A Century of Prolactin: Emerging Perspectives as a Metabolic Regulator.

Prolactin, a hormone that has been studied for almost a century, has evolved from a reproductive regulator to a key player in metabolic health. Initially identified for its lactogenic role, the impact of prolactin on glucose and lipid metabolism became evident in the 1970s, leading to a paradigm shift in our understanding. Deviations in prolactin levels, including hyperprolactinaemia and hypoprolactinaemia, have been associated with adverse effects on glucose and lipid metabolism. Mechanistically, prolactin regulates metabolic homoeostasis by maintaining islet abundance, regulating the hypothalamic energy regulatory centre, balancing adipose tissue expansion, and regulating hepatic metabolism. Given the widespread use of pharmaceutical agents that affect prolactin levels, it is important to examine prolactin-related metabolic effects. Recently, a profound exploration of the intricate metabolic role of prolactin has been conducted, encompassing its rhythm-dependent regulatory influence on metabolism and its correlation with cognitive impairment associated with metabolic diseases. In this review, we highlight the role of prolactin as a metabolic regulator, summarise its metabolic effects, and discuss topics related to the association between prolactin and metabolic comorbidities.

In-Situ Generated Trimetallic Molybdate Nanoflowers on Ni Foam Assisted with Microwave for Highly Enhanced Oxygen Evolution Reaction.

Oxygen evolution reaction (OER) is considered as a critical half-cell reaction of water splitting, the kinetics of which is sluggish even not favored, thus requiring highly active electrocatalysts to shrink the reaction energy barrier and improve the energy conversion efficiency. In this study, In-situ generated trimetallic molybdate nanoflowers on Ni foam by a straightforward and time-saving solvothermal method assisted with microwave, not only bring synergistic effect into full play between multiple metals, but also construct a well-defined nanoflower-like structure accompanied by larger specific area (273.3 m2 g-1 ) and smaller size than the pristine NiMoO4 . The resulting Ni0.9 Al0.1 MoO4 -NF requires a relatively low overpotential of 266 mV for OER at 10 mA cm-2 , which outperforms commercial RuO2 catalysts (274 mV). Such excellent performance compares favorably to most previously reported NiMoO4 -based electrocatalysts for OER. This work not only supplies a facile method to construct a well-defined nanoflower-like structure on foam, but also broadens our horizons into the mechanism of OER in alkaline conditions.

Highly efficient OER catalyst enabled by in situ generated manganese spinel on polyaniline with strong coordination.

The oxygen evolution reaction (OER), as the rate-determining step of electrochemical water splitting, is extremely crucial, and thus it is a requisite to engineer feasible and effective electrocatalysts to shrink the reaction energy barrier and accelerate the reaction. Herein, monodisperse Mn3O4 nanoparticles on a PANI substrate were synthesized by polymerization and in situ oxidation. Combining Mn3O4 nanoparticles and PANI fibers can not only maximize the strong coupling effect and synergistic effect but also construct a well-defined three-dimensional structure with extensive exposed active sites, where the permeation and adherence of the electrolyte are made exceedingly feasible, thus displaying excellent OER activity. Benefiting from the outstanding structural stability, the resulting Mn3O4/PANI/NF is able to deliver a low overpotential of 262 mV at a current density of 10 mA cm-2, which outperforms the commercial RuO2 catalyst (275 mV) as well as presently reported representative Mn-based and PANI-based electrocatalysts and state-of-the-art OER electrocatalysts. The synthetic method for Mn3O4/PANI not only provides a brand-new avenue for the rational design of inorganic material/conductive polymer composites but also broadens the understanding of the mechanism of Mn-based catalysts for highly enhanced OER.

Phenotypic spectrum and mechanism analysis of Schaff Yang syndrome: A case report on new mutation of MAGEL2 gene.

RATIONALE: The Schaaf-Yang syndrome (SYS) is an autosomal dominant multi-system genetic disease caused by melanoma antigen L2 (MAGEL2) gene mutations imprinted by mothers and expressed by fathers on the 15q11-15q13 chromosomes in the critical region of Prader-Willi. MAGEL2 is a single exon gene and one of the protein-coding genes of the Prader-Willi domain. MAGEL2 is a matrilineal imprinted gene (i.e., the maternal chromosome is methylated). It is only expressed by unmethylated paternal alleles, and the individual is affected only when the variation occurs on the paternal allele. PATIENT CONCERNS: We reported a patient with MAGEL2 gene new site mutation who had mild intellectual disability, social fear, small hands and feet, obesity issues, dyskinesia, growth retardation, language lag and sexual development disorder. DIAGNOSIS: Whole-exome sequencing showed a heterozygous variation in the MAGEL2 gene, NM_019066.4:c.1687C > T (p.Q563X) and diagnosed as Schaaf-Yang syndrome. INTERVENTIONS: Patient was advised to reduce weight, control blood lipids, blood glucose through appropriate strengthening of exercise and diet control in the future. At the same time, the family members were advised to provide mental training to the patient to strengthen the contact and communication with the outside world and improve the autistic symptoms. Because of the patient's bilateral cryptorchidism, it is recommended that the patient should be treated with bilateral cryptorchidism reduction fixation. OUTCOMES: After a follow-up of the patient for 2 months, the patient is still walking unsteadily and requires an auxiliary reference material to walk normally. There is no significant change in height compared to before, and the weight has dropped by about 2 kg in the past 2 months. The symptoms of autism have improved slightly. The patient is willing to communicate with outsiders; his intelligence has not improved significantly, and his academic performance in school is still at the middle and lower levels. LESSONS: The pathogenesis of SYS is complex, involving multiple pathways such as Leptin-POMC, MAGEL2-USP7-TRIM27 complex and oxytocin. Our study has also found that certain fatal phenotypes such as respiratory distress have a high incidence at individual sites, and early detection and timely intervention may prolong the life span of patients. Therefore, for patients in whom SYS is highly suspected, gene detection should be carried out as soon as possible.