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CR and milk hormone

 
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A1CR
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Joined: 18 Jan 2006
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PostPosted: Sat Nov 25, 2006 7:46 pm    Post subject: CR and milk hormone Reply with quote

The http://en.wikipedia.org/wiki/Lactogenic_hormone
prolactin is also
present in primates, so it is not apparent why Wiki appears
to exclude
primates. The paper below concludes:

"We speculate that the lactogens facilitate food intake in
response to
fasting or nutrient deprivation, when glucose levels decline
and cortisol
levels rise."

(Note from the Wiki description: "Sometimes, newborn babies
(males as well
as females) secrete a milky substance from their nipples.
This substance is
commonly known as Witch's milk." This may be seasonal).

Arumugam R, Fleenor D, Freemark M.
Lactogenic and somatogenic hormones regulate the expression
of neuropeptide
Y and CART in rat insulinoma (INS-1) cells: interactions
with glucose and
glucocorticoids.
Endocrinology. 2006 Oct 5; [Epub ahead of print]
PMID: 17023531

Lactogenic hormones stimulate food intake in rodents,
ungulates and
birds. To test the hypothesis that lactogens regulate
expression of
neuropeptides that control appetite, we used the prolactin
(PRL)-responsive
rat insulinoma (INS-1) cell line as an experimental
paradigm. INS-1 cells
express mRNAs for NPY and CART but little or no
agouti-related peptide or
POMC. As in the hypothalamus in vivo, the levels of NPY mRNA
in INS-1 cells
were increased by glucose deprivation. Conversely, high
media glucose
concentrations (11 mM) reduced the levels of NPY mRNA and
increased levels
of CART mRNA. Rat PRL stimulated a 4- to 7-fold increase in
NPY mRNA in
INS-1 cells (P < 0.001) and reduced by 50-80% the levels of
CART mRNA (P <
0.001). The effects of PRL on NPY mRNA were time- and
dose-dependent and
potentiated by glucose deprivation or exogenous
Dexamethasone (Dex).
Hormonal induction of NPY mRNA was accompanied by increased
secretion of NPY
peptide into cellular conditioned media. PRL stimulated a
1.8-3.5-fold
increase in expression of AMP-activated protein kinase
(AMPK), which
mediates in part the effects of hypoglycemia on NPY
expression in the
hypothalamus in vivo. Pharmacologic inhibition of AMPK
activity blunted
slightly the effects of PRL on NPY and CART but reversed
entirely the
effects of Dex or of PRL plus Dex on CART mRNA. The effects
of PRL on NPY,
CART, and AMPK mRNAs were mirrored by those of other
lactogens and
somatogens including placental lactogen and GH. Rat PRL and
rat GH in
combination had no additive or synergistic effects,
suggesting that
lactogenic and somatogenic hormones regulate neuropeptide
gene expression
through similar mechanisms. We conclude that lactogens act
in concert with
glucose deprivation and glucocorticoids to induce NPY
expression and inhibit
CART. We speculate that the lactogens facilitate food intake
in response to
fasting or nutrient deprivation, when glucose levels decline
and cortisol
levels rise.
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