Obesity and diabetes remain leading causes of reduced health span and life span throughout the world. Hence, it is not surprising that these areas are at the center of highly active areas of research. The identification of novel mechanisms underlying these metabolic disorders sets the stage for uncovering new potential therapeutic strategies. In this issue of Highlights in Arteriosclerosis, Thrombosis and Vascular Biology, we review recently published papers in the journal that add to our understanding of causes and consequences of obesity and diabetes and how these disorders impact metabolic function. Collectively, these studies in cultured cells to in vivo animal models to human subjects add to the growing body of evidence that both cell-intrinsic and cell-cell communication mechanisms collaborate in metabolic disorders to cause obesity, insulin resistance and diabetes and its complications. Adipocyte Biology: Effects on Vascular and Inflammatory HomeostasisAdipose tissue is a complex and highly active metabolic organ and adipose dysfunction is linked to cardiovascular disease 18 . Adipose tissues are diverse and specific depots have been characterized as "good fat" versus "bad fat." What accounts for these differences? Indeed, beyond adipocytes, multiple classes of immune cells, such as macrophages, T and B lymphocytes, T regulatory cells and NK cells; nerve tissue; stromovascular cells and endothelial cells (ECs), all housed within a biologically active connective tissue matrix, populate this tissue 19 . Recent studies have identified cell-intrinsic and cell-cell communication pathways linked to obesity and diabetes in adipose and other metabolic tissues, such as liver, skeletal muscle, and brain, and how their properties may affect vascular and inflammatory health and homeostasis. For example, cell-intrinsic roles for adipocytes in metabolic dysfunction were illustrated by studies in mice with adipocytespecific deletion of Nox4 (NADPH oxidase 4), using the Adipoq (Adiponectin) cre recombinase strategy for specific deletion of genes of interest in adipocytes. Mice were fed a high fat/high sucrose diet with added cholesterol. Mice devoid of adipocyte Nox4 exhibited
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.