Cell death and inflammation during obesity: “Know my methods, WAT(son)”

Hildebrandt, Ximena; Ibrahim, Mohamed A.; Peltzer, Nieves

doi:10.1038/s41418-022-01062-4

Cited by 120 publications

(45 citation statements)

References 113 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is thought that proliferation and differentiation of ASC are stimulated through paracrine feedback when hypertrophic growth has reached a defined limit of capacity. Pro-adipogenic signals released from engorged adipocytes may be triggered by mechanical strain [42], local hypoxia [43], or hypertrophy-induced cell death [44]. Recently, Li et al demonstrated that adipocytes from obese or insulin-resistant humans were prone to undergoing premature senescence [45], raising the possibility of a mechanism common to adipocytes that have either reached a critical size or the end of their lifespan.…”

Section: The Adipose Progenitor Pool Is Recruited To Expand Lipid Sto...mentioning

confidence: 99%

Maternal obesity and programming of metabolic syndrome in the offspring: searching for mechanisms in the adipocyte progenitor pool

Scheidl

Brightwell

Easson

et al. 2023

BMC Med

View full text Add to dashboard Cite

Background It is now understood that it is the quality rather than the absolute amount of adipose tissue that confers risk for obesity-associated disease. Adipose-derived stem cells give rise to adipocytes during the developmental establishment of adipose depots. In adult depots, a reservoir of progenitors serves to replace adipocytes that have reached their lifespan and for recruitment to increase lipid buffering capacity under conditions of positive energy balance. Main The adipose tissue expandability hypothesis posits that a failure in de novo differentiation of adipocytes limits lipid storage capacity and leads to spillover of lipids into the circulation, precipitating the onset of obesity-associated disease. Since adipose progenitors are specified to their fate during late fetal life, perturbations in the intrauterine environment may influence the rapid expansion of adipose depots that occurs in childhood or progenitor function in established adult depots. Neonates born to mothers with obesity or diabetes during pregnancy tend to have excessive adiposity at birth and are at increased risk for childhood adiposity and cardiometabolic disease. Conclusion In this narrative review, we synthesize current knowledge in the fields of obesity and developmental biology together with literature from the field of the developmental origins of health and disease (DOHaD) to put forth the hypothesis that the intrauterine milieu of pregnancies complicated by maternal metabolic disease disturbs adipogenesis in the fetus, thereby accelerating the trajectory of adipose expansion in early postnatal life and predisposing to impaired adipose plasticity.

show abstract

Section: The Adipose Progenitor Pool Is Recruited To Expand Lipid Sto...mentioning

confidence: 99%

Maternal obesity and programming of metabolic syndrome in the offspring: searching for mechanisms in the adipocyte progenitor pool

Scheidl

Brightwell

Easson

et al. 2023

BMC Med

View full text Add to dashboard Cite

show abstract

“…In agreement, NPY , an inducer of obesity and fat storage was found intact, possibly contributing to the overall fat profile in Cetacea [90]. Although, fat deposition and obesity trigger adipose tissue inflammation in most mammals, Cetacea exhibit a healthy fat phenotype [83, 91]. This could be concurrent with the loss of inflammatory modulation by NPFF , NPS , or NPB / NPW [15, 92, 93].…”

Section: Discussionmentioning

confidence: 88%

Alterations of Pleiotropic Neuropeptide-Receptor gene couples in Cetacea

Valente,

Cordeiro,

Pinto

et al. 2024

Preprint

View full text Add to dashboard Cite

BackgroundHabitat transitions have considerable consequences in organism homeostasis, as they require the adjustment of several concurrent physiological compartments to maintain stability and adapt to a changing environment. Within the range of molecules with a crucial role in the regulation of different physiological processes, neuropeptides are key agents. Here, we examined the coding status of several neuropeptides and their receptors with pleiotropic activity in Cetacea.ResultsAnalysis of 202 mammalian genomes, including 41 species of Cetacea, exposed an intricate mutational landscape compatible with gene sequence modification and loss. Specifically for Cetacea, in the twelve genes analysed we have determined patterns of loss ranging from species-specific disruptive mutations (e.g., Neuropeptide FF-Amide Peptide Precursor;NPFF) to complete erosion of the gene across the cetacean stem lineage (e.g., Somatostatin Receptor 4;SSTR4).ConclusionsImpairment of some of these neuromodulators, may have contributed to the unique energetic metabolism, circadian rhythmicity and diving response displayed by this group of iconic mammals.

show abstract

“…Chronic inflammation and metabolic dysregulation are common features among patients with obesity [205]. SHIP1 was found to be upregulated in diet‐induced obese mice [206].…”

Section: Therapeutic Avenuesmentioning

confidence: 99%

SHIP1 and its role for innate immune regulation—Novel targets for immunotherapy

Yeoh,

Krebs

2023

Eur J Immunol

View full text Add to dashboard Cite

Phosphoinositide‐3‐kinase/AKT (PI3K/AKT) signaling plays key roles for the regulation of cellular activity in both health and disease. In immune cells, this PI3K/AKT pathway is critically regulated by the phosphoinositide phosphatase SHIP1, which has been reported to modulate the function of most immune subsets. In this review, we summarize our current knowledge of SHIP1 with a focus on innate immune cells, where we reflect on the most pertinent aspects described in the current literature. We also present the several small molecule agonists and antagonists of SHIP1 developed the last two decades, which have led to improved outcomes in several pre‐clinical models of disease. We outline these promising findings and put them in relation with human diseases with unmet medical needs, where we discuss the most attractive targets for immune therapies based on SHIP1 modulation.This article is protected by copyright. All rights reserved

show abstract

Cell death and inflammation during obesity: “Know my methods, WAT(son)”

Cited by 120 publications

References 113 publications

Maternal obesity and programming of metabolic syndrome in the offspring: searching for mechanisms in the adipocyte progenitor pool

Maternal obesity and programming of metabolic syndrome in the offspring: searching for mechanisms in the adipocyte progenitor pool

Alterations of Pleiotropic Neuropeptide-Receptor gene couples in Cetacea

SHIP1 and its role for innate immune regulation—Novel targets for immunotherapy

Contact Info

Product

Resources

About