There is good news from Harvard Researches.
Summary from me:
>The study showed blood levels of fabkin were abnormally high in mice and human patients with either type 1 or type 2 diabetes. The researchers found that blocking the activity of fabkin prevented the development of both forms of diabetes in the animals. Fabkin likely plays a similar role in humans and the hormone complex could be a promising therapeutic target, according to the researchers.
...
>The authors showed that the insulin-producing beta cells of the pancreas are a target of fabkin and that the hormone is a driving force behind the development of diabetes. When the researchers used an antibody to neutralize fabkin in mice, the animals did not develop diabetes. When the antibody was given to obese, diabetic mice, they reverted to a healthy state.
I hope it's not another "funding" project but promising. Let's wait and see how it's going to happen.
Footnote: Yes, I know we are 5 years away from diabetes-free life... :D
Title is self-explanatory, I'm back in honeymoon phase all of a sudden. My carbohydrate ratio has changed almost twofold, I now only need one unit of insulin to cover 20 g of carbs. My blood sugar is crashing constantly, My basal rate has dropped two fold as well, I can't keep my blood sugar up at work either. I'm running on Skittles and mountain Dew just to get through the day without seizing up. I went from taking two shots of basal per day to one shot right after work, and it's beginning to look like I need a pump to manage this honeymoon BS.
Last night really confirmed it for me, I had a night time high of 250 for about an hour last night, with a sudden, automatic hard crash to a baseline level of 120, where I woke up at a couple hours after. I can understand how that might be typical of a non-diabetic or a type 2 diabetic, but I'm not insulin resistant, so obviously that insulin had to come from somewhere. The only thing I can theorize is that I developed new beta cells after recovering from covid-19.
title, testing tmrw so any quick answer will help, thank u!
https://doi.org/10.3390/antiox11010108
Metabolic Adaptions/Reprogramming in Islet Beta-Cells in Response to Physiological StimulatorsβWhat Are the Consequences
Abstract
Irreversible pancreatic Ξ²-cell damage may be a result of chronic exposure to supraphysiological glucose or lipid concentrations or chronic exposure to therapeutic anti-diabetic drugs. The Ξ²-cells are able to respond to blood glucose in a narrow concentration range and release insulin in response, following activation of metabolic pathways such as glycolysis and the TCA cycle. The Ξ²-cell cannot protect itself from glucose toxicity by blocking glucose uptake, but indeed relies on alternative metabolic protection mechanisms to avoid dysfunction and death. Alteration of normal metabolic pathway function occurs as a counter regulatory response to high nutrient, inflammatory factor, hormone or therapeutic drug concentrations. Metabolic reprogramming is a term widely used to describe a change in regulation of various metabolic enzymes and transporters, usually associated with cell growth and proliferation and may involve reshaping epigenetic responses, in particular the acetylation and methylation of histone proteins and DNA. Other metabolic modifications such as Malonylation, Succinylation, Hydroxybutyrylation, ADP-ribosylation, and Lactylation, may impact regulatory processes, many of which need to be investigated in detail to contribute to current advances in metabolism. By describing multiple mechanisms of metabolic adaption that are available to the Ξ²-cell across its lifespan, we hope to identify sites for metabolic reprogramming mechanisms, most of which are incompletely described or understood. Many of these mechanisms are related to prominent antioxidant responses. Here, we have attempted to describe the key Ξ²-cell metabolic adaptions and changes which are required for survival and function in various physiological, pathological and pharmacological conditions.
------------------------------------------ Info ------------------------------------------
Open Access: True (not always correct)
Authors:
- Philip Newsholme
- Jordan Rowlands
- Roselyn RoseβMeyer
- Vinicius Cruzat
Additional links:
What will happen to registered beta users once the update occurs? Will all of the beta content be introduced in the update? What do you think?
https://threadreaderapp.com/thread/1476221647417921536.html
https://www.medrxiv.org/content/10.1101/2021.12.26.21268380v1
>These results demonstrate that despite Omicron's extensive mutations and reduced susceptibility to neutralizing antibodies, the majority of T cell response, induced by vaccination or natural infection, cross-recognises the variant. Well-preserved T cell immunity to Omicron is likely to contribute to protection from severe COVID-19, supporting early clinical observations from South Africa.
