Type 2 diabetes is a leading cause of morbidity and a common risk of several disorders. Identifying the microbial ecology changes is essential for disease prediction, therapy, and prevention. Thus, our study is aimed at investigating the intestinal microbiota among healthy and type 2 diabetes individuals and exploring the effect of antidiabetic agents on gut bacterial flora. 24 type 2 diabetes (metformin, glimepiride, and nontherapeutic subgroups; N = 8 ) and 24 healthy control subjects were enrolled in this study, and intestinal bacterial microbiota was investigated by analyzing V3-V4 regions of 16S rRNA gene sequence. Numerous alterations were observed in the gut microbial community of diabetic individuals. These changes were characterized by a significant lowered abundance of Faecalibacterium, Fusobacterium, Dialister, and Elusimicrobium in the nontherapeutic subgroup compared to the healthy control group. Likewise, correlation analysis showed a substantial decline in gut microbiota richness and diversity with the duration of illness. Furthermore, antidiabetic agents restored to some extent the richness and diversity of gut microbiota and improved the abundance of many beneficial bacteria with a significant increase of Methanobrevibacter in the metformin subcategory compared to the nontherapeutic subgroup. In return, they decreased the abundance of some opportunistic pathogens. The findings of this study have added a novel understanding about the pathogenesis of the disease and the mechanisms underlying antidiabetic therapy, which are of potential interest for therapeutic lines and further studies.

Background Globally, urogenital and intestinal parasitosis remain significant health challenges. They are associated with rising morbidity, death, and many harmful outcomes. A little is known concerning parasitosis and type 2 diabetes mellitus. Our study planned to investigate the urogenital and intestinal parasitic infections among type 2 diabetes patients compare to non-diabetic (Control) individuals and examine the intensity of helminthiasis in both groups. Methods At Kosti Teaching Hospital (Sudan), 300 Urine and 300 stool samples have collected from 150 type 2 diabetes and 150 control individuals, along with the socio-demographic data using a structured questionnaire. The parasitic infections were examined by direct sedimentation technique for urine specimens. Whereas, for fecal samples, simple-direct saline, formal-ether concentration, Kato-Katz, and modified Ziehl–Neelsen techniques were used. Results Out of 150 type 2 diabetes patients studied, 31 (20.6%) and 14 (9.3%) had intestinal parasitosis and urogenital schistosomiasis, respectively. Whereas, 16 (10.6%) and 8 (5.3%) of the control group were infected, respectively. Compared to the control group, the odds of testing positive for either urogenital schistosomiasis (AOR: 2.548, 95% CI: 0.836–7.761, P = 0.100) or intestinal parasitic diseases (AOR: 2.099, 95% CI: 0.973–4.531, P = 0.059) were greater in diabetic individuals. Likewise, the intensities of helminthiasis were much higher in the diabetic patients and positively correlated with the duration of illness. The rate of urogenital schistosomiasis was also significantly different among the disease duration subcategories. Conclusions Our study has highlighted the relationship of type 2 diabetes with urogenital and intestinal parasitic infections and enhanced our knowledge about the frequency of particular urogenital and intestinal parasites as well as the intensity of helminths infection in type 2 diabetes compared to non-diabetic individuals, which are important for further studies.

Gut microbiota contributes to human health. Plenty of studies demonstrate that antibiotics can disrupt gut ecosystem leading to dysbiosis. Little is known about the microbial variation of appendix and its up/downstream intestine after antibiotic treatment. This study aimed to investigate the microbiome and mucosal morphology of jejunum, appendix, and colon of rats in health and dysbiosis. A rodent model of antibiotic-induced dysbiosis was employed. Microscopy was used to observe mucosal morphological changes. 16S rRNA sequencing was performed for identifying bacterial taxa and microbiome structure. The appendices of dysbiosis were found enlarged and inflated with loose contents. Microscopy revealed the impairment of intestinal epithelial cells. High-throughput sequencing showed the Operational Taxonomic Units changed from 361 ± 33, 634 ± 18, 639 ± 19 in the normal jejunum, appendix, colon to 748 ± 98, 230 ± 11, 253 ± 16 in the disordered segments, respectively. In dysbiosis, Bacteroidetes translocated inversely from the colon and appendix (0.26%, 0.23%) to the jejunum (13.87% ± 0.11%); the relative abundance of all intestinal Enterococcaceae increased, while Lactobacillaceae decreased. Several bacterial clusters were found correlated to the normal appendix, whereas nonspecific clusters correlated to the disordered appendix. In conclusion, species richness and evenness reduced in the disordered appendix and colon; similar microbiome patterns were shared between the appendix and colon regardless of dysbiosis; site-specific bacteria were missing in the disordered appendix. Appendix is likely a transit region involving in upper and lower intestinal microflora modulation. The limitation of this study is all the data were derived from rats. We must be cautious about translating the microbiome results from rats to humans.