Re: The Obesity Epidemic

Obesity ...The emphasis of treatment should be to commit
to the process of life-long healthy living including
eating more wisely and increasing physical activity.

Avoiding Persistent Organic Pollutants may also be help helpful.

Polychlorinated biphenyl-77 induces adipocyte differentiation and
proinflammatory adipokines and promotes obesity and atherosclerosis.
BACKGROUND: Obesity, an inflammatory condition linked to
cardiovascular disease, is associated with expansion of adipose
tissue. Highly prevalent coplanar polychlorinated biphenyls (PCBs)
such as 3,3',4,4'-tetrachlorobiphenyl (PCB-77) accumulate in adipose
tissue because of their lipophilicity and increase with obesity.
However, the effects of PCBs on adipocytes, obesity, and obesity-
associated cardiovascular disease are unknown. OBJECTIVES: In this
study we examined in vitro and in vivo effects of PCB-77 on adipocyte
differentiation, proinflammatory adipokines, adipocyte morphology,
body weight, serum lipids, and atherosclerosis. METHODS: PCB-77 or
2,2',4,4,5,5'-hexachlorobiphenyl (PCB-153) was incubated with 3T3-L1
adipocytes either during differentiation or in mature adipocytes.
Concentration-dependent effects of PCB-77 were contrasted with those
of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). For in vivo studies, we
treated C57BL/6 wild-type (WT) or aryl hydrocarbon receptor (AhR)(-/-)
mice with vehicle or PCB-77 (49 mg/kg, by intraperitoneal injection)
and examined body weight gain. In separate studies, we injected
ApoE(-/-) mice with vehicle or PCB-77 over a 6-week period and
examined body weight, adipocyte size, serum lipids, and
atherosclerosis. RESULTS: Low concentrations of PCB-77 or TCDD
increased adipocyte differentiation, glycerol-3-phosphate
dehydrogenase activity, and expression of peroxisome proliferator-
activated receptor gamma, whereas higher concentrations inhibited
adipocyte differentiation. Effects of PCB-77 were abolished by the AhR
antagonist alpha-naphthoflavone. PCB-77 promoted the expression and
release of various proinflammatory cytokines from 3T3-L1 adipocytes.
Administration of PCB-77 increased body weight gain in WT but not
AhR(-/-) mice. ApoE(-/-) mice injected with PCB-77 exhibited greater
body weight, adipocyte hypertrophy, serum dyslipidemia, and augmented
atherosclerosis. CONCLUSIONS: Our findings suggest that PCB-77 may
contribute to the development of obesity and obesity-associated
atherosclerosis. PMID: 18560532


White adipose tissue: storage and effector site for environmental
pollutants.
White adipose tissue (WAT) represents a reservoir of lipophilic
environmental pollutants, especially of those which are resistant to
biological and chemical degradation - so-called persistent organic
pollutants (POPs). Large amounts of different congeners and isomers of
these compounds exhibit a variety of adverse biological effects.
Interactions among different classes of compounds, frequently with
opposing effects, complicate hazard evaluation and risk assessment.
WAT is the key organ for energy homeostasis and it also releases
metabolites into the circulation and adipokines with systemic effects
on insulin sensitivity and fuel partitioning in muscles and other
tissues. Its beneficial role is lost in obesity when excessive
accumulation of WAT contributes to severe diseases, such as diabetes.
POPs may crossroad or modulate the effect of endogenous ligands of
nuclear transcription factors, participating in differentiation,
metabolism and the secretory function of adipocytes. These mechanisms
include, most importantly: i) endocrine disrupting potency of POPs
mixtures on androgen, estrogen or thyroid hormone metabolism/functions
in WAT, ii) interference of dioxin-like chemicals with retinoic acid
homeostasis, where impact on retinoid receptors is expected, and iii)
interaction with transcriptional activity of peroxisome proliferator-
activated receptors is likely. Thus, the accumulation and action of
POPs in WAT represents a unitary mechanism explaining, at least in
part, the effects of POPs in the whole organism. By modulating WAT
differentiation, metabolism and function, the POPs could affect not
only the physiological role of WAT, but they may also influence the
development of obesity-associated diseases. PMID: 16925464


For more related abstracts, search www.pubmed.com for "dioxin obesity"
.