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  #1   ^
Old Sat, Oct-13-18, 01:42
Demi's Avatar
Demi Demi is offline
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Plan: LCHF/IF
Stats: 217/192/160 Female 5'10"
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Default Fat: A new player expands our definition of diabetes

Quote:
Fat: A new player expands our definition of diabetes

Type 2 diabetes is reaching epidemic proportions around the world. The World Health Organization reports that more than 422 million people suffer from the disease, including over 1.2 million in Australia alone. The consequences of diabetes can be dire (cancer, kidney failure, and heart attacks) and its prevalence is rising fast. There is an urgent need to better understand how diabetes progresses -- and how it might be stopped.

A new study by Australian researchers, out today, is challenging what we know about the causes of diabetes. The new research points to fat tissue as a source of disease, and widens our understanding beyond the traditional focus on liver and pancreas as the main culprits.

The findings, uncovered in mice, are published in the high-impact journal Cell Metabolism.

A STARTLING DISCOVERY

The new research is centred around the surprising finding that protein kinase C epsilon (PKCε), known to be involved in diabetes, isn't acting in the liver or the pancreas as was once assumed.

Researchers have long known that PKCε is important for the development of diabetes. Mice that have no PKCε produced anywhere in the body don't develop diabetes-like symptoms -- even under conditions where other mice become diabetic.

"We have known for some time that if you remove PKCε entirely from mice and feed them a high-fat diet they do not become glucose intolerant. In fact, they are protected from becoming diabetes-like," says Associate Professor Carsten Schmitz-Peiffer (Garvan Institute of Medical Research), who led the research.

Diabetes researchers use a high-fat diet (HFD) to induce type 2 diabetes in mice. Following a HFD, most mice become 'glucose intolerant' -- they are unable to control their blood sugar after eating. In particular, the liver becomes 'insulin resistant' -- it no longer responds to the pancreatic hormone insulin.

"The big surprise was that when we removed PKCε production specifically in the liver -- the mice were not protected. For over a decade, it's been assumed that PKCε is acting directly in the liver -- by that logic, these mice should have been protected against diabetes."

"We were so surprised by this, that we thought we had developed our mice incorrectly. We confirmed the removal and tested it in several different ways, but they still became glucose intolerant when given a HFD."

A NEW ANSWER: FAT

If not the liver, then where? The hunt was on to determine where PKCε was working to progress glucose intolerance.

"What we found," explains A/Prof Schmitz-Peiffer, "is that if we removed PKCε production solely from fat tissue, the mice were protected from becoming glucose intolerant, similar to when we removed PKCε from the entire animal. So PKCε isn't progressing diabetes from the liver, but in fact, it is acting from fat tissue to worsen the disease."

PKCε has been known to be expressed in multiple tissues, but Prof Schmitz-Peiffer's findings now point to a new function in fat tissue.

A CHANGING LANDSCAPE FOR FAT TISSUE

A close examination of the fat tissue revealed a striking difference in the shape and size of the fat cells in the presence and absence of PKCε.

"Under the microscope, the fat cells looked very different," A/Prof Schmitz-Peiffer says. "In HFD-fed mice with PKCε removed from the fat tissue, we saw mostly small, healthy fat cells. And in HFD-fed mice with PKCε intact -- which are glucose intolerant -- we saw more of the unhealthy, engorged fat cells, that tend to have less access to oxygen and become inflamed."
For A/Prof Schmitz-Peiffer, it is clear this could have wide-ranging and complex implications for diabetes.

"We know that fat tissue is a lot more than just an inert mass for storing fat," explains A/Prof Schmitz-Peiffer, "it's a very dynamic organ, it sends many messages and releases factors that communicate with the rest of the body, including the liver."

"If PKCε is changing the nature of fat and affecting the overall health of fat cells, it's changing the types of messages it sends and factors it releases -- which could be acting on the liver and possibly other organs to interfere with glucose metabolism."

A BRAKE FOR PKCε -- 10 YEARS IN THE MAKING

This discovery is the latest in a long line of contributions made in this field by A/Prof Schmitz-Peiffer.

"10 years ago, we showed that removing PKCε entirely protected mice against glucose intolerance. We just never knew where PKCε was acting. But we knew we might be onto something therapeutically important, if we could find a way to block PKCε."

Today, Prof Schmitz-Peiffer is collaborating with Professor Ray Norton and Professor Jonathan Baell at the Fragment Based Drug Discovery Platform at the Monash Institute of Pharmaceutical Sciences to develop an orally available peptide that can disrupt PKCε activity.

"These results give us an even better idea about how to target PKCε to develop the most effective treatments possible. And therapeutically targeting PKCε would be a new possible approach for diabetes treatment."


