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#102
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What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)
(tcomeau) wrote in message . com...
Ron Ritzman wrote in message . .. On 27 Jan 2004 11:46:06 -0800, (tcomeau) wrote: And what "other mechanisms"? Your Google search term for today is "acylation stimulating protein" From Mr. "Ketogenic Diet" himself Lyle McDonald. http://groups.google.com/groups?q=%2...onr.com&rnum=1 Or http://tinyurl.com/2fbpf Here is a recent study on acylation stimulating protein. ** Acylation stimulating protein stimulates insulin secretion. Ahren B, Havel PJ, Pacini G, Cianflone K. Department of Medicine, Lund University, Lund, Sweden. Acylation stimulating protein (ASP) is a hormone produced by adipocytes and is of importance for the storage of energy as fat. We examined whether ASP might also have effects on islet function. In clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated insulin secretion. The lowest effective dose of ASP at 10 mmol/l glucose was 5 micro mol/l. The effect was glucose-dependent because ASP did not increase insulin secretion at 1 mmol/l glucose but had clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented glyceraldehyde-induced insulin secretion but the hormone did not enhance insulin secretion in response to depolarization by 20 mmol/l of KCl. ASP-induced insulin secretion was completely abolished by competitive inhibition of glucose phosphorylation by glucokinase with 5-thio-glucose and was partially inhibited by the calcium channel blocker, nifedipine, and by the protein kinase C inhibitor, GF109203. Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the endoplasmic reticulum, did not affect ASP-induced insulin secretion. ASP (5 micro mol/l) also augmented glucose-stimulated insulin secretion from islets isolated from C57BL/6J mice, and intravenous administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min) insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice. This was accompanied by an increased rate of glucose disposal. Minimal model analyses of data derived from the intravenous glucose tolerance test revealed that whereas ASP augmented insulin secretion, the hormone did not affect insulin sensitivity (S(I)) or glucose effectiveness (S(G)). We conclude that ASP augments glucose-stimulated insulin secretion through a direct action on the islet beta cells. The effect is dependent on glucose phosphorylation, calcium uptake and protein kinase C. Stimulation of insulin secretion by ASP in vivo results in augmented glucose disposal. PMID: 12917708 [PubMed - indexed for MEDLINE] ** Of interest: "We conclude that ASP augments glucose-stimulated insulin secretion through a direct action on the islet beta cells. The effect is dependent on glucose phosphorylation, calcium uptake and protein kinase C. Stimulation of insulin secretion by ASP in vivo results in augmented glucose disposal." These sentences: "...ASP augments glucose-stimulated insulin secretion..." "The effect is dependent on glucose phosphorylation..." Can we conclude that without "glucose-stimulated insulin secretion" and "glucose phosphorylation" the effects of ASP would be minimal if anything at all. TC No. What this study shows is that ASP enhances insulin secretion from the pancreas only in the presence of glucose; in other words, ASP can not stimulate insulin secretion on its own. However, the *primary* lipogenic effect of ASP is independent of insulin. ASP increases triglyceride synthesis in fat cells by stimulating the activity of the enzyme diacylglycerol acyltransferase (DGAT). DGAT catalyzes the last step in the making of a triglyceride molecule (when the third and final fatty acid is attached to the glycerol backbone). It's well known that insulin enhances fat-storage primarily by preventing lipolysis (triglyceride breakdown). ASP, on the other hand, promotes fat-storage primarily by stimulating lipogenesis (triglyceride synthesis). Think about it -- eating carbs causes insulin secretion; the insulin prevents fatty acid release from adipose tissue so that the carbs are burned for energy first. Eating fat causes ASP secretion; the ASP causes any extra fat to be stored in adipose tissue. This doesn't mean the insulin does not directly stimulate lipogenesis or that ASP doesn't directly prevent lipolysis, because they do. However, these are secondary effects. |
#103
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What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)
(September) wrote in message om...
