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<blockquote data-quote="Sean_Raymond" data-source="post: 2356611" data-attributes="member: 403497"><p>This is an interesting study. With a simple design. It isn't an RCT and it is conducted in free living individuals which need to be considered. One of the researcher's is Robert Lustig and I feel his clear position needs to also be considered in interpreting some of the things said here.</p><p></p><p>I'll put down some observations</p><p></p><p>The intro states that Insulin regulates Acetyl COA Carboxylase - which to a degree is true. ACC is the enzyme which converts Acetyl COA into Malonyl COA which is then converted to a fatty acid. In simple terms Insulin promotes the activity of an enzyme (ACC) which is instrumental in fat synthesis. BUT the enzyme insulin upregulates needs a substrate before fatty acids can be synthesised and that substrate is citrate. Citrate will only be available when the citric acid cycle becomes overwhelmed causing citrate to spill out of the mitochondria and into the cytosol of cells where it then can be used as a substrate (indirectly by insulin) for conversion into fat. BUT that spillage of citrate into the cytosol is NOT under hormonal/insulin control. It is driven by an abundance of energy which overwhelms the citric acid cycle.</p><p></p><p>I am working on trying to work out if, in an insulin resistant high blood sugar state, maybe this can cause this citrate spillage independent (to some degree) of positive energy balance. Basically insulin resistance causes a pseudo energy abundant state because of the high glucose/fat levels typical in insulin resistance fooling the body into thinking it has more than it has to promote fat storage (beyond hormonal control).</p><p></p><p>It then states that acute glucose stimulated secretion and fasting hyperinsulinaemia predicts weight gain - both claims are massively disputable and debatable. </p><p></p><p>May I ask why you say the weight loss WAS because of reduced insulin. The researchers acknowledged there could be other reasons for the reduced calorie intake other than insulin (they say these are less likely with no real evidence) and Ocretide has been shown to potentially reduce fat absorption in the gut. Also. he drug is a Somatostatin analog. Somatostatin has been shown to slow gastric motility and this can very plausibly cause a greater prolonged feeling of fullness after eating. So a compelling reason for why Octreotide may cause weight loss is because of its interaction with appetite regulation - promoting satiety. This fits in perfectly with this study as reduced hunger was reported. This warrants further investigation and I have not looked into this enough to say if it is the insulin or Octreotide acting on appetites regulation or a combo of both.</p><p></p><p>Also remember that in obese, insulin resistant individuals it isn't just insulin that is raised by glucagon, indeed we may very likely see hyperglucagonaemia accompany hyperinsulinaemia. Ocretide inhibits glucagon release as well as insulin.There may be implications for this reduction? I have no idea if there is a link - I am just throwing it out there to demonstrate much more is going on here than insulin reduction..</p><p></p><p>Regarding leptin reduction, this is not surprising given fat loss will cause Leptin reduction as leptin is released from adipose tissue. They had reduced hunger and less Leptin which may seem contradictory because Leptin promotes satiety but they were given a drug which has been shown to possibly reduce appetite.</p><p></p><p>I'm offering thoughts at this point although I am still more on the side of an explanation being it is insulin per se although I am trying to find a plausible mechanism to fit this. However it is correct that whatever is happening to explain the posters on here losing weight by reducing carbs/insulin and not calories IS happening. My initial rationale for this was that calories were reduced due to a massive reduction in calories by way of dietary carbohydrate reduction/removal and not fully compesating for this calorie reduction. Posters on here have shot that down with their testimonies that they eat as much if not more.</p></blockquote><p></p>
[QUOTE="Sean_Raymond, post: 2356611, member: 403497"] This is an interesting study. With a simple design. It isn't an RCT and it is conducted in free living individuals which need to be considered. One of the researcher's is Robert Lustig and I feel his clear position needs to also be considered in interpreting some of the things said here. I'll put down some observations The intro states that Insulin regulates Acetyl COA Carboxylase - which to a degree is true. ACC is the enzyme which converts Acetyl COA into Malonyl COA which is then converted to a fatty acid. In simple terms Insulin promotes the activity of an enzyme (ACC) which is instrumental in fat synthesis. BUT the enzyme insulin upregulates needs a substrate before fatty acids can be synthesised and that substrate is citrate. Citrate will only be available when the citric acid cycle becomes overwhelmed causing citrate to spill out of the mitochondria and into the cytosol of cells where it then can be used as a substrate (indirectly by insulin) for conversion into fat. BUT that spillage of citrate into the cytosol is NOT under hormonal/insulin control. It is driven by an abundance of energy which overwhelms the citric acid cycle. I am working on trying to work out if, in an insulin resistant high blood sugar state, maybe this can cause this citrate spillage independent (to some degree) of positive energy balance. Basically insulin resistance causes a pseudo energy abundant state because of the high glucose/fat levels typical in insulin resistance fooling the body into thinking it has more than it has to promote fat storage (beyond hormonal control). It then states that acute glucose stimulated secretion and fasting hyperinsulinaemia predicts weight gain - both claims are massively disputable and debatable. May I ask why you say the weight loss WAS because of reduced insulin. The researchers acknowledged there could be other reasons for the reduced calorie intake other than insulin (they say these are less likely with no real evidence) and Ocretide has been shown to potentially reduce fat absorption in the gut. Also. he drug is a Somatostatin analog. Somatostatin has been shown to slow gastric motility and this can very plausibly cause a greater prolonged feeling of fullness after eating. So a compelling reason for why Octreotide may cause weight loss is because of its interaction with appetite regulation - promoting satiety. This fits in perfectly with this study as reduced hunger was reported. This warrants further investigation and I have not looked into this enough to say if it is the insulin or Octreotide acting on appetites regulation or a combo of both. Also remember that in obese, insulin resistant individuals it isn't just insulin that is raised by glucagon, indeed we may very likely see hyperglucagonaemia accompany hyperinsulinaemia. Ocretide inhibits glucagon release as well as insulin.There may be implications for this reduction? I have no idea if there is a link - I am just throwing it out there to demonstrate much more is going on here than insulin reduction.. Regarding leptin reduction, this is not surprising given fat loss will cause Leptin reduction as leptin is released from adipose tissue. They had reduced hunger and less Leptin which may seem contradictory because Leptin promotes satiety but they were given a drug which has been shown to possibly reduce appetite. I'm offering thoughts at this point although I am still more on the side of an explanation being it is insulin per se although I am trying to find a plausible mechanism to fit this. However it is correct that whatever is happening to explain the posters on here losing weight by reducing carbs/insulin and not calories IS happening. My initial rationale for this was that calories were reduced due to a massive reduction in calories by way of dietary carbohydrate reduction/removal and not fully compesating for this calorie reduction. Posters on here have shot that down with their testimonies that they eat as much if not more. [/QUOTE]
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