Format

Send to

Choose Destination
See comment in PubMed Commons below
Gastroenterol Hepatol (N Y). 2007 Nov;3(11):856-63.

The pathophysiology of obesity and its clinical manifestations.

Author information

1
Dr. Redinger is Professor and Chairman of the Department of Medicine at the University of Louisville.

Abstract

Obesity is an exaggeration of normal adiposity and is a central player in the pathophysiology of diabetes mellitus, insulin resistance, dyslipidemia, hypertension, and atherosclerosis, largely due to its secretion of excessive adipokines. Obesity is a major contributor to the metabolic dysfunction involving lipid and glucose, but on a broader scale, it influences organ dysfunction involving cardiac, liver, intestinal, pulmonary, endocrine, and reproductive functions. Inflammatory, insulin-resistant, hypertensive, and thrombotic-promoting adipokines, which are atherogenic, are counterbalanced by anti-inflammatory and anti-atherogenic adipocyte hormones such as adiponectin, visfatin, and acylation-stimulating protein, whereas certain actions of leptin and resistin are pro-atherogenic. Adiponectin is protective against liver fibrosis due to its anti-inflammatory effect, whereas inflammatory cytokines such as tumor necrosis factor-α are detrimental for both fatty liver and pancreatic insulin release. Obesity contributes to immune dysfunction from the effects of its inflammatory adipokine secretion and is a major risk factor for many cancers, including hepatocellular, esophageal, and colon. Because of the accelerating effects that obesity has on the worsening of metabolic syndrome and cancer, it has the potential to be profoundly detrimental to our species if major methods of prevention and/or effective treatment are not realized. It is essential then to institute major educational efforts aimed at promoting better eating habits and physical exercise.

KEYWORDS:

Pathophysiology; clinical correlations; cytokines; inflammatory; lipotoxicity; obesity

PMID:
21960798
PMCID:
PMC3104148
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for PubMed Central
    Loading ...
    Support Center