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 > Dr.Bernstein & Diabetes
User Name
Password
FAQ Members Calendar Mark Forums Read Search Gallery My P.L.A.N. Survey


Reply
 
Thread Tools Display Modes
  #1   ^
Old Thu, Dec-20-18, 10:27
teaser's Avatar
teaser teaser is offline
Senior Member
Posts: 15,075
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
BF:
Progress: 104%
Location: Ontario
Default Hormone sensitive lipase as a drug target

https://www.sciencedaily.com/releas...81205134014.htm

Quote:
Type 2 diabetes: A therapeutic avenue is emerging

Diabetes is a disease in which blood sugar levels are high over a prolonged period (hyperglycemia). In the case of type 2 diabetes, this phenomenon which is caused by a disruption of the glucose metabolism develops progressively and insidiously. In France, the prevalence of diabetes is estimated at over 5 % of the 2015 population, with type 2 accounting for 90 % of cases. These figures do not include those who are unaware of their condition, particularly among the overweight or obese.

Hormone-sensitive lipase (HSL) is an enzyme which converts fats into fatty acids and releases them into the bloodstream. In obese patients, these fatty acids trigger the gradual insulin resistance at the origin of type 2 diabetes. Previous research by the Inserm team of Dominique Langin had shown that a decrease in HSL expression in the adipocytes led to a better response to insulin, a sign of good health for these cells.

Surprisingly, the researchers observed that the beneficial effect of a reduction in HSL was not actually due to the reduced release of fatty acid. It was explained by the increased synthesis of oleic acid, the principal fatty acid component of olive oil. This initial observation gave a glimpse of an interesting avenue for treating obese patients who are at greater risk of developing type 2 diabetes.


Feeding them oleic acid? Sorry. I'll try to behave.

Quote:
To envisage a therapeutic strategy, it therefore had to be elucidated how reducing HSL exerted this beneficial effect on the action of insulin. The group of Prof. Langin discovered the existence of a physical interaction between HSL and a transcription factor responsible for the synthesis of fatty acids, ChREBP. HSL, when binding to ChREBP, blocks its activity. As such, a decrease in HSL leads to the release of this factor in the nucleus, promoting its activity, oleic acid synthesis and sensitivity to insulin.

Preliminary results indicate that a known inhibitor of HSL blocks the interaction with ChREBP. These data therefore pave the way for the development of molecules which target this interaction. In collaboration with global biopharmaceutical company AstraZeneca, the researchers in Toulouse are currently testing different approaches to block the interaction between HSL and ChREBP. Ultimately this project could lead to the development of new drugs to treat the increasing global epidemic of type 2 diabetes.



Knockout of hormone sensitive lipase--I wanted to see if this would increase obesity. Doesn't seem to in mice, but does cause fatty liver.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5741266/


https://www.youtube.com/watch?v=VjQkqFSdDOc


Great talk by Prof. Robert Unger, explaining why peripheral insulin effects probably aren't the problem. Cliff notes--pancreatic alpha cells, which put out glucagon to raise blood glucose, are exposed to as much as 400 times the concentration of insulin as the periphery. This serves to lower glucagon, and increase the effect of insulin, so not as much is needed. The liver is exposed to 40 times the concentration that the peripheral tissues are exposed to. Peripheral insulin pushes on a wet noodle. Which is a good argument for Bernstein. At lower levels of insulin secretion, the effect of insulin on glucagon is negligible--you can see this in some of Unger's slides. I think you could look at it as the closer peripheral and central (liver and pancreas rather than brain) insulin requirements are one to the other, the closer to normal physiology injected insulin can get.
Reply With Quote
Sponsored Links
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 05:53.


Copyright © 2000-2024 Active Low-Carber Forums @ forum.lowcarber.org
Powered by: vBulletin, Copyright ©2000 - 2024, Jelsoft Enterprises Ltd.