Is this the mechanism by which toxic mold exposure can cause permanent weight gain?

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This looks interesting... BW is " body weight " , it appears...

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55: Peptides. 2000 Jun;21(6):793-801. Related Articles, Links

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Melanocortin signaling is decreased during neurotoxin-induced

transient hyperphagia and increased body-weight gain.

Dube MG, Pu S, Kalra SP, Kalra PS.

Department of Physiology, University of Florida Brain Institute

and College of Medicine, P.O. Box 100274, Gainesville, FL 32610, USA.

mdube@...

Hypothalamic neuropeptides play critical roles in the regulation

of feeding behavior and body weight (BW). Disruption of signaling in

the ventromedial nucleus by microinjection of the neurotoxin,

colchicine (COL), produces transient hyperphagia with corresponding BW

gain lasting for 4 days. Because the melanocortin system exerts an

inhibitory control on food intake, we hypothesized that hyperphagia in

COL-treated rats is due to decreased melanocortin-induced restraint on

feeding. Melanocortin restraint is exerted through

alpha-melanocortin-stimulating hormone derived from

proopiomelanocortin (POMC) and is antagonized by agouti-related

peptide produced in neurons located in the arcuate nucleus (ARC). COL

(4 microg/0.5 microl saline) or saline was microinjected bilaterally

into the ventromedial nucleus of adult male rats. In conjunction with

BW gain, blood leptin levels were elevated, whereas POMC mRNA in the

ARC was significantly decreased in COL-injected rats. Levels of

alpha-melanocortin-stimulating hormone were also decreased in the

micropunched paraventricular nucleus, dorsomedial nucleus, and

perifornical hypothalamus, sites implicated in the control of food

intake. That diminution in melanocortin signaling underlies

hyperphagia was supported by the observation that

intracerebroventricular injection of the MC3/MC4 melanocortin receptor

agonist, MTII, prevented the hyperphagia and BW gain. Surprisingly,

however, mRNA levels of the orexigenic peptide agouti-related peptide

in the ARC were decreased perhaps due to the action of elevated

leptin. These results show that transient hyperphagia and BW gain

induced by disruption of signaling in the ventromedial nucleus results

from two neurochemical rearrangements: development of leptin

resistance in POMC neurons and diminution in melanocortin signaling as

reflected by decreased POMC gene expression in the ARC and decreased

availability of alpha-melanocortin-stimulating hormone for release in

feeding relevant sites.