Diabetes has multiple causes.

http://en.wikipedia.org/wiki/GLUT4
GLUT4 is the insulin-regulated glucose transporter found in adipose
tissues and striated muscle (skeletal and cardiac) that is responsible
for insulin-regulated glucose disposal.

TCDD suppresses insulin-responsive glucose transporter (GLUT-4) gene
expression through C/EBP nuclear transcription factors in 3T3-L1
adipocytes.
TCDD is known to reduce significantly the level of the functionally
active form of glucose transporter type 4 (GLUT4) in vivo in adipose
tissue and muscles ... These results implicate the C/EBP proteins to
be the main mediator of suppressive action of TCDD on GLUT4 gene
expression in 3T3-L1 cells. PMID: 16615095

Differential effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the
"adipose- type" and "brain-type" glucose transporters in mice.
... We conclude that regulation by TCDD of glucose transport activity
in mice is an aryl, hydrocarbon receptor-dependent process and that
the adipose-type GLUT4 appears to be regulated at the mRNA level,
whereas the brain-type GLUT1 is affected mainly at the protein level.
PMID: 7530807

Associations of environmental exposure to dioxins with prevalent
diabetes among general inhabitants in Japan.
The aim of this study was to evaluate the associations of
environmental exposure to dioxins with diabetes among general
inhabitants in Japan. A cross-sectional study was performed on 1374
participants, who were not occupationally exposed to dioxins, aged
15-73 years, living widely in 75 different residential areas of 25
prefectures in Japan through 2002-2006. ...This recent representative
data from general inhabitants in Japan showed associations of
environmental exposure to dioxins, especially dioxin-like PCBs, with
diabetes. PMID: 18649880

Environmental contaminants as risk factors for developing diabetes.
The contribution of exposure to persistent organic pollutants (POPs)
to the incidence of diabetes has received little attention until
recently. A number of reports have emerged, however, concerning
elevated diabetes in persons occupationally exposed to dioxin. United
States (US) Air Force personnel in Vietnam who sprayed Agent Orange
containing dioxin as a contaminant had elevated rates of diabetes,
leading to US government compensation for diabetes in these veterans.
Recent studies in populations exposed to polychlorinated biphenyls
(PCBs) and chlorinated pesticides found a dose-dependent elevated risk
of diabetes. An elevation in risk of diabetes in relation to levels of
several POPs has been demonstrated by two different groups using the
National Health and Nutrition Examination Survey (NHANES), a random
sampling of US citizens. The strong associations seen in quite
different studies suggest the possibility that exposure to POPs could
cause diabetes. One striking observation is that obese persons that do
not have elevated POPs are not at elevated risk of diabetes,
suggesting that the POPs rather than the obesity per se is responsible
for the association. Although a specific mechanism is not known, most
POPs induce a great number and variety of genes, including several
that alter insulin action. Because diabetes is a dangerous disease
that is increasing in frequency throughout the world, further study of
the possibility that exposure to POPs contributes to the etiology of
diabetes is critical. PMID: 18557598

Increased risk of diabetes and polychlorinated biphenyls and dioxins:
a 24-year follow-up study of the Yucheng cohort.
OBJECTIVE: Polychlorinated biphenyls (PCBs) and polychlorinated
dibenzofurans (PCDFs) are important and persistent organic pollutants
(POPs) in humans. Recent cross-sectional studies have detected
increased concentrations of serum POPs in diabetic patients. We aimed
to examine the association between previous high exposures to PCBs and
PCDFs and the cumulative incidence of type 2 diabetes and
hypertension... CONCLUSIONS: Yucheng women, who had endured previous
exposure to PCBs and PCDFs, suffered from increased incidences of
diabetes, particularly those who had retained significant levels of
pollutant as evident from chloracne. When planning treatments against
diabetes, the body burden of PCBs and dioxins should be carefully
considered, especially for women. PMID: 18487481

Bisphenol-A disruption of the endocrine pancreas and blood glucose
homeostasis.
The link between endocrine disruptors and altered blood glucose
homeostasis has been recently suggested. Epidemiological studies have
correlated levels of phthalates, dioxins and persistent organic
pollutants with alterations of blood glucose homeostasis in humans.
Environmentally relevant doses of the ubiquitous endocrine disruptor
bisphenol-A (BPA) have profound effects on mice endocrine pancreas--an
essential tissue involved in glucose metabolism. BPA exerts rapid non-
genomic effects on insulin releasing beta-cells and glucagon releasing
alpha-cells within freshly isolated islets of Langerhans. In vivo, a
single BPA injection of 10 microg/kg rapidly increases plasma insulin
and concomitantly decreases glycaemia. When mice were treated with BPA
100 microg/kg/day for 4 days, the environmental oestrogen produced an
increase in beta-cell insulin content along with a post-prandial
hyperinsulinaemia and insulin resistance. The results reviewed here
demonstrate that doses well below the current lowest observed adverse
effect level considered by the US-EPA, disrupt pancreatic beta-cell
function producing insulin resistance in male mice. Therefore, this
altered blood glucose homeostasis by BPA exposure may enhance the risk
of developing type II diabetes. PMID: 17971160

Exposure to persistent organochlorine pollutants and type 2 diabetes
mellitus.
Persistent organochlorine pollutants (POPs), such as polychlorinated
biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), dichloro
diphenyl trichloroethane (DDT) and its major metabolite 1,1-
dichloro-2,2-bis (p-chlorophenyl)-ethylene (p,p' -DDE) have been
associated with type 2 diabetes mellitus (T2DM) in recent
epidemiological studies...The study shows an association between POP
serum concentrations and an increased prevalence of T2DM. PMID:
17623770

Association of a polychlorinated dibenzo-p-dioxin, a polychlorinated
biphenyl, and DDT with diabetes in the 1999-2002 National Health and
Nutrition Examination Survey.
The association of a polychlorinated dibenzo-p-dioxin, a
polychlorinated biphenyl, and p,p'-DDT with diabetes was evaluated
using the 1999-2002 National Health and Nutrition Examination
Survey. ... PCB 126 and p,p'-DDT were significantly associated with
undiagnosed diabetes. 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin (HxCDD)
was not associated with undiagnosed diabetes. ... These findings add
to the list of chemicals found to be associated with diabetes in the
1999-2002 National Health and Nutrition Examination Survey. PMID:
17187776

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

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