http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt
=Abstract&list_uids=16781084&query_hl=1&itool=pubmed_docsum

or     http://tinyurl.com/o7slp

Not knowing  what   visceral adipocytes were  I found this hypothesis.
due to Andrews post.

 "The inflammatory cytokines from visceral adipocytes are simply
deleterious.  They must be eliminated to reach the goal of optimal
health.
Prayerfully in Christ's amazing love,
Andrew B. Chung "

Thanks Andrew !

Bill

.................................

1: Med Hypotheses. 2006 Jun 14; [Epub ahead of print]
Related Articles, Links
 
The inflammatory consequences of psychologic stress: Relationship to
insulin resistance, obesity, atherosclerosis and diabetes mellitus, type
II.

Black PH.

Department of Microbiology, Boston University School of Medicine, 715
Albany Street, Room L-501, Boston, MA 02118, United States.

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 NF(kappa)B 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 visceral fat has both the proclivity and capacity to
undergo inflammation. It contains a rich blood and nerve supply as well
as proinflammatory molecules such as interleukin 6 (IL-6), tumor
necrosis factor alpha (TNFalpha), leptin, and resistin, the
adipocytokines, and acute phase proteins (APP) which are activated from
adipocytes and/or macrophages by sympathetic signaling. The inflammation
is linked to fat accumulation. Cortisol, IL-6, angiotensin II (angio
II), the enzyme 11(beta) hydroxysteroid dehydrogenase-1 and positive
energy balance, the latter due to increased appetite induced by the
major stress hormones, are factors which promote fat accumulation and
are linked to obesity. There is also the capacity of the host to limit
fat expansion. Sympathetic signaling induces TNF which stimulates the
production of IL-6 and leptin from adipocytes; these molecules promote
lipolysis and ffa fluxes from adipocytes. Moreover, catecholamines and
certain PIC inhibit lipoprotein lipase, a fat synthesizing enzyme. The
brain also participates in the regulation of fat cell mass; it is
informed of fat depot mass by molecules such as leptin and ffa. Leptin
stimulates corticotrophin releasing hormone in the brain which
stimulates the SNS and HPA axes, i.e. the stress response. Also, ffa
through portal signaling from the liver evoke a similar stress response
which, like the response to psychologic stress, evokes an innate immune
response (IIR), tending to limit fat expansion, which culminates in
inflammatory cascades, the IRS-MS, obesity and disease if prolonged.
Thus, the brain also has the capacity to limit fat expansion. A
competition apparently exists between fat expansion and fat loss. In
"western" cultures, with excessive food ingestion, obesity frequently
results. The linkage of inflammation to fat metabolism is apparent since
weight loss diminishes the concentration of inflammatory mediators. The
linkage of stress to inflammation is all the more apparent since the
efferent pathways from the brain in response to fat signals, which
results in inflammation to decrease and limit fat cell mass, is the same
as the response to psychologic stress, which strengthens the hypothesis
presented herein.

PMID: 16781084 [PubMed - as supplied by publisher]