Robinredbreast
Oracle
- Messages
- 18,446
- Location
- Planet Earth
- Type of diabetes
- Type 1
- Treatment type
- Insulin
- Dislikes
- Bullies, Liars, Trolls and dishonest cruel people
Indeed. If you've got a kindle, Thea Cooper's book Breakthrough, about the discovery of insulin, has got some really touching stuff about the close relationship between Banting, who seemed to be quite a stand-offish chap, and dog 92, Marjorie, who seems to have been the first to show his methods were working, but then had to die to prove the concept.
He made a point of telling all his patients how grateful they should be to that dog. And us too.
Here's a quote from him:
"I shall never forget that dog as long as I shall live,” Banting wrote of Dog 92 in 1940, “…when that dog died I wanted to be alone for the tears would fall despite anything I could do.”
http://www.breakthroughthebook.com/blog/2010/08/insulin-in-its-infancy-dogs-and-diabetes/
Flippin mice always seem to get the most cutting edge treatment before us mere humans do, and I bet ya none of them have ever paid taxes...
Spend more time with them and you could get yourself a pretty good support band if the pics of these wee critters are anything to go by! I wouldn't rate the groupies, though...
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'ere ows your Berts lumbago.Looks like old promo shots for the Small faces..
What about dogs 1 through 91?"I shall never forget that dog as long as I shall live,” Banting wrote of Dog 92 in 1940, “…when that dog died I wanted to be alone for the tears would fall despite anything I could do.”
All gone, gone I tellz ya.What about dogs 1 through 92?
What about dogs 1 through 91?
Looks like old promo shots for the Small faces..
so I reckoned my niche was just nibbling the neck of the guitar instead of hitting it and see how that worked out sound-wise. It's working out well
Dr Chhabra said that understanding how defective growth hormone receptors prevented diabetes at the cellular and tissue level could enable researchers to develop treatments for the general population.
He also makes it clear that it was neither him nor his team which first identified Laron dwarfs are being immune to cancer and diabetes. “A research first came out in 2011 about these people who don’t suffer from diabetes or cancer even though they are often obese,” adds Dr Chhabra.
Life span extending mutations in growth signaling pathways protect against age-dependent DNA damage in yeast and decrease insulin resistance and cancer in mice. To test their effect in humans, we monitored for 22 years Ecuadorian subjects with mutations in the growth hormone receptor gene leading to severe growth hormone receptor (GHR) and IGF-I deficiencies and combined this information with surveys to identify the cause and age of death for subjects who died before this period.
No matter how old they get, almost none die of cancer. No matter what they eat, they don't seem to develop diabetes.
This group represents approximately one-third of the global population of people who have what's known as Laron syndrome, a genetic disorder that makes the body unable to use growth hormone.
not at all. Does it matter when people post Urls without also posting a line on why you should click on someplace? I am so glad when someone visits the cluefree Url in place of me and my computer similar to watching someone other than self taste the jalapeno popper and save my tummy
“We discovered that a signalling molecule activated by the growth hormone receptors, called STAT5, was responsible for regulating this insulin sensitivity.
“Defective growth hormone receptors meant the STAT5 molecules weren’t activated properly.
“This switching off of the STAT5 activation improved prevented insulin resistance by improving insulin signalling.
“This increased insulin receptors and reduced glucose output from the liver.”
Growth hormone (GH) has an important function as an insulin antagonist with elevated insulin sensitivity evident in humans and mice lacking a functional GH receptor (GHR). We sought the molecular basis for this sensitivity by utilizing a panel of mice possessing specific deletions of GHR signaling pathways. Metabolic clamps and glucose homeostasis tests were undertaken in these obese adult C57BL/6 male mice, which indicated impaired hepatic gluconeogenesis.
Insulin sensitivity and glucose disappearance rate were enhanced in muscle and adipose of mice lacking the ability to activate the signal transducer and activator of transcription (STAT)5 via the GHR (Ghr-391−/−) as for GHR-null (GHR−/−) mice. These changes were associated with a striking inhibition of hepatic glucose output associated with altered glycogen metabolism and elevated hepatic glycogen content during unfed state. The enhanced hepatic insulin sensitivity was associated with increased insulin receptor β and insulin receptor substrate 1 activation along with activated downstream protein kinase B signaling cascades.
Although phosphoenolpyruvate carboxykinase (Pck)-1expression was unchanged, its inhibitory acetylation was elevated because of decreased sirtuin-2 expression, thereby promoting loss of PCK1. Loss of STAT5 signaling to defined chromatin immunoprecipitation targets would further increase lipogenesis, supporting hepatosteatosis while lowering glucose output. Finally, up-regulation of IL-15 expression in muscle, with increased secretion of adiponectin and fibroblast growth factor 1 from adipose tissue, is expected to promote insulin sensitivity.—Chhabra, Y., Nelson, C. N., Plescher, M., Barclay, J. L., Smith, A. G., Andrikopoulos, S., Mangiafico, S., Waxman, D. J., Brooks, A. J., Waters, M. J. Loss of growth hormone–mediated signal transducer and activator of transcription 5 (STAT5) signaling in mice results in insulin sensitivity with obesity.
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