The Clinical Phenotype and Genetic Analysis of Monogenic Non Syndromic Obesity Caused by MC4R Gene Variation.

The gut–kidney axis has been widely studied in recent years because the gastrointestinal tract can play a major role in the initiation of systemic inflammation in kidney diseases such as acute renal injury, chronic kidney disease (CKD), IgA nephropathy, and the final stage of CKD known as end‐stage renal disease., , Recent studies have shown that gut inflammation throughout the digestive tract may be associated with weakness of the epithelial tight‐junction barrier in the gut, leading to increased permeability (leaky gut), and allowing bacterial DNA and endotoxin to pass into the bloodstream. Therefore, uncontrolled inflammation in the gut causes detrimental effects on other organs by activating the innate and adaptive immune cells and triggering the inflammatory signaling pathways, particularly the Nuclear Factor kappa‑light‑chain‑enhancer of activated B cells (NF‐κB) Mitogen‑Activated Protein Kinase (MAPK), and Janus Kinase – Signal Transducer and Activator of Transcription (JAK–STAT) pathways, and releasing pro‐inflammatory and inflammatory cytokines., The different roles of autophagy signaling pathway have also been observed in inflammatory reactions and regulatory responses to inflammation; thus, it may be considered as a beneficial treatment for kidney disorders. Growing evidence has suggested the great potential of autophagy to protect kidneys from various types of kidney inflammation such as acute, chronic, metabolic, and aging‐related kidney disorders. Therefore, it seems that the activation of the autophagy process could reduce the severity of inflammatory diseases by modulating inflammation in different organs, especially kidneys. Autophagy is also known as the physiologic process in which the components of cells can break down directly in the degradation process in lysosomes and autophagosomes. This pathway helps the cells and tissues in different organs to keep their homeostasis balanced. To maintain homeostasis, the autophagy mechanisms can work together to break down intracellular substances and supply degraded products. Disturbances in autophagy can interrupt cellular homeostasis and lead to the development of several infectious diseases and inflammatory‐related disorders. Past studies have reported that autophagy is involved both in inflammatory‐related diseases and in aging and lifespan extension., The studies have provided an overview of the close relationship between the gut and other organs (gut–organ axis) in inflammation control in numerous inflammatory diseases via triggering different inflammatory responses. and are two important groups of probiotics utilized in both human and animal health. According to recent research, there is strong evidence that probiotics may exhibit several therapeutic features, including anti‐inflammatory and immune‐modulatory abilities, through increasing the expression of genes involved in inflammatory signaling pathways, particularly NF‐κB, MAPK, and JAK–STAT pathways., Moreover, probiotics play an advantageous role in decreasing the level of pro‐inflammatory cytokines efficiently and increasing the level of anti‐inflammatory cytokines. As mentioned in previous studies, probiotics are also known as a natural biotreatment agent due to their numerous health‐promoting features and inherent ability to fight inflammatory‐related diseases, particularly CKD., Indeed, the advantageous effects of probiotics can assist in decreasing uremic toxin production and improving renal function in in vitro and animal models. In addition, human studies on probiotics in chronic inflammatory kidney disorders have attracted the attention of scientists and encouraged the scientific community in the past decade to comprehensively explore the therapeutic potentials of probiotics.,