Adipotide and the Bad Fat
Just a brief respite from mitochondria:
Adipotide is a drug which targets the blood vessels supplying adipose tissue. It causes impressive fat loss by killing fat cells. Anon posted these two links on the last post.
There are other processes which can produce adipocyte destruction. We've discussed both acquired and congenital lipodystrophes in the past. They produce whole body fat loss with progressively deteriorating glucose tolerance because fatty acids have no adipocytes to enter, so end up accumulating in all tissues, producing pathological insulin resistance and diabetes. This is basic physiology and exactly what you would expect.
Adipotide is different. It produces fat loss with improving metabolic conditions and decreased hunger. How come a dead adipocyte is good from Adipotide and bad from auto immune attack?
Alex emailed me the full text. Here is the snippet from the email conversation which was my initial take on what might be happening:
"How does the drug get any improvement? You'd need to see the data and how they generated it but if the drug preferentially targets abdominal fat there would be an improvement in systemic insulin resistance until enough total [whole body] fat cells were lost for the overall for deterioration in insulin sensitivity due to muscle lipid accumulation to precipitate diabetes.
Of course during lipolysis you would have FFA release acting like an obese fat cell becoming insulin resistant and sending FFAs systemically to most non CNS mitochondria... Reduced need for food and increased ATP for activity from the metabolic flexibility perspective..."
Look here: Surgical removal of visceral fat improves peripheral insulin sensitivity (there's a lot I could write about this paper but no time). This paper looks OK, other papers by this group are very dubious.
Visceral fat seems quite important, here's an early brief review.
And here is the only quote we need from the Adipotide paper (thank you Alex for the full text):
"MRI and DEXA imaging confirmed that weight loss in the rhesus monkeys occurred primarily because of visceral fat loss."
Now, that's all hunky dory. What is the question we need to ask? Actually, there are a few:
Why is visceral fat Bad Fat? Why do we make it? If we get rid of the Bad Fat, will health be Good for ever? Did we evolve Bad Fat to kill ourselves? Is there a survival benefit from Bad Fat if we continue to drink >30% of our calories from fructose based drinks? Would having our omentum removed do good or bad things long term if we continue to mainline fructose? Would we need to get rid of our Bad Fat if we poured the Fanta down the urinal rather than down our throats?
I rather like Bad Fat. It opens all sorts of avenues of thought. There's so much about it that fits together but no more time to blog at the moment.
Adipotide is a drug which targets the blood vessels supplying adipose tissue. It causes impressive fat loss by killing fat cells. Anon posted these two links on the last post.
There are other processes which can produce adipocyte destruction. We've discussed both acquired and congenital lipodystrophes in the past. They produce whole body fat loss with progressively deteriorating glucose tolerance because fatty acids have no adipocytes to enter, so end up accumulating in all tissues, producing pathological insulin resistance and diabetes. This is basic physiology and exactly what you would expect.
Adipotide is different. It produces fat loss with improving metabolic conditions and decreased hunger. How come a dead adipocyte is good from Adipotide and bad from auto immune attack?
Alex emailed me the full text. Here is the snippet from the email conversation which was my initial take on what might be happening:
"How does the drug get any improvement? You'd need to see the data and how they generated it but if the drug preferentially targets abdominal fat there would be an improvement in systemic insulin resistance until enough total [whole body] fat cells were lost for the overall for deterioration in insulin sensitivity due to muscle lipid accumulation to precipitate diabetes.
Of course during lipolysis you would have FFA release acting like an obese fat cell becoming insulin resistant and sending FFAs systemically to most non CNS mitochondria... Reduced need for food and increased ATP for activity from the metabolic flexibility perspective..."
Look here: Surgical removal of visceral fat improves peripheral insulin sensitivity (there's a lot I could write about this paper but no time). This paper looks OK, other papers by this group are very dubious.
Visceral fat seems quite important, here's an early brief review.
And here is the only quote we need from the Adipotide paper (thank you Alex for the full text):
"MRI and DEXA imaging confirmed that weight loss in the rhesus monkeys occurred primarily because of visceral fat loss."
Now, that's all hunky dory. What is the question we need to ask? Actually, there are a few:
Why is visceral fat Bad Fat? Why do we make it? If we get rid of the Bad Fat, will health be Good for ever? Did we evolve Bad Fat to kill ourselves? Is there a survival benefit from Bad Fat if we continue to drink >30% of our calories from fructose based drinks? Would having our omentum removed do good or bad things long term if we continue to mainline fructose? Would we need to get rid of our Bad Fat if we poured the Fanta down the urinal rather than down our throats?
I rather like Bad Fat. It opens all sorts of avenues of thought. There's so much about it that fits together but no more time to blog at the moment.
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Fax: 0086-0371-66837889
Mobile:0086-13592439230
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