Reading THIS article sure makes one wonder.
Here is part of the article:
"The toxic byproducts produced by the breakdown of unsaturated fats lead to a higher likelihood of severe inflammation, cell death and multi-system organ failure among acute pancreatitis patients who are obese, say researchers at the University of Pittsburgh School of Medicine. Their findings, published online in Science Translational Medicine, provide new insight into how fat can induce complications after sudden inflammatory, non-infectious illnesses."
Should we start calling saturated fats, SAFE FATS?
asked byAnonymous_Chump (6418)
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on November 07, 2011
at 01:41 AM
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-??m 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 ??M) but not palmitic acid (1200 ??M) 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 ??M) of linoleic acid [which increased cytosolic calcium (fig. S9B)] but not palmitic acid increased mRNA levels for tumor necrosis factor????? (TNF-??) 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 proinflammatory.
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.
on November 06, 2011
at 11:42 PM
Well, obese folks should skew towards healthy fats, whether MUFAs, good PUFAs, or SFAs. I wouldn't be too concerned about this research unless you an obese person with acute pancreatitis.