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<blockquote data-quote="KenMacK" data-source="post: 2052637" data-attributes="member: 506757"><p>P.S. Outside of the researchers who perform portal hormone measurements, there seems to be little understanding of the non-diabetic and diabetic islet function.</p><p>Hyperglycemia due to dietary carb's (i.e. portal/islet glucose) CANNOT be compensated for with sub-Q insulin. Even in the non-diabetic there is a hyperglycemic response to prandial glucose, but there is a strong acute insulin response and (hence) a total suppression of glucagon secretion. This is a negative feedback, and hence regulatory in nature.</p><p>By contrast, in the diabetic there is a weak or absent GSIS (glucose stimulated insulin secretion) and an INCREASE in GSIG (glucagon secretion). This is a POSITIVE feedback, and fundamentally unstable in nature. Those who understand control/regulatory systems, either in engineering or in nature, should recognize that during the prandial or meal-absorptive interval this will induce an oscillatory and amplified hormone response that is unpredictable, capable of producing both hyperglycemia and hypoglycemia at different times if one attempts to compensate with exogenous insulin.</p><p>This IS THE REASON that a diabetic (excepting MODY2) should eliminate carb's in the diet. It is not simply that carb's generate a stronger (gram for gram) acute insuin response than most AAs -- this reflects a very simplistic and incomplete understanding of the endocrinology.</p><p>People who talk about rapidity of release of various forms of fast-acting manufactured insulins simply do not understand insulin therapy and what it does and does not do. All fast-acting forms of insulin (mimetics or analogs) are attempts to compensate for dietary carb's, and all cannot work (well or consistently and predictably, at least). There is no substitute, presently, for the elimination of significant amounts of carb's in meals. All meals should be AA-dominated, in terms of required compensatory insulin bolus.</p><p>By contrast, the islet response to AAs is quite different. AASIS will be deficient in most diabetics (notably excepting early T2DM), and hence AASGS will be excessive. However, the excess of glucagon will be predictable and largely proportional to mass of animal-sourced protein (each individual AA has its own unique potency of AASGS, acting directly upon both alpha cells and beta cells, and so proportions matter) ingested during absorption. The feedback will never become positive -- it will remain negative albeit weak or deficient. This is WHY an insulin bolus will have a consistent and predictable compensatory effect to diabetic hyperglycemia from dietary protein.</p><p>The definition of carb elimination, as a practical matter for the diabetic, is a meal composition that produces a protein-dominated requirement for insulin bolus quantity (i.e. number of units).</p><p>The diabetic practicing a ketogenic diet MUST use only insulin Regular (e.g. Novolin R or Humilin R). This is the only form of insulin that has appropriate time-release/flux profile for absorption of protein from the small intestines. All other forms of insulin are inappropriate for bolus application. Fast-acting, intermediate-acting, and long-acting insulin analogs must be avoided in covering meals, and will result in both prandial hypoglyemia and prandial hyperglycemia in the best case.</p><p>Diabetics should also be aware that there is a lag (typically about a half hour) between capillary blood glucose and serum BG. Not only do home meters/strips rely upon capillary/interstitial BG, but so do CGMs (all or most, I think, although I do not use one). For basal compensation (i.e. non-absorptive intervals) this is not a huge problem, although even in this state any stress-hormone induced hyperglycemia will not be compensated for properly. But for bolus compensation a CGM cannot fulfill the function of sensor (operating in paralle with endocrine pancreas).</p><p>Furthermore, for correct bolus compensation and feedback (using a pump, for example) it is the ISLET blood that would have to be sensed. Not even portal blood would be adequately adequate, although this would be better than serum blood and serum blood is better than capillary blood. During the absorptive period the portal blood glucose can be up to 40 times that of peripheral blood and islet blood glucose can be up to 400 times that of peripheral blood! This is what the lab measurements illustrate. This is why quantitative analysis is essential.</p><p>I cannot overemphasize how incorrect any whole-body IR model is. It is metaphorical at best, very misleading in general, and incorrect. IR is a measureable independent characteristic of each individual tissue in the body -- there is no such thing, physiologically, as whole-body IR. And there is no such thing as "hepatic IR", although one can find this term extensively used in the clinical research literature. It is just as much a mere metaphor as is whole-body IR. The liver is normal, without significant defect, in most diabetes. It is responding normally to an imbalance of portal hormones. The defect is at the level of the islets.</p><p>For those who might mention fatty liver as an example of hepatic abnormality -- this is an effect, and not a cause, of T2DM and pre-diabetes (MetS) and generally not present at all in other forms of diabetes. It is a manifestation of disrupted fatty-acid metabolism in liver. In MetS ALL of the insulin-expressing tissues are similarly disrupted, and filled with ectopic FA intermediates (aka lipotoxicity). These include muscle, kidney, intestine, and adipose.</p><p>NAFLD is not universally present in either pre-diabetes or in T2DM. It is not required, and is certainly not causal.</p></blockquote><p></p>
