from patients with CD. Results: The study included >263 different GF-labeled foodstuffs, and 55% of them were made in Mexico. The Mexican items were principally flours, sausages, bread and bakery, milk-type products, and tortillas, while pasta, snacks, and breakfast cereals were mainly imported. The cost ratio of GF products to the conventional mean was 3.5, ranging principally from 1 to 13. The most common GF-labeled foods were flours and pasta (34), cookies and snacks (32), breakfast cereals, sausages, and milk-type products (18-20). Although 36% of the products were certified, 17.4% of the analyzed samples contained >20 mg gluten/kg, mainly the non-certified ones and those made in Mexico. IgA from patients with CD reacted in vitro against gluten proteins from the contaminated GF-labeled products. Conclusion: The accessibility of GF products in the northwestern Mexican market is wide; however, such products are expensive, and some could be risky for patients with CD because they contain gluten, which is recognized by the immune systems of these patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Calderón de la Barca, Luna-Alcocer, Valenzuela-Miranda and Mejía-León.)

Background: Intestinal bacterial dysbiosis and increased gut permeability are associated with higher risk of developing type 1 diabetes (T1D) or celiac disease (CD). There is a lack of information on parasitism involved in gut disturbance of predisposed children. We evaluated the effect of enteropathogenic parasites ( Cryptosporidium spp., Cyclospora spp. G. lamblia , and Blastocystis spp.) on the bacterial structure of feces from children with autoantibodies for T1D or CD. Participants included 37 children under 18 years of age, from whom stools were analyzed for enteric parasites by qPCR and 22/37 for bacterial profile by sequencing the V3-V4 region of the 16s rRNA gene. Dietary, clinical, and socioeconomic data was recorded., Results: Pathogens parasitized 28/37 participants, Cryptosporidium spp. was the most prevalent (62.2%), followed by both Cyclospora cayetanensis and Blastocystis spp (37.8%). There were no dietary differences ( p  > 0.05) attributable to parasitism. Co-infected participants with Cryptosporidium and Cyclospora did not differ (p = 0.064) from non-infected participants in bacterial alpha phylogenetic diversity. The same parasites' co-infection was associated with a decreased abundance of the Ruminococaceae (p = 0.04) and Verrucomicrobioceae families, of the Akkermansia genus (p = 0.009). There was a lower Firmicutes/Bacteroidetes ratio (p = 0.02) in infected than in uninfected participants., Conclusions: Cryptosporidium and Cyclospora affected the bacterial structure at family and genus levels, decreasing the ratio between Firmicutes and Bacteroidetes in children with auto-antibodies for T1D or CD, which could increase the risk of illness onset., Competing Interests: Competing interestsAuthors declare no conflict of interests., (© The Author(s) 2020.)

Objective: Gut dysbiosis in type 1 diabetes (T1D), characterized by high Bacteroides proportion, tends to reverse as T1D progresses, without reaching full recovery. Since diet influences microbiota structure, the aim was to evaluate the impact of dietary changes on Bacteroides proportion the first year of T1D evolution., Methods: Dietary intake was assessed by 24-hour recalls and Bacteroides proportion by quantitative polymerase chain reaction, in 10 Mexican children (11.6 ± 1.92 years) with T1D at baseline and 3, 6 and 9 months' follow-up. Repeated measures analysis of variance and multiple linear regression were performed to compare ingested nutrients in relation with Bacteroides proportion. Effects over time were evaluated by mixed regression models., Results: Patients with T1D decreased their energy (2621.89 to 1867.85 kcal, p = 0.028), protein (83.06 to 75.17 g, p = 0.012), and saturated fat consumption (40.83 to 25.23 g, p = 0.031) from baseline to 3 months, without posterior changes. Bacteroides proportion increased in the first months and tended to decrease at around 9 months (p > 0.05) and was positively correlated with saturated fat (β = 3.70, p = 0.009) and total carbohydrates (β = 0.73, p = 0.005) at 3 months. Carbohydrate consumption was related to decreased Bacteroides abundance over time (β = -14.9, p = 0.004), after adjusting for glycosylated hemoglobin., Conclusions: Besides autoimmunity, diet appears to have a central role determining the T1D-associated dysbiosis evolution.

