3 ms·
You know what else inhibits fatty acid oxidation? CPT1A (Carnitine palmitoyltransferase I) Deficiency. Does this make people live longer? Nope. You know why? C
by FollowingTheDao 3y ago
You know what else inhibits fatty acid oxidation? CPT1A (Carnitine palmitoyltransferase I) Deficiency.
Does this make people live longer? Nope. You know why? Cause it can give people heart disease:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4358228/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4358228/
I carry a mild form of CPT1A deficiency (I have Inuit heritage) and this prevents ketosis on a high fat (think ocean fats like blubber) diet. But put me under with propanol (A CPT1 inhibitor) and they have to pump me full of glucose.
Sorry, but you all are thick and dull because you never think genetics matter when it comes to diet. You think we are all the same and almost every study on nutrition does not account for genetics. In mice, they all have the same genetics, but as humans we vary more than you think.
The bad forms of CPT1 Deficiency lead to lifelong problems of hypoglycemia because they are homozygous for the change. They are a sacrifice that enabled the Inuit to survive on the diet we are provided in our ecosystem and we cherish these children.
You all are trying to be something you are not, something far from your ancestors. It is sad.
- hattmall 3y agoGenetics matter a lot here for sure, mainly in that the genetics of mice vary greatly from all humans. It's still important to study and understand these interactions.
- fasteo 3y ago>>> You know what else inhibits fatty acid oxidation? CPT1A (Carnitine palmitoyltransferase I) Deficiency. If I am not mistaken, the problem with CPT1A is upstream, way before oxidation occurs, in the breakdown of the long chain fatty acids before they can go into the mitochondria for oxidation. Unrelated to inhibiting oxidation
- c0pium 3y ago> you all are thick and dull because you never think genetics matter This is uncalled for and untrue. There are a lot of human nutrition studies which account for genetics. It sounds like you’re angry, you should think about why that is before lashing out.
- FollowingTheDao 3y agoI know why I am angry. If you think there is something wrong with anger you have a problem with being human.
- c0pium 3y agoThere’s something wrong with being a terrible member of the community because you feel entitled to it. Which is what you’re doing.
- FollowingTheDao 3y agoMaybe live my life and talk to me after that. I do not feel "entitled" to be angry, I am just effing angry. And you did not even ask why I am angry, so what kind of terrible person in the community are you?
- c0pium 3y agoI’m angry, so screw all these other people who had nothing to do with it? Classic. I didn’t need to ask, you’re not exactly an enigma. Look at your post history for like 2 seconds.
- anon84873628 3y ago>In mice, they all have the same genetics, but as humans we vary more than you think. This is deliberate, so that the research question can be isolated from variation in mouse genetics as much as possible. Different types of research use different mouse lineages according to their purposes. Do you think scientists are not aware of the role of genetics, or the great variability? The goal is to elucidate fundamental aspects of cell function: >We conclude that metabolic maturation shapes the epigenetic landscape of cardiomyocytes No one is trying to make you take a pill or alter your lifestyle because of this research.
- mikewarot 3y ago>This is deliberate, so that the research question can be isolated from variation in mouse genetics as much as possible. The breeding process for said mice may represent an evolutionary pressure[1] that alters them sufficiently that they are no longer suitable for an analog to humans[2], unlike their wild brethren. Or so sayeth the evolutionary biologists. [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC113886/#:~:text=Established%20inbred%20mouse%20strains%20have,11%2C14%E2%80%9316 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC113886/#:~:text...). [2] https://pubmed.ncbi.nlm.nih.gov/34008434/ https://pubmed.ncbi.nlm.nih.gov/34008434/