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2 Oct, 5 tweets, 2 min read
1/ BOOM! Want to know how fat gets directed to muscle, cardiac, and adipose tissue...

ANGPTL3-4-8 model of fatty acid trafficking! So elegant! It's like evolution is an engineer .@DaveKeto .@Ad_SotoMota

Video Here 👇👇
2/ The model describes how three ANGPTL family members act in concert to promote tissue-specific LPL activity corresponding to the body’s nutritional status. Interestingly, all three proteins are LPL inhibitors; however, they are differentially induced by fasting and feeding ...
3/ ...and preferentially effect different tissues. ANGPTL4 is induced by fasting and inhibits LPL specifically in adipocytes, directing direct FFA to skeletal and cardiac muscles in the unfed state. By contrast, ANGPTL8 is induced by feeding and...
4/ ANGPTL8 is induced by feeding and, by interacting with ANGPTL3, inhibits LPL activity in specifically in cardiac and skeletal muscle. ...
5/ Thus, in the fasted state, LPL activity is relatively suppressed in adipocytes and FFA are directed to lean tissue; whereas in the fed state, LPL activity in adipocytes increases relative to lean tissue to facilitate the storge of circulating TG.

The End 📙 (but not really)

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More from @nicknorwitz

Nick Norwitz Profile picture
1 Oct
1/ I'm so happy! 🥲 Thread

Today @harvardmed we started metabolism, metabolic regulation, and had a carb metabolism lecture...

I've had a handful of peers (6 thus far today), unprompted, contact me to ask some version of the following question...
2/ I've very intentionally kept a low profile, and I'm not looking to make "my thing" (metabolic health) the focus of lectures not get myself a troublemaker label. Plus, I'm genuinely happy to use listen and learn.

BUT...
3/ I'm incredibly excited to note that my peers are asking what I personally think should be the obvious questions -->

e.g. Why treat a disease of high blood sugar and high insulin with carbs and insulin?

I find it very informative. But now, one of two things could happen...
Read 5 tweets
Nick Norwitz Profile picture
28 Sep
Full after fruit?
1)That’s an atypical satiation response
2) The is probably accurate bc of what the peach 🍑 would replace
3) most modern fruit isn’t “natural.” 10,000 gen of selection for sweetness …
4) Ppl would also lose weight eating more hard boiled eggs 🥚

Cont’…
5) of all fruit, I think peach isn’t a “bad” choice, and I’m not anti fruit. But the notion that fruits are healthy by virtue of being fruits is problematic. Most people think dried fruit is healthy, including dried 🍍 at the extreme. May as well be eating sour patch kids…
6) again, I’m not anti-fruit but let’s try to discuss in what context the fruit is being consumed and how “processed” the fruit is re artificial selection or other processing. Let’s also discuss the actual nutrient content and other options…
Read 6 tweets
Nick Norwitz Profile picture
19 Sep
1/ Another in my biology series of How it Works. This time... How Does You Body Get Rid of Excess Nitrogen? #Protein

The short answer is that it transforms the nitogenous group (amino group) into urea, and it gets peed out. But let's dig in a bit...
2/ The first step is to get the Nitrogen-containing amino group off of the donor amino acid. This is done by a "transamination reaction" in which transaminase enzymes effectively shuffle the amino group, transfering it from one donor amino acid to an acceptor alpha keto acid...
3/ Again, just a simple shuffling. In the example shown Alanine is the donor amino acid, and it's amino group is transfered to alpha-ketoglutarate to make their respective alpha keto acid and amino acid pairs: Pyruvate & Glutamate...
Read 6 tweets
Nick Norwitz Profile picture
24 Jul
1/ Why does LDLc go up more if you're leaner and have higher energy demands, one explaination by @DaveKeto (and hopefully I recount it corrently):

In a low-carb state, dependence on fat metabolism is increased. Thus, ur fat cells r shrinking& growing in a more dynamic fashion...
2/ In order to expand, the fat cell (and other cells) needs material that can be provided by circulating lipoproteins.

Now let's pause and remeber that leanness & metabolic health are characterized by small fat cells (even if there are more). This is healthy but...
3/ If you fat cell is small its going to have a higher surface area to volume ratio than large fat cells. Thus, to grow and the same amount in terms of volume (as the TG pool is turned over more quickly) small fat cells will require more membrane components provided by LDL...
Read 4 tweets
Nick Norwitz Profile picture
24 Jul
1/ What does Lipid Trafficking and VLDL have to do with type II #diabetes?

Check out my new video on the "Twin Cycle Hypothesis"

In 9 min, you'll be smarter than you were before!
🤓🤓🤓👇👇👇
#LEM #Lipids #Insulin
2/ After you watch the video, can you answer the following "quiz" questions?

(i) How does the contribution of de novo lipogenesis to Triglyceries in VLDL change as liver fat accumulates?
...
3/ T/F and why?
(ii) Palmitic acid is transported by VLDL1 to the pancreas, harming beta cells in the pancreas. Palmitic acid is a major saturated fat (16:0) found in animal foods. So, you should eat less red meat and dairy and substitue in healthy whole grains & fruit, like 🍌?
Read 4 tweets
Nick Norwitz Profile picture
14 Jul
1/ New Human study supports twin-cycle hypothesis of #diabetes … thread incoming!
#metabolism #insulinresistance

sciencedirect.com/science/articl…
2/ The twin cycle hypothesis postulates that accumulation of liver fat can drive diabetes in the following way: more liver fat promotes hepatic insulin resistance which increases gluconeogenesis and thus increases insulin to promote more de novo lipogenesis. Basically…
3/ Basically, more liver fat more insulin resistance more liver fat and so on. New human data provide support for the model. One of the key findings of the paper is that more liver fat = more de novo lipogenesis, creating specifically the saturated fat palmitic acid (PA)…
Read 14 tweets

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