https://doi.org/10.1016/j.celrep.2021.109488
https://pubmed.ncbi.nlm.nih.gov/34348139
Abstract
Hyperglycemia affects over 400 million individuals worldwide. The detrimental health effects are well studied at the tissue level, but the inΒ vivo effects at the organelle level are poorly understood. To establish such an inΒ vivo model, we used mice lacking TXNIP, a negative regulator of glucose uptake. Examining mitochondrial function in brown adipose tissue, we find that TXNIP KO mice have a lower content of polyunsaturated fatty acids (PUFAs) in their membrane lipids, which affects mitochondrial integrity and electron transport chain efficiency and ultimately results in lower mitochondrial heat output. This phenotype can be rescued by a ketogenic diet, confirming the usefulness of this model and highlighting one facet of early cellular damage caused by excess glucose influx.
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Open Access: True
Authors: Althea N. Waldhart - Brejnev Muhire - Ben Johnson - Dean Pettinga - Zachary B. Madaj - Emily Wolfrum - Holly Dykstra - Vanessa Wegert - J. Andrew Pospisilik - Xianlin Han - Ning Wu -
Additional links:
Thank you for your time :)
You may or may not have read my article on the theory behind obesity.
https://designedbynature.design.blog/2020/05/13/hyprocico-the-theory-behind-obesity/
I'm still looking for papers and see if they validate or invalidate my theory. As such I came across the following paper.
It's a rat study but what I found interesting about it is that they let the control group eat freely and then they did isocaloric feeding of the experimental groups.
One of the effects in my theory is that you need to burn more fat through the addition of thermogenesis (via WAT and BAT activation) to produce the same amount of protection from protein breakdown versus a high carb diet. The protection comes from the combination of glucose and BHB but a given volume of BHB production requires a given amount of fat metabolism. Glucose on the other hand, from diet, is readily available according to the quantity eaten.
The protective effect from fat metabolism isn't just BHB production but also glucose production from the glycerol. And I suspect accessing the glycerol is the main driver for metabolising fat.
"Isoenergetic Feeding of Low Carbohydrate-High Fat Diets Does Not Increase Brown Adipose Tissue Thermogenic Capacity in Rats"
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0038997
The diet of the different groups (carb - fat - prot):
- 64.3 - 16.7 - 19.0 - control,
- 01.7 - 92.8 - 05.5 - low-carbohydrate-high-fat-low protein (LC-HF-LP);
- 02.2 - 78.7 - 19.1 - low carbohydrate-high-fat-normal-protein (LC-HF-NP);
- 19.4 - 61.9 18.7 - normal carbohydrate-high fat-normal protein (high fat)
All of these diets used identical macro-nutrient sources (protein-source: casein; fat-source: beef tallow; carbohydrate-source: starch)
https://preview.redd.it/tytca2tjav151.png?width=2939&format=png&auto=webp&s=f3d1e201a633e79ed803908a3b8a2639a686224f
What we see here first of all is that the dogmatic thinking of "all that matters are calories" is not true. Isocaloric feeding gives different results in body weight and composition.
What you need to recognize is that part of the ingested protein is converted to glucose. This will help to understand the differences here. Glucose from carbs together with glucose fro
... keep reading on reddit β‘It is well known that cells of brown adipose tissue, used for thermogenesis, express uncoupling proteins which dissipate the proton gradient across the inner mitochondrial membrane, generating heat. There are also medications (2,4-dinitrophenol) that do the same thing, leading to higher energy usage but uncontrolled heat production.
However, in explanations of this phenomenon, the exact explanation of how this photon transport leads to heat generation is always handwaved away as something like "the energy of the proton gradient is wasted as heat" in more or less complex formulations. I am interested in the exact physical mechanism which links the proton influx into the mitochondrial matrix to an increase in temperature, which I have never been able to find explained anywhere.
Also, a further question which may or may not be answered by my primary question: why does dissipation of a concentration gradient not lead to heat generation in other scenarios (e.g. when concentration gradients across neuronal cell membranes are dissipated at the postsynapse or the axon, during signal transmission; or during a large scale calcium influx into muscle cells)?
Hyperbaric Oxygen Ameliorates Insulin Sensitivity by Increasing GLUT4 Expression in Skeletal Muscle and Stimulating UCP1 in Brown Adipose Tissue in T2DM Mice.
https://twitter.com/BenBikmanPhD/status/1231791307988717569
https://www.ncbi.nlm.nih.gov/pubmed/32082261
https://www.frontiersin.org/articles/10.3389/fendo.2020.00032/full
Abstract
Hyperbaric oxygen (HBO) therapy is a treatment modality useful for diseases. Hypoxia could stimulate the induction of insulin resistance. Therefore, we sought to determine whether hyperbaric oxygen would ameliorate insulin sensitivity by promoting glucose transporter type 4 (GLUT4) expression in muscle and by stimulating UCP1 in brown adipose tissue (BAT) in a streptozocin (STZ)-induced type 2 diabetes mellitus (T2DM) mouse model. Male C57BL/6J mice were treated three times with low-dose of streptozocin (60 mg/kg, i.p.) and were fed with high-fat diets (HFD) to establish the T2DM model. HBO was administered daily as 100% oxygen at 2.0 atmosphere absolute (ATA) for 1 h for a week. We found that HBO significantly reduced blood glucose levels and attenuated insulin resistance in T2DM mice. HBO modulated food intake by influencing the activity of neuropeptide Y (NPY)-positive neurons in the arcuate nucleus (Arc). HBO treatment increased GLUT4 amount and level of phosphorylated Akt (p-Akt) in muscles of T2DM mice whereas this treatment stimulated the phosphorylation of AMPK in muscles of both T2DM and HFD mice. The morphological staining of BAT and the increased expression of uncoupling of protein 1 (UCP1) demonstrated the promotion of metabolism after HBO treatment. These findings suggest that HBO ameliorates insulin sensitivity of T2DM mice by stimulating the Akt signaling pathway and by promoting GLUT4 expression in muscle, and by increasing UCP1 expression in BAT.
Copyright Β© 2020 Liu, Zhang, Yuan, Song, Zhang, Lin, Li, Sheng, Ma, Lv, Gao and Dong.
KEYWORDS:
UCP1; glucose transporter type 4; hyperbaric oxygen; insulin sensitivity; type 2 diabetes mellitus
http://diabetes.diabetesjournals.org/content/61/3/674
Brown fat transplant. Not insulin producing cells transplant.
BAT transplants result in euglycemia, normalized glucose tolerance, reduced tissue inflammation, and reversal of clinical diabetes markers such as polyuria, polydipsia, and polyphagia. These effects are independent of insulin but correlate with recovery of the animalsβ white adipose tissue
