Whereas type 1 diabetes is caused by an autoimmune response directed against the insulin-producing beta islet cells of the pancreas, type 2 diabetes is caused by exhausting those beta cells through excessive energy consumption.
Essentially, if one eats too much and has high blood glucose levels, the beta cells have to produce more and more insulin to keep up, eventually leading to accumulation of damage and death. This state is referred to as insulin resistance, and it is considered to be a major contributor to the further development of type 2 diabetes.
Johns Hopkins University Rövid összefoglaló This research is being done to find out whether subjects previously treated with the implantable insulin pump IIP therapy, and now taking insulin by injection, will benefit from re-implantation of IIP. The investigators will see if IIP causes more stable control of blood sugar, with fewer highs and lows. Részletes leírás If the participant joins the study and chooses to have a new pump implanted, the study is expected to last months for each participant, and each participant will continue to be followed, with 3-monthly refills and research visits for as long as the pump lasts, until the participant chooses to withdraw, until the FDA approves the pump for regular care, or until the company stops supporting the pump. During the first months of the study, there will be an estimated 13 clinic visits and one hospital stay for days.
A major problem encountered by scientists seeking to study obesity and diabetes is that treatments developed in mice have failed to have any impact on humans, underlying their limited utility as a model organism for the disease. Given this stumbling block, researchers have increasingly begun to study other animals, as in a recent paper that focused on grizzly bears.
Johns Hopkins Medicine Summary: People with pre-diabetes who lose roughly 10 percent of their body weight within six months of diagnosis dramatically reduce their risk of developing type 2 diabetes over the next three years, according to new research.
During the months leading up to hibernation, they are capable of doubling their levels of body fat. Such massive weight gain would result in serious health problems for humans, but bears are capable of tolerating these fluctuations, leading the authors to investigate how exactly this was possible.
As it turns out, bears are capable of uniquely regulating a protein called PTEN phosphatase and tensin homologwhich has a role in shutting off insulin signaling among other things.
During the fall, while bears are bulking up, they turn off PTEN, which results in increased insulin sensitivity and stable blood sugar levels despite weight gain. While hibernating, PTEN is turned back on, making the bears more insulin resistant and slowing weight loss during their long winter snooze.
These findings with PTEN actually mirror a previous study in humans, in which patients who only had one copy of PTEN instead of two were more resistant to complications associated with weight gain, namely diabetes and heart disease. So all we have to do is turn off PTEN in people and their type 2 diabetes will go away, right?
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Remember how PTEN does more than simply shutting down insulin signaling? Well, one of those things is kind of important: It prevents cancer.
PTEN is an essential tumor suppressor that has been implicated in dozens of malignancies. Indeed, those patients who lacked one copy of PTEN were found to develop aggressive cancers at a much higher rate than normal.
Though this may be potentially circumvented by targeting PTEN in fat cells only, it is still obviously a major concern for therapeutic development. While diabetes is certainly a cause of reduced quality of life, making patients more insulin sensitive will also result latest type 1 diabetes research news increased weight gain.
It found that type 2 diabetes is associated with a higher risk of mortality in hospitalised COVID patients than type 1 diabetes. The combination of an older age and high C-reactive protein CRP was also linked to a higher risk of death. Younger people under 70 years old with chronic kidney disease, a common long-term complication of diabetes, also had a higher likelihood of dying.
Since the obesity epidemic shows no signs of slackingaddressing the associated comorbidities is a major priority for biomedical researchers. And while this research is certainly promising, there are significant barriers that need to be overcome before a drug can even begin to be conceptualized.