Journal Reference:
Amanda E. Brandon, Bing M. Liao, Barbara Diakanastasis, Benjamin L. Parker, Katy Raddatz, Sophie A. McManus, Liam O'Reilly, Erica Kimber, A. Gabrielle van der Kraan, Dale Hancock, Darren C. Henstridge, Peter J. Meikle, Gregory J. Cooney, David E. James, Saskia Reibe, Mark A. Febbraio, Trevor J. Biden, Carsten Schmitz-Peiffer. Protein Kinase C Epsilon Deletion in Adipose Tissue, but Not in Liver, Improves Glucose Tolerance. Cell Metabolism, 2018; DOI: 10.1016/j.cmet.2018.09.013





https://www.sciencedaily.com/releas...81012110203.htm
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  #2   ^
Old Sat, Oct-13-18, 09:13
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
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Default

Have to wonder about effects on total body fat. Smaller, healthier adipocytes, but there'd have to be more of them if they contained the same fat as in an animal with more engorged fat cells.
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  #3   ^
Old Sat, Oct-13-18, 10:07
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Plan: Ketogenic (LCHFKD)
Stats: 227/186/185 Male 6' 0"
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This seems plausible, as fat contributes and receives metabolic information much like an organ, and we are starting to learn more about its role. I'm curious about the HFD fed to the mice. I know that I become glucose intolerant when I eat a high carb diet whether or not fat is present, but my glucose intolerance was eliminated by a high fat, very low carb diet. Mice react differently in many cases than humans would to a diet mix, and what the researchers refer to as a HFD may also contain a much higher carb component, so the combination of fat and carbs could have an influence as well?
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  #4   ^
Old Sat, Oct-13-18, 21:02
Zei Zei is offline
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Plan: Carb reduction in general
Stats: 230/213/180 Female 5 ft 9 in
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Default

Here's a pair of rodent high fat and control lab chows from Bio-Serv with their ingredient lists:
https://www.bio-serv.com/product/HFPellets.html
Quote:
F3282/S3282
Lard, Casein, Maltodextrin, Sucrose, Mineral Mix, Vitamin Mix, DL-Methionine, Choline Chloride

F4031 (Control)
Cornstarch, Sucrose, Casein, Maltodextrin, Lard, Mineral Mix,Vitamin Mix, DL Methionine, Choline Chloride

Both list maltodextrin and sucrose as prominent ingredients. The high fat chow is plentiful in carbohydrates with the fat and is not a ketogenic product.
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  #5   ^
Old Sun, Oct-14-18, 07:51
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WereBear WereBear is offline
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Plan: Epi-Paleo/IF
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This article makes it obvious they donít want results so much as a pill they can sell.
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  #6   ^
Old Sun, Oct-14-18, 08:25
Bonnie OFS Bonnie OFS is offline
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Plan: Dr. Bernstein
Stats: 188/175/135 Female 5 ft 4 inches
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Quote:
Originally Posted by Zei
Here's a pair of rodent high fat and control lab chows from Bio-Serv with their ingredient lists:
https://www.bio-serv.com/product/HFPellets.html
Both list maltodextrin and sucrose as prominent ingredients. The high fat chow is plentiful in carbohydrates with the fat and is not a ketogenic product.


Thanks! I was wondering if it was more a high fat/sugar mix rather than just high fat. When are the researchers going to be honest about this?
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  #7   ^
Old Sun, Oct-14-18, 08:55
GRB5111's Avatar
GRB5111 GRB5111 is offline
Posts: 2,410
 
Plan: Ketogenic (LCHFKD)
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
Default

Quote:
Originally Posted by Zei
Here's a pair of rodent high fat and control lab chows from Bio-Serv with their ingredient lists:
https://www.bio-serv.com/product/HFPellets.html
Both list maltodextrin and sucrose as prominent ingredients. The high fat chow is plentiful in carbohydrates with the fat and is not a ketogenic product.

That's exactly what I was assuming. Thanks, this information puts things in better perspective and combined with the fact that rodents aren't going to react the same as humans, it's a mistake to represent the outcome as representing a human mechanism without direct human studies. It simply forms a hypothesis about the role of PKCε in humans and its possible reaction to a diet high in fat and carbs (SAD). It would have to be tested on human subjects in ketosis to determine an accurate metabolic response for that WOE.
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  #8   ^
Old Sun, Oct-14-18, 14:24
deirdra's Avatar
deirdra deirdra is offline
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Plan: HF/vLC/GF,CF,SF
Stats: 197/136/150 Female 66 inches
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Progress: 130%
Location: Alberta
Default

Thanks, Zei. The "high fat" diet is essentially SAD and that 35.7% carbs would be like a human eating 175g carbs on 2000 cals/day; not low carb even in the loosest sense (~100-150g). It is not really testing high fat either, since 36% is not high for a wild rat eating nuts & seeds. The study is really comparing SAD fiber-free junkfood to a Pritikinesque very low fat diet, but with zero fiber.

Last edited by deirdra : Sun, Oct-14-18 at 14:53.
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  #9   ^
Old Sun, Oct-14-18, 14:34
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Plan: atkins
Stats: 247/217/153 Female 5'8"
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Location: Massachusetts
Default

Quote:
Originally Posted by WereBear
This article makes it obvious they donít want results so much as a pill they can sell.

Yes.

I was looking for a dietary solution. But they are not.
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