जर्नल ऑफ़ डायबिटीज़ एंड क्लिनिकल प्रैक्टिस

खुला एक्सेस

हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।

ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं

अमूर्त

Diabetic Nephropathy in Pregnancy and Derived Metabolites Inmodulation

Eunyong Kim

The main cause of kidney disorders that are at their final stages is diabetic renal disease, which is a growing public health burden. Host-gut microbiota interactions have become increasingly important for maintaining host homeostasis in recent years. There is growing evidence for a bidirectional microbiota-kidney interaction in the setting of nephropathies, which is particularly noticeable with progressive kidney dysfunction [1]. In fact, chronic kidney disease alters the "healthy" microbiota structure, causing intestinal microbes to produce large amounts of uremic solutes that damage the kidneys [2]. On the other hand, the uremic state, fuelled by decreased renal clearance, causes changes in microbial metabolism and composition, creating a vicious cycle in which dysbiosis and renal dysfunction worsen over time [3]. We shall synthesise the data from clinical and experimental research in this review [4]. Since the previous several decades, there has been a marked increase in the frequency of both type 1 and type 2 diabetes worldwide, which has resulted in a significant increase in the prevalence of micro- and macrovascular complications [5]. The most frequent microvascular consequence and the main cause of end-stage renal disease, diabetic kidney disease, are thought to develop in 30 to 40% of diabetic individuals. Angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors, along with novel glucose-lowering medications like sodium-glucose transporter 2 inhibitors, have been shown to be effective in the traditional treatment of DKD. This has been shown to reduce diabetes-related cardiovascular morbidity and slow the progression of CKD in T2D patients [6]. However, the continued danger of developing ESKD is considerable, calling for the development of and strategies to effectively treat DKD or stop its resurgence [7]. Modifying kidney inflammation and the gut-kidney axis may be attractive therapeutic targets to stop DKD from developing into ESKD, for which renal transplantation is the only effective treatment [8]. Trillions of bacteria that coexist with the host in the digestive system, especially the large intestine, are housed there [9]. The native microorganisms supply the host with crucial metabolites through the bacterial manufacture of vitamins, secondary bile acids, and metabolism of food proteins and carbohydrates, while the host ensures an anaerobic habitat and nourishment for the microbiome [10].