Posts Tagged: obesity

Extracellular Vesicles in Metabolic Syndrome

Extracellular Vesicles in Metabolic Syndrome

M. Carmen Martínez, Ramaroson Andriantsitohaina

Extracellular vesicles (EVs) participate in the development of atherosclerotic plaque. EVMP from smooth muscle cells (pink) induce endothelial dysfunction and macrophage infiltration in the vessel wall through the reactive oxygen species (ROS) production and p38 activation in endothelial cells. EVEXO derived from dendritic cells (blue) increase endothelial inflammation by activation of nuclear factor-κB (NF-κB) pathway and increasing expression of proinflammatory molecules, including vascular cell adhesion molecule (VCAM), intercellular adhesion molecule (ICAM1), and E-selectin. [Powerpoint File]

Extracellular Vesicles in Metabolic Syndrome

Extracellular Vesicles in Metabolic Syndrome

M. Carmen Martínez, Ramaroson Andriantsitohaina

Effects of extracellular vesicles (EVs) on blood vessel. EVMP from endothelial cells (dark pink) transfer miR-503 to pericytes and subsequently inhibit vascular endothelial growth factor (VEGF) expression, resulting in decreased migration and proliferation. EVEXO from smooth muscle cells (pink) induce downregulation of LC3 II, ATG5, and Beclin-1 expression in endothelial cells. EVEXO from macrophages (green) evoke intercellular adhesion molecule 1 (ICAM1) overexpression in endothelial cells and reduce level of miR-17. Also, macrophage foam cell–derived EVs favor both migration and adhesion of vascular smooth muscle cells by activating ERK (extracellular signal-regulated kinase) and Akt (protein kinase B/AKT) pathways and by transfer integrins β1 and α5 into vascular smooth muscle cells. EVMP from metabolic syndrome (MetS) patients act on smooth muscle cells and induce overexpression of inducible nitric oxide synthase (iNOS) and monocyte chemoattractant molecule (MCP)-1, leading to vascular hyporeactivity. Also, these EVMP directly act on endothelial cells evoking reduced nitric oxide (NO) production, enhanced cytosolic and mitochondrial reactive oxygen species (ROS) production, and unfolding protein response (UPR). All effects of EVMP from MetS patients are mediated by the interaction Fas/FasL. [Powerpoint File]

Treatment of Obesity: Weight Loss and Bariatric Surgery

Treatment of Obesity: Weight Loss and Bariatric Surgery

Bruce M. Wolfe, Elizaveta Kvach, Robert H. Eckel

Diagram of surgical options. Image credit: Walter Pories, MD, FACS. [Powerpoint File]

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

José J. Fuster, Noriyuki Ouchi, Noyan Gokce, Kenneth Walsh

Functional adipose tissue (left), predominantly found in lean organisms, tends to express anti-inflammatory adipokines that protect against cardiovascular disease. In contrast, excess adipose tissue expansion promotes dysfunction (right), leading to the expression of proinflammatory adipokines that promote cardiovascular disease. Dysfunctional adipose tissue is characterized by enlarged adipocytes, vascular rarefaction, increased inflammatory cell infiltrate, and the appearance of crown-like structures. [Powerpoint File]

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

José J. Fuster, Noriyuki Ouchi, Noyan Gokce, Kenneth Walsh

Obesity leads to adipose tissue dysfunction, triggering the release of proinflammatory adipokines that can directly act on cardiovascular tissues to promote disease. The adipokine imbalance can also affect the function of metabolically important tissues and the microvasculature, promoting insulin resistance and indirectly contributing to cardiovascular disease. [Powerpoint File]

