Lang F, et al. – This research entailed the appraisal of the pathophysiology of suboptimal fluid intake in the general population. The data disclosed that suboptimal fluid intake could lead to an enhancement of vasopressin and glucocorticoid levels. This, in turn, aided in up–regulating serum– and glucocorticoid–inducible kinase 1 (SGK1) expression and favouring the development of SGK1 related pathologies.

• Enhanced copeptin levels (reflecting enhanced vasopressin levels) in 25% of the common population were related to enhanced risk of metabolic syndrome with abdominal obesity, type 2 diabetes, hypertension, coronary artery disease, heart failure, vascular dementia, cognitive impairment, microalbuminuria, chronic kidney disease, inflammatory bowel disease, cancer, and premature mortality.
• Vasopressin was found to stimulate the release of glucocorticoids which in turn up-regulate the serum- and glucocorticoid-inducible kinase 1 (SGK1).
• Dehydration upregulated the transcription factor NFAT5, thereby stimulating the SGK1 expression.
• SGK1 was activated via insulin, growth factors and oxidative stress through phosphatidylinositide-3-kinase, 3-phosphoinositide-dependent kinase PDK1 and mTOR. SGK1 is a powerful stimulator of Na⁺/K⁺-ATPase, carriers (e.g. the Na⁺,K⁺,2Cl^- cotransporter NKCC, the NaCl cotransporter NCC, the Na⁺ /H⁺ exchanger NHE3, and the Na⁺ coupled glucose transporter SGLT1), and ion channels (e.g. the epithelial Na+ channel ENaC, the Ca2⁺ release activated Ca2⁺ channel Orai1 with its stimulator STIM1, and diverse K⁺ channels).
• SGK1 took part in the regulation of the transcription factors nuclear factor kappa-B NFΚB, p53, cAMP responsive element binding protein (CREB), activator protein-1, and forkhead transcription factor FKHR-L1 (FOXO3a).
• Enhanced SGK1 activity aided in the development of hypertension, obesity, diabetes, thrombosis, stroke, inflammation including inflammatory bowel disease and autoimmune disease, cardiac fibrosis, proteinuria, renal failure, along with the tumor growth.