Well, I agree with Beth that one big reason why this study may not have general applicability is that it's just about people who already have chronic or acute pancreatitis. But since I'm procrastinating right now I went and read the article [abstract here]. I have a few things to share.
First thing is that the summary Anonymous Chump linked to is a little misleading. The unsaturated fat that was causing the damage was not (or they have very good reason to think it was not) coming from the diet. It was coming from the fat deposits around the pancreas itself: "intrapancreatic" fat. Basically what is going on in these cases of pancreatitis is that the enzymes that the pancreas releases, which are supposed to go through the pancreatic duct into the duodenum (the most proximal, or first, part of the small intestine), leak out instead. When that happens they break down the fat that's been gathering around the pancreas.
So, in any event, I have gathered from the following gobbledygook:
Pancreatic acinar cells, which are
polarized, normally release their
digestive enzymes from the apical pole
(25) into the ductal lumen (Fig. 1A,
inset). These enzymes normally do not
contact the basal surface where
adipocytes are located. Disruption of
apically directed, polarized
trafficking, such as from an insult
that causes pancreatitis (25–27),
results in interstitial leakage of
enzymes and other macromolecules
during pancreatitis (17).
(Acinar = berry-like. It's what they call the cells in the pancreas that release the exocrine stuff, the stuff that goes into the digestive system. Had to look that up.)
So in order to check that this was really what was happening they simulated it:
To explore whether this macromolecular
diffusion contributes to fat-induced
acinar necrosis, we simulated
pathological interstitial leakage by
coculturing adipocytes and pancreatic
acini using a Transwell system in
which the 3-μm pores allowed
macromolecular diffusion (fig. S3)
while avoiding contamination of one
cell type by the other (fig. S4A).
When individually cultured, each cell
type appeared morphologically and
physiologically normal (figs. S5 and
S6). However, coculture resulted in
acinar cell necrosis.
So the leaking of the digestive enzymes led to some necrosis -- the bad kind of cell death. It appears that this happens because the digestive enzymes are breaking down the fat that's hanging around the pancreas and the released NEFAs (non-esterified fatty acids, fats that are no longer bound to triglycerides) are damaging to the pancreatic cells.
But it's not really all the fat that's damaging. It's mostly the unsaturated fat, and among that pool mostly the polyunsaturated fat. (Now the basic gist of the article should be coming into view.)
There were a bunch of ways that they approached this, but here's an excerpt:
To determine which fatty acids are
responsible for acinar cell necrosis
in coculture, we exposed acinar cells
to individual fatty acids at
concentrations less than or equal to
those in coculture or debridement
fluid. Intracellular calcium
concentrations were increased when
acinar cells were treated with UFAs
(Fig. 4A). [...] UFAs also caused lactate
dehydrogenase (LDH) leakage into the
medium (Fig. 4C and fig. S8A). [...] Linoleic
acid (300 μM) but not palmitic acid
(1200 μM) inhibited mitochondrial
complexes I and V (Fig. 4, D and E,
and fig. S10), causing a drop in ATP
concentrations and necrotic cell death
(fig. S11). Additionally, sublethal
concentrations (200 μM) of linoleic
acid [which increased cytosolic
calcium (fig. S9B)] but not palmitic
acid increased mRNA levels for tumor
necrosis factor–α (TNF-α) and the
neutrophil chemoattractants CXCL1 and
CXCL2 (Fig. 4, F to H). These findings
support the hypothesis that UFAs
generated as a result of lipolysis
induce acinar cell necrosis and are
Wow, that's some Dr. K sh*t right there. [That's supposed to be a fun compliment, just in case.] It's all a little difficult to understand, but I believe the basic message is: PUFAs are responsible for the cell death.
So we have a very specific finding, but a very interesting one nonetheless.