Active Low-Carber Forums
Atkins diet and low carb discussion provided free for information only, not as medical advice.
Home Plans Tips Recipes Tools Stories Studies Products
Active Low-Carber Forums
A sugar-free zone


Welcome to the Active Low-Carber Forums.
Support for Atkins diet, Protein Power, Neanderthin (Paleo Diet), CAD/CALP, Dr. Bernstein Diabetes Solution and any other healthy low-carb diet or plan, all are welcome in our lowcarb community. Forget starvation and fad diets -- join the healthy eating crowd! You may register by clicking here, it's free!

Go Back   Active Low-Carber Forums > Main Low-Carb Diets Forums & Support > Low Carb Health & Technical Forums > Cholesterol, Heart Disease
User Name
Password
Register FAQ Members Calendar Mark Forums Read Search Gallery My P.L.A.N. Survey


Reply
 
Thread Tools Display Modes
  #1   ^
Old Fri, Oct-20-17, 13:17
nawchem's Avatar
nawchem nawchem is offline
Senior Member
Posts: 8,212
 
Plan: No gluten, CAD
Stats: 163.5/161.0/149.0 Female 62
BF:36/27.7/27.3
Progress: 17%
Default How glucose becomes cholesterol and cholesterols function

Basic lipid science. (Its not cholymicron, its chylomicron)

https://www.youtube.com/watch?v=PkKH8lTxvzA
Reply With Quote
Sponsored Links
  #2   ^
Old Fri, Oct-20-17, 16:43
teaser's Avatar
teaser teaser is offline
Senior Member
Posts: 12,558
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
BF:
Progress: 104%
Location: Ontario
Default

This seems as good a place to put this as any;

Quote:
Insulin signaling molecule in liver controls levels of triglyceride in blood

A new animal study shows how insulin controls the movement and storage of fat molecules in the liver and how a breakdown in this system could lead to non-alcoholic fatty liver disease and changes in circulating lipid levels associated with cardiovascular disease. Researchers from the Perelman School of Medicine at the University of Pennsylvania published their findings this week in the Journal of Clinical Investigation (JCI).

"The production of triglyceride in the liver and its secretion into blood are closely linked to nutrient availability and insulin levels," said senior author Paul Titchenell, PhD, an assistant professor of Physiology and a member of the Institute for Diabetes, Obesity, and Metabolism. "After a meal, insulin tells the liver to package and secrete excess nutrients into triglyceride-rich lipid particles into the blood for use by the rest of the body."

After eating, glucose rises, which induces insulin release to control blood sugar levels by increasing glucose uptake and reducing glucose production by the liver. In addition to glucose regulation, insulin also controls blood lipid levels in part by increasing lipid synthesis, uptake, and storage in fat cells.

In the JCI paper, the team demonstrated that mTOR complex 1 (mTORC1), a protein super-molecule made up of several smaller proteins, is essential for very low density lipoprotein (VLDL)-triglyceride production. VLDL-triglyceride molecules are exported by the liver and carry lipids to peripheral tissues. "This is important because in metabolic diseases associated with insulin resistance the liver makes more triglycerides, which leads to increased levels in the blood and eventually cardiovascular disease," Titchenell said.

In mice, the absence of mTORC1 in liver cells caused a build-up of triglycerides in the liver, thereby reducing circulating triglycerides. On the other hand, activation of mTORC1 depleted liver triglycerides and increased blood triglycerides. Titchenell identified an important cellular process controlled by mTORC1 and demonstrated that mTORC1 controls the production of another class of molecules called phospholipids, which are essential for the triglyceride export from the liver. Phospholipids are necessary to form a barrier around triglyceride molecules allowing for their export and transport throughout the body.

"In insulin-resistant disorders such as diabetes and obesity, hyperactive mTORC1 in liver leads to excess fat production and export," Titchenell said. "mTORC1 is what we want to target pharmacologically to decrease the risk of cardiovascular disease that is associated with obesity and diabetes. If we could affect mTORC1 in a balanced way, then maybe could help prevent non-alcoholic fatty liver disease and heart disease."

In the future, the researchers aim to unravel the precise mechanisms that mediate mTORC1's control of phospholipid synthesis to uncover novel drug targets with the goal of reducing the excess lipid burden during metabolic disease.


https://www.sciencedaily.com/releas...71019142857.htm

Pharmacological balance, eh? Low carb diet, meal timing. Insulin should be pulsatile, not chronically elevated.

Something that happens sometimes with type II diabetics when they first start insulin--because they're insulin resistant, all that stuff that's supposed to deplete the liver of triglycerides is messed up, the increased insulin actually helps to clear their liver of fat. In the short-term at least, eventually the system is liable to become overloaded again.
Reply With Quote
Reply

Thread Tools
Display Modes

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

vB code is On
Smilies are On
[IMG] code is On
HTML code is Off



All times are GMT -6. The time now is 17:53.


Copyright © 2000-2018 Active Low-Carber Forums @ forum.lowcarber.org
Powered by: vBulletin, Copyright ©2000 - 2018, Jelsoft Enterprises Ltd.