Insulin-like peptide 5 (INSL5) is a member of the insulin-like family of peptides. It has been reported to be orexigenic in rodent models of obesity with impaired glucose metabolism. We attempted to confirm this property as a first step in establishing the ability of INSL5 to successfully integrate with other agents more proven in their ability to reverse obesity and improve metabolism. INSL5 was chemically synthesized by two alternative methods to a native form and one that was site-specifically conjugated to a 20 KDa polyethylene glycol (PEG) polymer. The pharmacology of each peptide was assessed by high-dose chronic administration in normal and obese mice. INSL5 failed to produce pharmacologically relevant effects on food intake, body weight or glucose control indicative of a negligible role of the peptide in the control of feeding and glucose metabolism.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.peptides.2019.170116 | DOI Listing |
Alzheimers Dement
December 2024
Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by synapse and memory failure, and severe cognitive impairment. Physical exercise stimulates neuroprotective pathways, has pro-cognitive actions, and has been reported to alleviate memory impairment in AD. Irisin, an exercise-induced hormone, is secreted following proteolytic cleavage of fibronectin type-III-domain-containing 5 (FNDC5).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Rush University Medical Center, Chicago, IL, USA.
Background: Abnormal brain insulin signaling has been associated with Alzheimer's disease pathology and a faster rate of late-life cognitive decline. However, the underlying mechanisms remain unclear. In this study, we examined whether AD-related cortical proteins identified using targeted-proteomics play a role in the association of brain insulin signaling and cognitive decline.
View Article and Find Full Text PDFSci Rep
January 2025
Departments of Ophthalmology, Sapporo Medical University School of Medicine, S-1 W-16, Chuo-Ku, Sapporo, 060-8543, Japan.
To elucidate the role of IGF1R inhibition in the pathogenesis of Graves' orbitopathy (GO), the effects of linsitinib (Lins) on a recombinant human TSHR antibody (M22) and IGF1 to activate TSHR and IGF1R of human orbital fibroblasts (HOFs) obtained from patients without GO (HOFs) and patients with GO (GHOFs) were studied using in vitro three-dimensional (3D) spheroid models in addition to their 2D planar cell culture. For this purpose, we evaluated 1) cellular metabolic functions by using a seahorse bioanalyzer (2D), 2) physical properties including size and stiffness of 3D spheroids, and mRNA expression of several extracellular matrix (ECM) proteins, their modulators (CCL2 LOX, CTGF, MMPs), ACTA2 and inflammatory cytokines (IL1β, IL6). Administration of IGF1 and M22 induced increases of cellular metabolic functions with the effect on HOFs being much more potent than the effect on GHOFs, suggesting that IGF1R and TSHR of GHOFs may already be stimulated.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Kidney stone disease is a major risk factor for impaired renal function, leading to renal fibrosis and end-stage renal disease. High global prevalence and recurrence rate pose a significant threat to human health and healthcare resources. Investigating the mechanisms of kidney stone-induced injury is crucial.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Plastic and Reconstructive Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Insulin-like growth factor 2 (IGF2) is a mitogenic peptide hormone expressed by various tissues. Although it is three times more abundant in serum than IGF1, its physiological and pathological roles are yet to be fully understood. Previous transcriptome sequencing studies have shown that IGF2 expression is increased in hypertrophic scar (HS); however, its role in HS formation and the underlying mechanism remains elusive.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!