Alphaβs swift success has left scientists wondering how the variant conquered the world. A new study points to one secret to its success: Alpha disables the first line of immune defense in our bodies, giving the variant more time to multiply.
- New York Times
- By Carl Zimmer
- June 7, 2021
#####How the βAlphaβ Coronavirus Variant Became So Powerful
βItβs very impressive,β said Dr. Maudry Laurent-Rolle, a physician and virologist at the Yale School of Medicine who was not involved in the new study. βAny successful virus has to get beyond that first defense system. The more successful it is at doing that, the better off the virus is.β
The report was posted online on Monday and has not yet been published in a scientific journal.
They found that lung cells with Alpha made drastically less interferon, a protein that switches on a host of immune defenses. They also found that in the Alpha cells, the defensive genes normally switched on by interferon were quieter than in cells infected with other variants.
Somehow, the immune systemβs most important alarm bells were barely ringing in the presence of the Alpha variant. βItβs making itself more invisible,β Dr. Towers said
To investigate how Alpha achieved this invisibility, the researchers looked at how the coronavirus replicated inside of infected cells. They found that Alpha-infected cells make a lot of extra copies β some 80 times more than other versions of the virus β of a gene called Orf9b.
βItβs off the chart,β said Nevan Krogan, a molecular biologist at the University of California, San Francisco, and a co-author of the new study.
In previous research, Dr. Krogan and his colleagues had found that Orf9b makes a viral protein that locks onto a human protein called Tom70. And it just so happens that Tom70 is essential for a cellβs release of interferon in the face of an invading virus.
Putting all of the evidence together, Dr. Krogan and his colleagues argue that the Alpha variant carries a mutation that forces the production of a lot more Orf9b proteins. Those proteins swarm the human Tom70 proteins, dampening the production of interferon and a full immune response. The virus, protected from attack, has better odds of making copies of itself.
An infected cell can gradually remove the Orf9b proteins from its Tom70 molecules, however. By about 12 hours after infection, the alarm system starts coming back online.
Dr. Kroganβs team has also started similar experiments on other variants, inclu
... keep reading on reddit β‘Iβm a 22f and just super curious, Iβve had t1 diabetes for 5 years and Iβm starting to get to that age where children are something Iβm considering for the future. I know that generally when a woman is pregnant her immune system is weak, but does it weaken enough to stop the t-cells? Iβm just so intrigued about how it all works lol.
I just came across this post from the Sunnybrook Research Institute here in Toronto which announced new research that sounds promising.
https://sunnybrook.ca/media/item.asp?i=2376&f=pioneering-diabetes-treatment
100 years after the discovery of insulin, researchers at Sunnybrook are working on a new approach to treat diabetes.
βWeβre interested in better understanding why insulin producing beta cells canβt regenerate like other cells,β says Dr. Rob Screaton, a senior scientist in Biological Sciences at Sunnybrook Research Institute and an associate professor in The Department of Biochemistry at The University of Toronto.
In patients with type I diabetes, the immune system destroys insulin-producing cells in the pancreas. These cells canβt regenerate when theyβre gone, meaning patients need regular insulin injections to replace what they can no longer produce themselves.
βDirecting stem cells to become beta cells is an exciting strategy to replace lost beta cells in patients with diabetes, but so far these cells have remained largely unresponsive to glucose,β says Dr. Screaton. βAn alternative approach is to encourage beta cells to regenerate again, while suppressing the ongoing immune attack.β
Above, take a look inside the Screaton lab to see how the team is working to identify the pathways that prevent beta cell regeneration, in an effort to develop new treatments or diabetes.
(See video at link posted above)
If this press release had been from Moderna for some new vaccine their stock would have most likely went up 10 or 20 percent. Their market caps is 151 B. Complete crap. Although I think SRNE should have put this press release out in the morning.
