Neuroprotective role of vitamin B12 in streptozotocin-induced type 1 diabetic rats.

Chronic hyperglycemia-induced neuropathological changes include neuronal apoptosis, astrogliosis, decrease in neurotrophic support, impaired synaptic plasticity, and impaired protein quality control (PQC) system. Vitamin B12 is indispensable for neuronal development and brain function. Several studies reported the neuroprotective effect of B12 supplementation in diabetic patients. However, the underlying molecular basis for the neuroprotective effect of B12 supplementation in diabetes needs to be thoroughly investigated. Two-month-old Sprague-Dawley rats were randomly assigned into three groups: Control (CN), diabetes (D; induced with streptozotocin; STZ), and diabetic rats supplemented with vitamin B12 (DBS; vitamin B12; 50 µg/kg) for four months. At the end of 4 months of experimentation, the brain was dissected to collect the cerebral cortex (CC). The morphology of CC was investigated with H&E and Nissl body staining. Neuronal apoptosis was determined with TUNEL assay. The components of neurotrophic support, astrogliosis, synaptic plasticity, and PQC processes were investigated by immunoblotting and immunostaining methods. H& E, Nissl body, and TUNEL staining revealed that diabetes-induced neuronal apoptosis and degeneration. However, B12 supplementation ameliorated the diabetes-induced neuronal apoptosis. Further, B12 supplementation restored the markers of neurotrophic support (BDNF, NGF, and GDNF), and synaptic plasticity (SYP, and PSD-95) in diabetic rats. Interestingly, B12 supplementation also attenuated astrogliosis, ER stress, and ameliorated autophagy-related proteins in diabetic rats. Overall, these findings suggest that B12 acts as a neuroprotective agent by inhibiting the neuropathological changes in STZ-induced type 1 diabetes. Thus, B12 supplementation could produce beneficial outcomes including neuroprotective effects in diabetic patients.

Diets, Lifestyles and Metabolic Risk Factors among Corporate Information Technology (IT) Employees in South India.

(1) Information Technology (IT) Business Process Outsourcing (BPO), the largest employment sector of India, contributes to rapid economic growth. However, the work of IT employees is sedentary, and the food environments of their worksites expose them to an obesogenic environment. This study aimed to assess their metabolic and lifestyle risk factors. (2) Methods: To examine the health and nutrition status of IT employees, anthropometric, biochemical and clinical assessments were conducted among 183 employees from three IT organizations of varied operational sizes. Their health-, diet- and physical activity-related practices were assessed using a questionnaire. The prevalence of MetS was assessed. Selected biomarker levels were assessed and associated with their self-perceived stress levels. (3) Results: The median age of the employees was 30 years (26-35 years). While 44.02% of employees were overweight, 16.85% of employees were obese. About 3.89% of employees were found to be diabetic, and HDL-C levels were lower than recommended in 64.93% of employees. In all, 29.87% of the study population were considered to have metabolic syndrome since they had metabolic risk scores ≥ 3. Those with metabolic syndrome were significantly older (p = 0.000), and levels of MDA (p = 0.003), homocysteine (p = 0.001), IL-6 (p = 0.017) and IL-4 (p = 0.000) were significantly higher among them. Although the prevalence of MetS was significantly lower among those aged >30 years, the lifestyle risk factors were significantly higher among them. (4) Conclusions: The assessed parameters indicate a high risk of developing NCDs among employees in the IT industry in India. This shows the need for the modification of lifestyle and workplace food and physical activity environments.

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

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, ß-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.

Dysbiosis in the Gut Microbiome in Streptozotocin-Induced Diabetes Rats and Follow-Up During Retinal Changes.

Purpose: To analyze the gut bacterial microbiome of streptozotocin-induced diabetic rats and rats with retinal changes. Methods: Induction of diabetes was confirmed by an increase in blood sugar (>150 mg/dL), and the progression of diabetes with retinal changes was assessed by histology and immunohistochemistry of retinal sections. Microbiomes were generated using fecal DNA, and the V3-V4 amplicons were sequenced and analyzed by QIIME and R. Results: Dysbiosis in the gut microbiome of diabetic rats and diabetic rats with retinal changes was observed at the phylum and genus levels compared with the control rats. Heat-map analysis based on the differentially abundant genera indicated that the microbiomes of controls and diabetic rats separated into two distinct clusters. The majority of the microbiomes in diabetic rats with retinal changes also formed a distinct cluster from the control rats. ß-diversity analysis separated the microbiome of control rats from the microbiome of diabetic rats and diabetic rats with retinal changes, but the microbiomes of diabetic rats and diabetic rats with retinal changes showed an overlap. Functional analysis indicated that the enhanced inflammation in diabetic rats showing retinal changes could be ascribed to a decrease in anti-inflammatory bacteria and an increase in pathogenic and proinflammatory bacteria. Conclusions: This study showed that the gut bacterial microbiome in diabetic rats with retinal changes was different compared with control rats. The results could help develop novel therapeutics for diabetics and diabetic individuals with retinal changes.