(tcomeau) wrote in message . com... Ron Ritzman wrote in message . .. On 27 Jan 2004 11:46:06 -0800, (tcomeau) wrote: And what "other mechanisms"? Your Google search term for today is "acylation stimulating protein" From Mr. "Ketogenic Diet" himself Lyle McDonald. http://groups.google.com/groups?q=%2...onr.com&rnum=1 Or http://tinyurl.com/2fbpf Here is a recent study on acylation stimulating protein. ** Acylation stimulating protein stimulates insulin secretion. Ahren B, Havel PJ, Pacini G, Cianflone K. Department of Medicine, Lund University, Lund, Sweden. Acylation stimulating protein (ASP) is a hormone produced by adipocytes and is of importance for the storage of energy as fat. We examined whether ASP might also have effects on islet function. In clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated insulin secretion. The lowest effective dose of ASP at 10 mmol/l glucose was 5 micro mol/l. The effect was glucose-dependent because ASP did not increase insulin secretion at 1 mmol/l glucose but had clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented glyceraldehyde-induced insulin secretion but the hormone did not enhance insulin secretion in response to depolarization by 20 mmol/l of KCl. ASP-induced insulin secretion was completely abolished by competitive inhibition of glucose phosphorylation by glucokinase with 5-thio-glucose and was partially inhibited by the calcium channel blocker, nifedipine, and by the protein kinase C inhibitor, GF109203. Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the endoplasmic reticulum, did not affect ASP-induced insulin secretion. ASP (5 micro mol/l) also augmented glucose-stimulated insulin secretion from islets isolated from C57BL/6J mice, and intravenous administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min) insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice. This was accompanied by an increased rate of glucose disposal. Minimal model analyses of data derived from the intravenous glucose tolerance test revealed that whereas ASP augmented insulin secretion, the hormone did not affect insulin sensitivity (S(I)) or glucose effectiveness (S(G)). We conclude that ASP augments glucose-stimulated insulin secretion through a direct action on the islet beta cells. The effect is dependent on glucose phosphorylation, calcium uptake and protein kinase C. Stimulation of insulin secretion by ASP in vivo results in augmented glucose disposal. PMID: 12917708 [PubMed - indexed for MEDLINE] ** Of interest: "We conclude that ASP augments glucose-stimulated insulin secretion through a direct action on the islet beta cells. The effect is dependent on glucose phosphorylation, calcium uptake and protein kinase C. Stimulation of insulin secretion by ASP in vivo results in augmented glucose disposal." These sentences: "...ASP augments glucose-stimulated insulin secretion..." "The effect is dependent on glucose phosphorylation..." Can we conclude that without "glucose-stimulated insulin secretion" and "glucose phosphorylation" the effects of ASP would be minimal if anything at all. TC No. What this study shows is that ASP enhances insulin secretion from the pancreas only in the presence of glucose; in other words, ASP can not stimulate insulin secretion on its own. However, the *primary* lipogenic effect of ASP is independent of insulin. ASP increases triglyceride synthesis in fat cells by stimulating the activity of the enzyme diacylglycerol acyltransferase (DGAT). DGAT catalyzes the last step in the making of a triglyceride molecule (when the third and final fatty acid is attached to the glycerol backbone). It's well known that insulin enhances fat-storage primarily by preventing lipolysis (triglyceride breakdown). ASP, on the other hand, promotes fat-storage primarily by stimulating lipogenesis (triglyceride synthesis). Think about it -- eating carbs causes insulin secretion; the insulin prevents fatty acid release from adipose tissue so that the carbs are burned for energy first. Eating fat causes ASP secretion; the ASP causes any extra fat to be stored in adipose tissue. This doesn't mean the insulin does not directly stimulate lipogenesis or that ASP doesn't directly prevent lipolysis, because they do. However, these are secondary effects. Thanks for the info. One or two questions... "Acylation stimulating protein (ASP) is a hormone produced by adipocytes and is of importance for the storage of energy as fat." Under what circumstances do the adipocytes produce ASP? What triggers the fat cells to increase or decrease production of ASP? TC |
#104
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What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)
On 30 Jan 2004 08:46:15 -0800, (tcomeau) wrote:
Under what circumstances do the adipocytes produce ASP? The presence of "dietary fat" (chylomicrons) in the blood triggers the ASP system Look, I'm not bashing Atkins or low carb. I lost 80 pounds LC and another 80 on a "politically correct" ordinary low calorie diet. I lost weight on both approaches but felt less hungry on LC so I know how it really works. LC/Atkins benefits some people because there is no insulin "spike and crash" effect that makes you hungry too soon after a big carby meal, not because of some mysterious fat burning enzyme that magically makes excess calories go away. On top of that, carbs represent over 50% of the average American diet so it's not surprising that many people lose weight on Atkins. -- Ron Ritzman http://www.panix.com/~ritzlart Smart people can figure out my email address |
#105
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What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)
(tcomeau) wrote in message . com...
