Adropin is a novel 76-amino acid-peptide that is expressed in different tissues and cells including the liver, pancreas, heart and vascular tissues, kidney, milk, serum, plasma and many parts of the brain. Adropin, encoded by the Enho gene, plays a crucial role in energy homeostasis. The literature review indicates that adropin alleviates the degree of insulin resistance by reducing endogenous hepatic glucose production. Adropin improves glucose metabolism by enhancing glucose utilization in mice, including the sensitization of insulin signaling pathways such as Akt phosphorylation and the activation of the glucose transporter 4 receptor. Several studies have also demonstrated that adropin improves cardiac function, cardiac efficiency and coronary blood flow in mice. Adropin can also reduce the levels of serum triglycerides, total cholesterol and low-density lipoprotein cholesterol. In contrast, it increases the level of high-density lipoprotein cholesterol, often referred to as the beneficial cholesterol. Adropin inhibits inflammation by reducing the tissue level of pro-inflammatory cytokines such as tumor necrosis factor alpha and interleukin-6. The protective effect of adropin on the vascular endothelium is through an increase in the expression of endothelial nitric oxide synthase. This article provides an overview of the existing literature about the role of adropin in different pathological conditions.

Diabetes mellitus (DM) is a chronic illness with an increasing global prevalence. More than 537 million cases of diabetes were reported worldwide in 2021, and the number is steadily increasing. The worldwide number of people suffering from DM is projected to reach 783 million in 2045. In 2021 alone, more than USD 966 billion was spent on the management of DM. Reduced physical activity due to urbanization is believed to be the major cause of the increase in the incidence of the disease, as it is associated with higher rates of obesity. Diabetes poses a risk for chronic complications such as nephropathy, angiopathy, neuropathy and retinopathy. Hence, the successful management of blood glucose is the cornerstone of DM therapy. The effective management of the hyperglycemia associated with type 2 diabetes includes physical exercise, diet and therapeutic interventions (insulin, biguanides, second generation sulfonylureas, glucagon-like peptide 1 agonists, dipeptidyl-peptidase 4 inhibitors, thiazolidinediones, amylin mimetics, meglitinides, α-glucosidase inhibitors, sodium-glucose cotransporter-2 inhibitors and bile acid sequestrants). The optimal and timely treatment of DM improves the quality of life and reduces the severe burden of the disease for patients. Genetic testing, examining the roles of different genes involved in the pathogenesis of DM, may also help to achieve optimal DM management in the future by reducing the incidence of DM and by enhancing the use of individualized treatment regimens.

Unlike other organs, the importance of VD in a normal stomach is unknown. This study focuses on understanding the physiological role of vitamin D in gastric epithelial homeostasis. C57BL/6J mice were divided into three groups that were either fed a standard diet and kept in normal light/dark cycles (SDL), fed a standard diet but kept in the dark (SDD) or fed a vitamin D-deficient diet and kept in the dark (VDD). After 3 months, sera were collected to measure vitamin D levels by LC-MS/MS, gastric tissues were collected for immunohistochemical and gene expression analyses and gastric contents were collected to measure acid levels. The VDD group showed a significant decrease in the acid-secreting parietal cell-specific genes Atp4a and Atp4b when compared with the controls. This reduction was associated with an increased expression of an antral gastrin hormone. VDD gastric tissues also showed a high proliferation rate compared with SDL and SDD using an anti-BrdU antibody. This study indicates the requirement for normal vitamin D levels for proper parietal cell functions.

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Spexin is a newly discovered gastrointestinal tract (GIT) peptide. Preliminary biochemical analysis showed that spexin was localized to secretory granules in a transfected pancreatic cell line. Spexin was also expressed in the submucosal cells of the mouse stomach indicating that it is a resident peptide in the GIT and may thus influence pancreatic function. It has been suggested that spexin may play a role in the regulation of physiological homeostasis. Our aim was to determine whether spexin is present in the pancreas of normal and streptozotocin‐induced diabetic rats. We also wanted to know whether spexin co‐localizes with pancreatic hormones in the islet of Langerhans. Immunohistochemical, immunofluorescence and transmission electron microscopy (TEM) methods were used to determine the cellular localization of spexin in the endocrine pancreas of non‐diabetic and diabetic rats. Immunofluorescence study showed that a significant number of cells in the core of rat pancreatic islet contains spexin, where insulin‐positive cells are located. We used double labelling immunofluorescence method to determine whether spexin and insulin co‐localize together in the same cell. We observed that these spexin‐immunoreactive cells also contain insulin. There was no evidence of co‐localization of spexin with either somatostatin or pancreatic polypeptide. The number of spexin‐ and insulin‐immunopositive cells was significantly (p <0.05) reduced after the onset of diabetes mellitus. Moreover, TEM showed that the secretory granules of pancreatic beta cells contain spexin‐labelled immunogold particles. In conclusion, the presence of spexin in pancreatic beta cells suggests a role in the regulation of pancreatic endocrine function.