The inflammatory consequences of psychologic stress
(Referred by Marcelo Gustavo Colominas [mgcolominas@gigared.com])
The inflammatory consequences of psychologic
stress: Relationship to insulin resistance, obesity,
atherosclerosis and diabetes mellitus, type II
Paul H. Black *
Department of Microbiology, Boston University School of Medicine, 715 Albany Street, Room L-501, Boston, MA 02118, United States
Received 31 March 2006; accepted 4 April 2006
Summary Inflammation is frequently present in the visceral fat and vasculature in certain patients with cardiovascular disease (CVD) and/or adult onset Diabetes Mellitus Type II (NIDDM). An hypothesis is presented which argues that repeated acute or chronic psychologically stressful states may cause this inflammatory process. The mediators are the major stress hormones norepinephrine (NE) and epinephrine (E) and cortisol together with
components of the renin–angiotensin system (RAS), the proinflammatory cytokines (PIC), as well as free fatty acids (ffa), the latter as a result of lipolysis of neutral fat. NE/E commence this process by activation of NFjB in macrophages, visceral fat, and endothelial cells which induces the production of toll-like receptors which, when engaged, produce a cascade of inflammatory reactions comprising the acute phase response (APR) of the innate immune system (IIS). The inflammatory process is most marked in the visceral fat depot as well as the vasculature, and
is involved in the metabolic events which culminate in the insulin resistance/metabolic syndromes (IRS/MS), the components of which precede and comprise the major risk factors for CVD and NIDDM./.../
The inflammatory consequences of psychologic
stress: Relationship to insulin resistance, obesity,
atherosclerosis and diabetes mellitus, type II
Paul H. Black *
Department of Microbiology, Boston University School of Medicine, 715 Albany Street, Room L-501, Boston, MA 02118, United States
Received 31 March 2006; accepted 4 April 2006
Summary Inflammation is frequently present in the visceral fat and vasculature in certain patients with cardiovascular disease (CVD) and/or adult onset Diabetes Mellitus Type II (NIDDM). An hypothesis is presented which argues that repeated acute or chronic psychologically stressful states may cause this inflammatory process. The mediators are the major stress hormones norepinephrine (NE) and epinephrine (E) and cortisol together with
components of the renin–angiotensin system (RAS), the proinflammatory cytokines (PIC), as well as free fatty acids (ffa), the latter as a result of lipolysis of neutral fat. NE/E commence this process by activation of NFjB in macrophages, visceral fat, and endothelial cells which induces the production of toll-like receptors which, when engaged, produce a cascade of inflammatory reactions comprising the acute phase response (APR) of the innate immune system (IIS). The inflammatory process is most marked in the visceral fat depot as well as the vasculature, and
is involved in the metabolic events which culminate in the insulin resistance/metabolic syndromes (IRS/MS), the components of which precede and comprise the major risk factors for CVD and NIDDM./.../
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