Visceral adiposity is associated with metabolic disorders, but little is known on the underlying pathophysiological mechanism. One possible link might be the release of various signalling and mediator proteins, named adipokines. Our hypothesis was that dependent on genetic background factors are released which might trigger a primary disease susceptibility. This study characterizes the adipokines released from visceral adipose tissue from two metabolic healthy mouse strains, i.e. C57BL/Ks (BKS) and C57BL/6 (C57), of which the former genetic background is more sensitive to develop diabetes following metabolic challenge. Using liquid chromatography (LC)-electrospray ionization (ESI)-MS/MS, a reference map comprising 597 adipokines was generated (http://www.diabesityprot.org). Thirty-five adipokines, including six not previously described ones, were differentially released between the mouse strains. Most notable is the reduced release of the adiponectin-binding protein T-Cadherin (CAD13) in BKS mice. This observation highlights the importance of secretome profiling in unravelling the complex interplay between genetic diversity and lifestyle.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3109/13813455.2014.970197 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The genetic and observational nexus between diabetes and arthritis: a national health survey and mendelian randomization analysis.
Nutr Diabetes
December 2024
Department of International Medical, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, China.
Background: Diabetes mellitus (DM) and arthritis are prevalent conditions worldwide. The intricate relationship between these two conditions, especially in the context of various subtypes of arthritis, remains a topic of interest.
Objective: To investigate the relationship between diabetes and arthritis, with a focus on Rheumatoid Arthritis (RA), using data from the National Health and Nutrition Examination Survey (NHANES) and Mendelian Randomization (MR) analysis.
A novel de novo GABRA2 gene missense variant causing developmental epileptic encephalopathy in a Chinese patient.
Ann Clin Transl Neurol
December 2024
Department of Pediatrics, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, P. R. China.
Background: Variants in the GABRA2 gene, which encodes the α2 subunit of the γ-aminobutyric acid A receptor, have been linked to a rare form of developmental and epileptic encephalopathy (DEE) referred to as DEE78. Only eight patients have been reported globally. This study presents the clinical presentation and genetic analysis of a Chinese family with a child diagnosed with DEE78, due to a novel GABRA2 variant.
View Article and Find Full Text PDFIncreasing and Alarming Prevalence of Trichophyton indotineae as the Primary Causal Agent of Skin Dermatophytosis in Iran.
Mycoses
January 2025
Mycology Reference Laboratory, Isfahan University of Medical Sciences, Isfahan, Iran.
Background: Trichophyton indotineae, formerly described as T. mentagrophytes rDNA-ITS genotype VIII, has recently been identified as a novel species within the T. mentagrophytes complex.
View Article and Find Full Text PDFUnraveling the Causal Relationship Between Blood Metabolites and Acne: A Metabolomic Mendelian Randomization Study.
J Cosmet Dermatol
January 2025
Department of Dermatology, Chinese People's Liberation Army Western Theater Command General Hospital, Chengdu, China.
Background: Acne is a common skin disorder that may be linked to metabolic dysfunction. However, the causal impact of blood metabolites on acne has not been thoroughly investigated.
Methods: We performed a metabolome-wide Mendelian randomization (MR) analysis on 486 blood metabolites and acne using a genome-wide association dataset.
JAK inhibition decreases the autoimmune burden in Down syndrome.
Elife
December 2024
Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, United States.
Background: Individuals with Down syndrome (DS), the genetic condition caused by trisomy 21 (T21), display clear signs of immune dysregulation, including high rates of autoimmunity and severe complications from infections. Although it is well established that T21 causes increased interferon responses and JAK/STAT signaling, elevated autoantibodies, global immune remodeling, and hypercytokinemia, the interplay between these processes, the clinical manifestations of DS, and potential therapeutic interventions remain ill defined.
Methods: We report a comprehensive analysis of immune dysregulation at the clinical, cellular, and molecular level in hundreds of individuals with DS, including autoantibody profiling, cytokine analysis, and deep immune mapping.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!