[QUOTE="KenMacK, post: 2052637, member: 506757"] P.S. Outside of the researchers who perform portal hormone measurements, there seems to be little understanding of the non-diabetic and diabetic islet function. Hyperglycemia due to dietary carb's (i.e. portal/islet glucose) CANNOT be compensated for with sub-Q insulin. Even in the non-diabetic there is a hyperglycemic response to prandial glucose, but there is a strong acute insulin response and (hence) a total suppression of glucagon secretion. This is a negative feedback, and hence regulatory in nature. By contrast, in the diabetic there is a weak or absent GSIS (glucose stimulated insulin secretion) and an INCREASE in GSIG (glucagon secretion). This is a POSITIVE feedback, and fundamentally unstable in nature. Those who understand control/regulatory systems, either in engineering or in nature, should recognize that during the prandial or meal-absorptive interval this will induce an oscillatory and amplified hormone response that is unpredictable, capable of producing both hyperglycemia and hypoglycemia at different times if one attempts to compensate with exogenous insulin. This IS THE REASON that a diabetic (excepting MODY2) should eliminate carb's in the diet. It is not simply that carb's generate a stronger (gram for gram) acute insuin response than most AAs -- this reflects a very simplistic and incomplete understanding of the endocrinology. People who talk about rapidity of release of various forms of fast-acting manufactured insulins simply do not understand insulin therapy and what it does and does not do. All fast-acting forms of insulin (mimetics or analogs) are attempts to compensate for dietary carb's, and all cannot work (well or consistently and predictably, at least). There is no substitute, presently, for the elimination of significant amounts of carb's in meals. All meals should be AA-dominated, in terms of required compensatory insulin bolus. By contrast, the islet response to AAs is quite different. AASIS will be deficient in most diabetics (notably excepting early T2DM), and hence AASGS will be excessive. However, the excess of glucagon will be predictable and largely proportional to mass of animal-sourced protein (each individual AA has its own unique potency of AASGS, acting directly upon both alpha cells and beta cells, and so proportions matter) ingested during absorption. The feedback will never become positive -- it will remain negative albeit weak or deficient. This is WHY an insulin bolus will have a consistent and predictable compensatory effect to diabetic hyperglycemia from dietary protein. The definition of carb elimination, as a practical matter for the diabetic, is a meal composition that produces a protein-dominated requirement for insulin bolus quantity (i.e. number of units). The diabetic practicing a ketogenic diet MUST use only insulin Regular (e.g. Novolin R or Humilin R). This is the only form of insulin that has appropriate time-release/flux profile for absorption of protein from the small intestines. All other forms of insulin are inappropriate for bolus application. Fast-acting, intermediate-acting, and long-acting insulin analogs must be avoided in covering meals, and will result in both prandial hypoglyemia and prandial hyperglycemia in the best case. Diabetics should also be aware that there is a lag (typically about a half hour) between capillary blood glucose and serum BG. Not only do home meters/strips rely upon capillary/interstitial BG, but so do CGMs (all or most, I think, although I do not use one). For basal compensation (i.e. non-absorptive intervals) this is not a huge problem, although even in this state any stress-hormone induced hyperglycemia will not be compensated for properly. But for bolus compensation a CGM cannot fulfill the function of sensor (operating in paralle with endocrine pancreas). Furthermore, for correct bolus compensation and feedback (using a pump, for example) it is the ISLET blood that would have to be sensed. Not even portal blood would be adequately adequate, although this would be better than serum blood and serum blood is better than capillary blood. During the absorptive period the portal blood glucose can be up to 40 times that of peripheral blood and islet blood glucose can be up to 400 times that of peripheral blood! This is what the lab measurements illustrate. This is why quantitative analysis is essential. I cannot overemphasize how incorrect any whole-body IR model is. It is metaphorical at best, very misleading in general, and incorrect. IR is a measureable independent characteristic of each individual tissue in the body -- there is no such thing, physiologically, as whole-body IR. And there is no such thing as "hepatic IR", although one can find this term extensively used in the clinical research literature. It is just as much a mere metaphor as is whole-body IR. The liver is normal, without significant defect, in most diabetes. It is responding normally to an imbalance of portal hormones. The defect is at the level of the islets. For those who might mention fatty liver as an example of hepatic abnormality -- this is an effect, and not a cause, of T2DM and pre-diabetes (MetS) and generally not present at all in other forms of diabetes. It is a manifestation of disrupted fatty-acid metabolism in liver. In MetS ALL of the insulin-expressing tissues are similarly disrupted, and filled with ectopic FA intermediates (aka lipotoxicity). These include muscle, kidney, intestine, and adipose. NAFLD is not universally present in either pre-diabetes or in T2DM. It is not required, and is certainly not causal. [/QUOTE]
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