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Gut mycobiome dysbiosis in rats showing retinal changes indicative of diabetic retinopathy.

ABSTRACT: The current study compared the gut mycobiomes of diabetic rats generated by a streptozotocin chemical challenge, diabetic rats with retinal changes and normal control rats over a period of 4 months. Sustained increase in blood sugar levels (>150 mg/dL) confirmed the induction of diabetes. Histology and immunohistochemistry were used to identify changes in the retinal tissues in the diabetic rats indicative of the animals progressing into diabetic retinopathy. Gut mycobiomes generated using faecal DNA, indicated dysbiosis at the genus level in both diabetic (DM) and diabetic rats with retinal changes (DRC) when compared with the control rats. In Tables 3-6 the specific genera that were significantly increased/decreased in DM1 and DM2 and in DRC1 and DRC2 respectively compared to the respective controls CT1-CT4 rats are listed. Further, the mycobiomes of the DM and DRC rats separated into distinct clusters following heat-map analysis of the discriminating genera. In addition, β-diversity analysis separated the mycobiomes of DM and DRC rats from that of the control rats, but the mycobiomes of diabetic rats and diabetic rats with retinal changes showed an overlap. Based on the inferred functions of the discriminating genera in the mycobiomes, we speculated that increase in pathogenic fungi might contribute to the inflammatory status both in diabetic rats and rats showing retinal changes.

SUBMITTER: Padakandla SR

PROVIDER: S-EPMC9017887 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Gut mycobiome dysbiosis in rats showing retinal changes indicative of diabetic retinopathy.

Padakandla Shalem Raj SR Das Taraprasad T Sai Prashanthi Gumpili G Angadi Kiran Kumar KK Reddy S Sreenivasa SS Reddy G Bhanuprakash GB Shivaji Sisinthy S

PloS one 20220419 4

The current study compared the gut mycobiomes of diabetic rats generated by a streptozotocin chemical challenge, diabetic rats with retinal changes and normal control rats over a period of 4 months. Sustained increase in blood sugar levels (>150 mg/dL) confirmed the induction of diabetes. Histology and immunohistochemistry were used to identify changes in the retinal tissues in the diabetic rats indicative of the animals progressing into diabetic retinopathy. Gut mycobiomes generated using faeca ...[more]

PMID: 35439275

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Project description:IntroductionDiabetic retinopathy (DR) is the most common complication of diabetes. Neuronal apoptosis, activated microglia, and microvascular changes are early features of DR. The gut microbiota is critical for the maturation and activation of microglia in the brain, and DR patients exhibit gut dysbiosis. However, the effect of the gut microbiota on retinal microglia under normal or diabetic conditions is still unclear.MethodsType 2 diabetes (T2D) was established in male adult Brown Norway (BN) rats, and they were treated with gavage of broad-spectrum antibiotic (ABX) suspension. Retinal fundus fluorescein angiography was performed to observe the dynamic growth process and leakage of blood vessels. Retro-orbital injection of FITC-Dextran was performed to observe the changes in blood-retinal barriers. After treatment with ABX and diabetes lasting for more than 6 months, 16S RNA sequencing of stool samples was performed to determine changes in the gut microbiome and mass spectrometry was used to analyze metabolome changes. IBA1, IB4, and Brn3 staining were performed on adult rats' retinal wholemount or sections to observe the changes in microglia, blood vessels and the number of ganglion cells.ResultsLong-term (6 months) T2D caused gut dysbiosis with increased average taxa numbers. We showed that broad-spectrum antibiotics (ABXs) gavage can reduce the average number of gut microbiota taxa and retinal microglia in adult male BN rats with or without T2D. Interestingly, adult male BN rats with T2D for more than 6 months showed a loss of retinal ganglion cells (RGCs) without significant changes in retinal microglia or retinal vascular vessels. However, ABX gavage reduced retinal microglia and alleviated RGC damage in these T2D rats.ConclusionOur data suggests that ABX gavage-induced gut dysbiosis can reduce retinal microglia in adult rats and alleviate RGC loss in long-term T2D rats. Targeting the gut microbiota may be a future therapeutic strategy for DR management.

Project description:IntroductionDiphenyl diselenide (DPDS) ameliorates nephropathy in streptozotocin (STZ)-induced type 1 diabetic rats by inhibiting oxidative stress and inflammatory reactions. However, it has not been clarified whether DPDS alleviates type 1 diabetic kidney disease (DKD) is related to the inhibition of extracellular matrix (ECM) production and the regulation of intestinal flora disorder.MethodsThe present study investigated the effects of DPDS on ECM generation in the kidney and intestinal microflora composition in feces. The rats were orally administered DPDS or metformin for eight weeks. Various indices were measured to assess the severity of renal injury. After euthanizing the rats, oxidative stress markers in serum and kidney were assessed using biochemical methods, and the expressions of ECM-related proteins in kidney were analyzed using Western blot. Additionally, 16S rRNA high-throughput sequencing was used to evaluate the diversity and composition of the intestinal flora in feces.ResultsThe results showed DPDS and metformin improved the DKD in STZ rats, as evidenced by decreased blood glucose, BUN, urine volume, urine microalbumin, urinary β2 microglobulin, and improvement of renal pathological morphology. Furthermore, DPDS intervention markedly reduced the protein expression of α-SMA, COI Ⅳ, FN, and vimentin in the kidneys. Besides, DPDS not only improved dyslipidemia in STZ diabetic rats, but also enhanced the activities of antioxidant enzymes, decreased the level of MDA in serum and kidney, and regulated the expression of proteins related to the Nrf2/Keap1 signaling pathway in the kidney. Moreover, we found that DPDS could selectively improve the relative abundance of probiotics as well as the diversity of flora, thus ameliorating the intestinal microbial composition of the STZ rats, significantly regulating the intestinal microbial homeostasis.DiscussionOverall, DPDS inhibited ECM production and improved renal pathological changes, which may be related to reducing oxidative stress damage in the kidney and improving intestinal flora imbalance, providing data support for the further development and application of DPDS in DKD.

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Gut mycobiome dysbiosis in rats showing retinal changes indicative of diabetic retinopathy.

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Gut mycobiome dysbiosis in rats showing retinal changes indicative of diabetic retinopathy.

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