Type 1 diabetes (T1D) is the second most frequent autoimmune disease in childhood. The long-term micro- and macro-vascular complications of diabetes are associated with the leading causes of disability and even mortality in young adults. Understanding the T1D etiology will allow the design of preventive strategies to avoid or delay the T1D onset and to help to maintain control after developing. T1D development involves genetic and environmental factors, such as birth delivery mode, use of antibiotics, and diet. Gut microbiota could be the link between environmental factors, the development of autoimmunity, and T1D. In this review, we will focus on the dietary factor and its relationship with the gut microbiota in the complex process involved in autoimmunity and T1D. The molecular mechanisms involved will also be addressed, and finally, evidence-based strategies for potential primary and secondary prevention of T1D will be discussed.

Background: Type 1 diabetes (T1D) is currently an autoimmune disease occurring more frequently and early in life. T1D development requires genetic predisposition and environmental factors, which influence the gut microbiota in early infancy and could increase the risk for T1D-associated autoimmunity. In Mexico there are no published microbiota studies in children <6 years old with T1D., Case Reports: We report two contrasting Mexican T1D cases of children <6 years of age and a third case of a healthy child prior to autoimmunity and T1D onset. Perinatal factors, feeding regimes in the first year of life and gut microbiota composition are discussed and related to the T1D onset. The three cases show a particular microbiota profile with decreased bacterial diversity as compared with healthy children, which could be related to environmental factors prior to the development of T1D and disease control., Conclusions: T1D infant cases presented a decreased bacterial diversity, which appeared before autoimmunity and T1D onset. Glycemic control could tend to correct the gut dysbiosis in T1D children. Prospective studies are needed to follow-up healthy children at high genetic risk to assess factors related to the microbiota structure., (Copyright © 2015 Hospital Infantil de México Federico Gómez. Publicado por Masson Doyma México S.A. All rights reserved.)

Background: Type 1 diabetes (T1D) and celiac disease (CD) are the 2 most common autoimmune childhood diseases that share their HLA-DQ2 and DQ8 genetic origin. There has currently been an increase in both diseases worldwide. In children from the low-population State of Sonora (15 inhabitants/km(2)) in north-western Mexico, there is no information on their genetic risk or the distribution of the related alleles in the general population., Aims: To compare the HLA-DQ allele frequency in a representative sample of newborns from Sonora with that of T1D and CD patients to determine the risk gradient, and to identify the presence of celiac autoimmunity in the T1D group., Methods: The study included 397 Sonoran newborns, with 44 cases of T1D, and 25 CD cases. The CD and T1D cases were clinically diagnosed by specialists at the Hospital Infantil del Estado de Sonora, and the autoantibodies were determined by ELISA. Whole blood was collected, gDNA was extracted, and HLA-DQ2 and DQ8 were typed by PCR-SSP. The risk gradient was calculated by comparing the allele frequencies of the cases with those of the newborns., Results: The Sonoran HLA-DQ risk heterodimer proportion was 16.1% for HLA-DQ2 and 13.6% for HLA-DQ8, with an HLA-DQ2:HLA-DQ8 ratio of 1.2:1. The DQ8/DQ2 genotype represented a 1:14 risk for T1D, whereas the DQ8/DQB1*0201 combination showed a 1:6 risk for CD. The prevalence of CD autoimmunity in T1D children was 7%., Conclusion: The Sonoran population has a distinctive HLA-DQ allele distribution due to its ancestry. The HLA-DQ8 combinations with DQ2 or one of its alleles conferred the highest risk for both diseases, and T1D and CD frequently appear together., (Copyright © 2015 Asociación Mexicana de Gastroenterología. Published by Masson Doyma México S.A. All rights reserved.)

Dysbiosis of the intestinal microbiota affecting the gut barrier could be triggering Type 1 Diabetes (T1D), the second most frequent autoimmune disease in childhood. This study compared the structure of the fecal microbiota in 29 mestizo children aged 7-18 years, including 8 T1D at onset, 13 T1D after 2 years treatment, and 8 healthy controls. Clinical information was collected, predisposing haplotypes were determined; the fecal DNA was extracted, the V4 region of the 16S rRNA gene amplified and 454-pyrosequenced. The newly diagnosed T1D cases had high levels of the genus Bacteroides (p < 0.004), whereas the control group had a gut microbiota dominated by Prevotella. Children with T1D treated for ≥2 years had levels of Bacteroides and Prevotella compared to those of the control group. The gut microbiota of newly diagnosed T1D cases is altered, but whether it is involved in disease causation or is a consequence of host selection remains unclear.