Linking Lipid Metabolism to Chromatin Regulation in Aging.

The adolescent transition begins with the onset of puberty which, upstream in the brain, is initiated by the gonadotropin-releasing hormone (GnRH) pulse generator that activates the release of peripheral sex hormones. Substantial research in human and animal models has revealed a myriad of cellular networks and heritable genes that control the GnRH pulse generator allowing the individual to begin the process of reproductive competence and sexual maturation. Here, we review the latest knowledge in neuroendocrine pubertal research with emphasis on genetic and epigenetic mechanisms underlying the pubertal transition.

Emerging Genetic and Epigenetic Mechanisms Underlying Pubertal Maturation in Adolescence.

Resistin: Potential biomarker and therapeutic target in atherosclerosis.

Caenorhabditis elegans has been used as a major model organism to identify genetic factors that regulate organismal aging and longevity. Insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) regulates aging in many species, ranging from nematodes to humans. C. elegans is a nonpathogenic genetic nematode model, which has been extensively utilized to identify molecular and cellular components that function in organismal aging and longevity. Here, we review the recent progress in the role of IIS in aging and longevity, which involves direct regulation of protein and RNA homeostasis, stress resistance, metabolism and the activities of the endocrine system. We also discuss recently identified genetic factors that interact with canonical IIS components to regulate aging and health span in C. elegans. We expect this review to provide valuable insights into understanding animal aging, which could eventually help develop anti-aging drugs for humans.

https://www.molcells.org/journal/download_pdf.php?doi=10.14348/molcells.2022.0097

Recent Progress in Regulation of Aging by Insulin/IGF-1 Signaling in Caenorhabditis elegans

Cross-talk between SIRT1 and endocrine factors: effects on energy homeostasis

The development of human calcified aortic stenosis (AS) includes age-dependent processes that have been involved in atherosclerosis, such as infiltration of macrophages in aortic valves, which then promote production of many pro-inflammatory cytokines, including resistin. However, the molecular mechanisms contributing to these processes are not established. Since Sirt1 has been shown to modulate macrophage biology and inflammation, we examined its levels in human AS and tested its impact on resistin expression. Sirt1 mRNA (p = 0.01) and protein (p<0.05) levels were reduced in explanted valves from AS patients (n = 51) compared to those from control (n = 11) patients. Sirt1 mRNA levels were negatively associated with resistin mRNA levels quantified in AS valves (p = 0.02). Stimulation of Sirt1 by resveratrol or virus-driven overexpression robustly diminished resistin mRNA and protein expression in macrophages, whereas down-regulation of Sirt1 triggered a large increase in resistin expression. These effects were direct, as chromatin immunoprecipitation assays showed that Sirt1 physically interacted with the resistin promoter region at an AP-1 response element. Moreover, Sirt1 blocked c-jun-induced resistin transactivation in gene reporter assays. These findings demonstrate that, in calcified AS, levels of Sirt1 are reduced whereas those of resistin are increased within aortic valve leaflets. Our results also suggest that this loss of Sirt1 expression alleviates its inhibition of resistin transcription in macrophages. Although the overall contribution of this process to the underlying mechanisms for AS disease development remains unresolved, these observations suggest that modification of Sirt1 expression and/or activity could represent a novel approach against inflammation in AS.

/pdf/sirt1-inhibits-resistin-expression-in-aortic-stenosis-13vx05xzjg.pdf

Sirt1 Inhibits Resistin Expression in Aortic Stenosis

Despite many advances, the molecular links between energy metabolism and longevity are not well understood. Here, we have used the nematode model Caenorhabditis elegans to study the role of the yet-uncharacterized gene R148.3 in fat accumulation and lifespan. In wild-type worms, a R148.3p::GFP reporter showed enhanced expression throughout life in the pharynx, in neurons, and in muscles. Functionally, a protein fusing a predicted 22 amino acid N-terminal signal sequence (SS) of R148.3 to mCherry displayed robust accumulation in coelomyocytes, indicating that R148.3 is a secreted protein. Systematic depletion of R148.3 by RNA interference (RNAi) at L1 but not at young-adult stage enhanced triglyceride accumulation, which was associated with increased food uptake and lower expression of genes involved in lipid oxidation. However, RNAi of R148.3 at both L1 and young-adult stages robustly diminished mean and maximal lifespan of wild-type worms, and also abolished the long-lived phenotypes of eat-2 and daf-2/InsR mutants. Based on these data, we propose that R148.3 is an SS that modulates fat mass and longevity in an independent manner.

The R148.3 Gene Modulates Caenorhabditis elegans Lifespan and Fat Metabolism.

It is shown herein that the expression of the OcaB protein is modulated, in adipocytes, during adipogenesis, the development of insulin resistance, the glucose intolerance and ageing. The application thus provides methods of characterizing an individual susceptibility to develop adipogenesis, insulin resistance and/or glucose intolerance methods of diagnosing insulin resistance and/or glucose intolerance, methods of characterizing the effectiveness of an agent in the treatment, prevention or alleviation of symptoms of adipogenesis, insulin resistance and/or glucose intolerance, screening assays to identify agents useful in the treatment, prevention or alleviation of symptoms of adipogenesis, insulin resistance and/or glucose intolerance based on the assessment of a parameter of an OcaB-based reagent.

Diagnostic, screening and therapeutic applications of ocab-based tools

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Sirt1 Inhibits Resistin Expression in Aortic Stenosis

The R148.3 Gene Modulates Caenorhabditis elegans Lifespan and Fat Metabolism.

Diagnostic, screening and therapeutic applications of ocab-based tools