Lipid Use and Misuse by the Heart

Lipid Use and Misuse by the Heart

P. Christian Schulze, Konstantinos Drosatos, Ira J. Goldberg

Cellular fatty acid uptake. Fatty acids generated by lipoprotein lipase (LpL) or as nonesterified fatty acids associated with albumin enter cells via a cell surface receptor such as cluster of differentiation 36 (CD36) or at high levels are acquired via nonspecific movement across the cell membrane. Once inside the cells, fatty acids are complexed to CoA and then either used for ATP generation or stored within lipid droplets. ATGL indicates adipose triglyceride lipase; DGAT, DAG acyl transference; FFA, first fatty acid; PPAR, peroxisomal proliferator–activated receptor; and VLDL, very low–density lipoprotein. [Powerpoint File]

Lipid Use and Misuse by the Heart

Lipid Use and Misuse by the Heart

P. Christian Schulze, Konstantinos Drosatos, Ira J. Goldberg

Metabolism of circulating triglyceride-rich lipoproteins. Triglycerides (TG) within the circulation are predominantly carried by chylomicrons and very low–density lipoprotein (VLDL). Chylomicrons carry dietary lipids. Along with the lipids, it contains apolipoproteins including apoB-48 and C-II, the activator of lipoprotein lipase (LPL). VLDL contains apoB-100 and carry triglycerides secreted from the liver. Lipolysis converts triglycerides to fatty acids (FA) and also leads to the shedding of surface components that contain cholesterol (Chol). Defective lipolysis leads to reduced acquisition of fatty acids, cholesterol, and vitamin A by the heart. CE indicates cholesteryl ester; LDL, low-density lipoprotein; and LDL-R, low-density lipoprotein receptor. [Powerpoint File]

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

José J. Fuster, Noriyuki Ouchi, Noyan Gokce, Kenneth Walsh

Adipose tissue depots occur throughout the body. Studies suggest that visceral adipose tissue accumulation is a major risk factor for cardiometabolic disease, whereas subcutaneous fat seems to be neutral or protective. Other adipose tissue depots of note include the epicardium, the perivascular space, and bone marrow, but the functional significance of these tissues is largely unknown. Brown adipose tissue occurs in the supraclavicular and paraspinal regions. In contrast to white adipose tissue, brown adipose tissue is metabolically active, and it functions to utilize fuel to produce heat. In addition, ectopic lipid can accumulate in tissues, such as liver, in metabolically dysfunctional organisms. [Powerpoint File]

Lipid Use and Misuse by the Heart

Lipid Use and Misuse by the Heart

P. Christian Schulze, Konstantinos Drosatos, Ira J. Goldberg

Intracellular triglyceride storage and release. Triglycerides are stored within cardiomyocytes in lipid droplets (shown in yellow) that are surrounded by phospholipids and several proteins; the most abundant are the perilipins (PLINs such as PLIN 2, 3, and 5). These proteins modulate the actions of the major triglyceride hydrolytic enzyme adipose triglyceride lipase (ATGL), which removes the first fatty acid (FFA) from triglyceride. The second fatty acid is removed by hormone-sensitive lipase (HDL) and the final by monoglycerol lipase (MGL). The released fatty acid complex with CoA via long chain acyl coA synthetases (ACSL). [Powerpoint File]

Adipose Tissue Biology and Cardiomyopathy: Translational Implications

The cardiovascular system is influenced by adipose tissue, not only through effects on systemic insulin sensitivity but also through direct and indirect effects of adipokines.

Adipose Tissue Biology and Cardiomyopathy: Translational Implications

Aslan T. Turer, Joseph A. Hill, Joel K. Elmquist, Philipp E. Scherer

The cardiovascular system is influenced by adipose tissue, not only through effects on systemic insulin sensitivity but also through direct and indirect effects of adipokines. Adipokines have effects on the central nervous system, which, in turn, influence sympathetic outflow, peripheral metabolism, and (at least in the liver) organ steatosis. Better understood are the direct effects of adipokines on the heart, which may influence substrate metabolism, detoxify lipid intermediates, and promote cell survival (illustration credit: Ben Smith). [Powerpoint File]