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Interesting study about ketones and carbohydrate metabolism
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<blockquote data-quote="LittleGreyCat" data-source="post: 2433737" data-attributes="member: 6467"><p><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/</a></p><p></p><p>I can't vouch for the accuracy of this, but it does have some (at least mildly) mind boggling statement.</p><p></p><p>Try for size:</p><p>"Contrary to popular belief supported by the leading physiology and biochemistry textbooks, there is sufficient population of glucose transporters in all cell membranes at all times to ensure enough glucose uptake to satisfy the cell's respiration, even in the absence of insulin [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/#B21" target="_blank">21</a>]. Insulin can and does increase the number of these transporters in some cells but glucose uptake is <em>never </em>truly insulin dependent. Even under conditions of extreme ketoacidosis there is no significant membrane barrier to glucose uptake – the block occurs "lower down" in the metabolic pathway where the excess of ketones competitively blocks the metabolites of glucose entering the citric acid cycle. Thus, insulin is <em>not </em>needed for glucose uptake and utilization in man [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/#B21" target="_blank">21</a>]. In fact, the process appears to be general for all polar (water-soluble) substrates, as transporters are the mechanism by which they are transported across the highly non-polar (lipid) cell membranes. When insulin is administered to people with diabetes who are fasting, blood glucose concentrations falls. It is generally assumed that this is because insulin increases glucose uptake into tissues. However, this is <em>not </em>the case and is just another metabolic legend arising from <em>in vitro </em>rat data. It has been shown that insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production"</p></blockquote><p></p>
[QUOTE="LittleGreyCat, post: 2433737, member: 6467"] [URL]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/[/URL] I can't vouch for the accuracy of this, but it does have some (at least mildly) mind boggling statement. Try for size: "Contrary to popular belief supported by the leading physiology and biochemistry textbooks, there is sufficient population of glucose transporters in all cell membranes at all times to ensure enough glucose uptake to satisfy the cell's respiration, even in the absence of insulin [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/#B21']21[/URL]]. Insulin can and does increase the number of these transporters in some cells but glucose uptake is [I]never [/I]truly insulin dependent. Even under conditions of extreme ketoacidosis there is no significant membrane barrier to glucose uptake – the block occurs "lower down" in the metabolic pathway where the excess of ketones competitively blocks the metabolites of glucose entering the citric acid cycle. Thus, insulin is [I]not [/I]needed for glucose uptake and utilization in man [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/#B21']21[/URL]]. In fact, the process appears to be general for all polar (water-soluble) substrates, as transporters are the mechanism by which they are transported across the highly non-polar (lipid) cell membranes. When insulin is administered to people with diabetes who are fasting, blood glucose concentrations falls. It is generally assumed that this is because insulin increases glucose uptake into tissues. However, this is [I]not [/I]the case and is just another metabolic legend arising from [I]in vitro [/I]rat data. It has been shown that insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production" [/QUOTE]
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