Ron Ritzman wrote in message . ..
On 27 Jan 2004 11:46:06 -0800, (tcomeau) wrote:

And what "other mechanisms"?

Your Google search term for today is "acylation stimulating
protein"

From Mr. "Ketogenic Diet" himself Lyle McDonald.

http://groups.google.com/groups?q=%2...onr.com&rnum=1

Or

http://tinyurl.com/2fbpf

Here is a recent study on acylation stimulating protein.

**
Acylation stimulating protein stimulates insulin secretion.

Ahren B, Havel PJ, Pacini G, Cianflone K.

Department of Medicine, Lund University, Lund, Sweden.


Acylation stimulating protein (ASP) is a hormone produced by
adipocytes and is of importance for the storage of energy as fat. We
examined whether ASP might also have effects on islet function. In
clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated
insulin secretion. The lowest effective dose of ASP at 10 mmol/l
glucose was 5 micro mol/l. The effect was glucose-dependent because
ASP did not increase insulin secretion at 1 mmol/l glucose but had
clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented
glyceraldehyde-induced insulin secretion but the hormone did not
enhance insulin secretion in response to depolarization by 20 mmol/l
of KCl. ASP-induced insulin secretion was completely abolished by
competitive inhibition of glucose phosphorylation by glucokinase with
5-thio-glucose and was partially inhibited by the calcium channel
blocker, nifedipine, and by the protein kinase C inhibitor, GF109203.
Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the
endoplasmic reticulum, did not affect ASP-induced insulin secretion.
ASP (5 micro mol/l) also augmented glucose-stimulated insulin
secretion from islets isolated from C57BL/6J mice, and intravenous
administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min)
insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice.
This was accompanied by an increased rate of glucose disposal. Minimal
model analyses of data derived from the intravenous glucose tolerance
test revealed that whereas ASP augmented insulin secretion, the
hormone did not affect insulin sensitivity (S(I)) or glucose
effectiveness (S(G)). We conclude that ASP augments glucose-stimulated
insulin secretion through a direct action on the islet beta cells. The
effect is dependent on glucose phosphorylation, calcium uptake and
protein kinase C. Stimulation of insulin secretion by ASP in vivo
results in augmented glucose disposal.

PMID: 12917708 [PubMed - indexed for MEDLINE]
**


Of interest:

"We conclude that ASP augments glucose-stimulated insulin secretion
through a direct action on the islet beta cells. The effect is
dependent on glucose phosphorylation, calcium uptake and protein
kinase C. Stimulation of insulin secretion by ASP in vivo results in
augmented glucose disposal."

These sentences:

"...ASP augments glucose-stimulated insulin secretion..."

"The effect is dependent on glucose phosphorylation..."

Can we conclude that without "glucose-stimulated insulin secretion"
and "glucose phosphorylation" the effects of ASP would be minimal if
anything at all.

TC