Adipose tissue insulin sensitivity

[Commander]

http://journals.cambridge.org/downlo...451e4f5abcf862
http://www.pubmedcentral.nih.gov/art...i?artid=297156
http://www.sportsci.org/encyc/adipose/adipose.html

"Insulin reduces mobilization of fatty acids from adipose tissue by inhibiting triglyceride lipase" - from the last link

My summary in laymens term's:
Bigger fat cells = more insulin resistant adipose tissue
Too much insulin -> represses fat mobilization
Vicious cycle, get fatter.

Question:
Do the same things which increase muscle tissue insulin sensitivity, (i.e. proper timing of carbs, exercise, supplementation with chromium, ALA, etc, etc) also increase adipose tissue insulin sensitivity?

Or are there other things we can do to improve adipose tissue insulin sensitivity?

[Venom]

This is a great post.

Yeah that is a visous cycle. Interesting studies, though: endurance athletes have high intramuscular triglercides, yet there insulin sensativity is amazing. Whearas obese people and diabetics also have high IMTs but can't handle carbs. Thought is that athletes are constantly recycling triglycerides; whearas fat people just have old triglycerides stored in tissue, and they get oxidized, and oxidized fat and their metabolites causes insulin resistance. But yeah, its a physcious cycle from a lot of perspectives. Getting fat will promote getting fatter from endless physiological and psychological perspectives.


In my assessment, you would not want adipose tissue to be sensitive to insulin, because glucose taken up into adipose will be converted in triglycerides.

What you named above will primarily promote muscle sensitivity. Example: when you exercise, oxidative stress builds up mostly in your muscles. ALA therefore reduces oxidative stress in your muscles and directly improves sensitivity there - not fat. Now carbs, our lab has shown that if you go low carb <150 your muscle and liver mostly handle that and insulin sensitivity in those tissues is much greater - i.e. greater PI3 kinase, etc. But there are barely any adaptations in adipose, so you dont take up carbs in adipose. And you consequently lose more fat. I have heard that glutamine actually may cause insulin resistance in adipose, but dont have reference on hand.

[Commander]

Venom wrote: "This is a great post.
Yeah that is a visous cycle. Interesting studies, though: endurance athletes have high intramuscular triglercides, yet there insulin sensativity is amazing. Whearas obese people and diabetics also have high IMTs but can't handle carbs. Thought is that athletes are constantly recycling triglycerides; whearas fat people just have old triglycerides stored in tissue, and they get oxidized, and oxidized fat and their metabolites causes insulin resistance."

Cool, I didn't catch that. It makes sense though.

I may have misunderstood some of the studies. It sounded like when adipose tissue was insulin sensitive it mobilized fat easier (because there was less insulin present to reduce the mobilization), which I thought was good.

But you are saying, that we don't want adipose tissue to be insulin sensitive, correct?

When you said that "there are barely any adaptations in adipose" do you mean that there isn't much we can do to change how it reacts, etc? Meaning we should focus our efforts on adapting our muscle tissue?

[Venom]

No I mean that most of the carbs dont reach adipose so it does not adapt (I.e. does not increase PI3 kinase, AKT, etc.). If you have a high carb diet on other hand, there will be spill over of carbs into adipose, and it will make similar adaptations as liver and muscle.

[Commander]

Ok, thank you.