Very little is generally known about another hormone co produced with insulin by the beta cells of pancreas. The hormone first reported in 1987 and is called "AMYLIN".
The secretory and plasma concentration profiles of insulin and AMYLIN are similar with low fasting concentration and increases in response to nutrient intake.
AMYLIN works with insulin to help coordinate the rate glucose appearance and disappearance in the circulation by preventing an abnormal rise in glucose concentrations. AMYLIN complements the effect of insulin on circulating concentrations via two main mechanism. AMYLIN suppresses Post Prandial Glucagone secretions, thereby decreasing glucagone stimulated hepatic glucose output following food ingestion.
IMPORTANTLY AMYLIN does NOT suppress glucagone secretions during insulin induced hypoglycemia .
AMYLIN also slows the rate of gastric emptying and thus the rate at which nutrients are delivered from stomach to small intestine for absorption. In addition to its effects on glucagone secretion and rate of gastric emptying AMYLIN reduces food intake and body weight.
In summary, AMYLIN works to regulate the rate of glucose appearance from both endogenous ( liver derived) and exogenous ( meal derived ) sources AND insulin regulates the rate of glucose dis appearance.
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patliputra
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Probably because majority of people come to forums looking for solutions. Now here's the take from a diabetic who looks for solutions followed by all technicalities discussed in your post and no solutions offered:
With increased need for insulin by diabetics, there's an excess need/secretion of ProIAPP. However, the enzymes cannot keep pace with excess secretion when it comes to converting these precursor molecules into insulin and IAPP (or Amylin as Americans call it), respectively, and , as a result, leads to the accumulation of proIAPP. The muted processing of proIAPP, which occurs at N-terminal cleavage site, is a driving factor in the triggering of amyloid which may fuel amyloid-induced apoptosis of beta-cells ie programmed beta cell death. In layman terms all this mumbo jumbo is stated in one sentence:
"High Glucose levels lead to beta cell death" Jenny Ruhl (whom you consider as some commercial writer but we consider as mother of T2 self management) says that elevated glucose levels leads to cellular death. These plain sentences are easier to understand.
This was just the theory which again is incomplete in any discussion for a diabetic who is looking for solution and the theoretical discussion abruptly ends with no solution on offer is obviously of no help to a diabetic looking for solutions. They want SOLUTIONS, much like when one goes to a restaurant one wants the meal served and not know which brand of salt or oil was used in cooking.
Question:
So, what does one do to reduce/minimize amyloid-induced apoptosis of beta-cells which is making diabetes a progressive disease which finally leads to exogenous insulin if ADA diet is followed for decades?
Answer:
Get away from ADA's High Carb Low Fat broken dietary guideline and reduce the need for ProIAPP, leaving less of unprocessed ProIAPP and thus less of amyloid formation and hence reduced chances of beta cell death. Besides, this also offers a far better sugar control, lowered insulin resistance and hence still less unprocessed ProIAPP and lower need for DRUGS. A healthy cycle sets in. No textbooks or so called great websites will talk these things. These come from one's open mindedness to understand beyond the dated information that's presented on so called great websites. All it needs is "common sense"
I am sure the "so called experts" sitting at ADA/WHO/AMA/AHA etc know all this but still they keep pushing the diet that is only making things go from BAD to WORSE not just wrt glucose control but CVD/CHD, Obesity, Cancer, Neuropathy etc. Yet, all attempts are only to find new patented (read criminally profitable) drugs, insulin and expensive procedures. In the end who is funding ADA/WHO/AMA/AHA etc? They care a hoot for patients. They care for their profits even if that means pushing a FAILED DIET.
wise and naughty .....(By the way fbs is 120 for 2 dyas., its a achievement sort of.,) AG thanks., and ppbs around 147 to 180., happy with progress..AND an OPEN thanks to you in this forum.
AG works as a stress buster, though ADA camp may not agree. Even TID dose is fine. For PPBS you have to count carbs and adhere to LCHF and get your proIAPP secretion down, which can also reduce Insulin Resistance thereby further cutting down proIAPP secretion
If strict adherence also doesn't get to the target values, then walk after meals. User ram_latha has posted about walking after meals on the other site.
If LCHF and walking also doesn't get you to target levels, then comes drug. Drug should be last.
Glad that you are getting your numbers down. Just get hold of LCHF game's rules. The more thanks I get, the more indiacratus and company will insult and abuse me and start hitting Report button to get me booted off from here
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Insulin resistance (IR)
ALL YOU WANTED TO KNOW ABOUT METHI.. ( FENUGREEK)