(September) wrote in message om... (tcomeau) wrote in message . com... Ron Ritzman wrote in message . .. On 27 Jan 2004 11:46:06 -0800, (tcomeau) wrote: And what "other mechanisms"? Your Google search term for today is "acylation stimulating protein" From Mr. "Ketogenic Diet" himself Lyle McDonald. http://groups.google.com/groups?q=%2...onr.com&rnum=1 Or http://tinyurl.com/2fbpf Here is a recent study on acylation stimulating protein. ** Acylation stimulating protein stimulates insulin secretion. Ahren B, Havel PJ, Pacini G, Cianflone K. Department of Medicine, Lund University, Lund, Sweden. Acylation stimulating protein (ASP) is a hormone produced by adipocytes and is of importance for the storage of energy as fat. We examined whether ASP might also have effects on islet function. In clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated insulin secretion. The lowest effective dose of ASP at 10 mmol/l glucose was 5 micro mol/l. The effect was glucose-dependent because ASP did not increase insulin secretion at 1 mmol/l glucose but had clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented glyceraldehyde-induced insulin secretion but the hormone did not enhance insulin secretion in response to depolarization by 20 mmol/l of KCl. ASP-induced insulin secretion was completely abolished by competitive inhibition of glucose phosphorylation by glucokinase with 5-thio-glucose and was partially inhibited by the calcium channel blocker, nifedipine, and by the protein kinase C inhibitor, GF109203. Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the endoplasmic reticulum, did not affect ASP-induced insulin secretion. ASP (5 micro mol/l) also augmented glucose-stimulated insulin secretion from islets isolated from C57BL/6J mice, and intravenous administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min) insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice. This was accompanied by an increased rate of glucose disposal. Minimal model analyses of data derived from the intravenous glucose tolerance test revealed that whereas ASP augmented insulin secretion, the hormone did not affect insulin sensitivity (S(I)) or glucose effectiveness (S(G)). We conclude that ASP augments glucose-stimulated insulin secretion through a direct action on the islet beta cells. The effect is dependent on glucose phosphorylation, calcium uptake and protein kinase C. Stimulation of insulin secretion by ASP in vivo results in augmented glucose disposal. PMID: 12917708 [PubMed - indexed for MEDLINE] ** Of interest: "We conclude that ASP augments glucose-stimulated insulin secretion through a direct action on the islet beta cells. The effect is dependent on glucose phosphorylation, calcium uptake and protein kinase C. Stimulation of insulin secretion by ASP in vivo results in augmented glucose disposal." These sentences: "...ASP augments glucose-stimulated insulin secretion..." "The effect is dependent on glucose phosphorylation..." Can we conclude that without "glucose-stimulated insulin secretion" and "glucose phosphorylation" the effects of ASP would be minimal if anything at all. TC No. What this study shows is that ASP enhances insulin secretion from the pancreas only in the presence of glucose; in other words, ASP can not stimulate insulin secretion on its own. However, the *primary* lipogenic effect of ASP is independent of insulin. ASP increases triglyceride synthesis in fat cells by stimulating the activity of the enzyme diacylglycerol acyltransferase (DGAT). DGAT catalyzes the last step in the making of a triglyceride molecule (when the third and final fatty acid is attached to the glycerol backbone). It's well known that insulin enhances fat-storage primarily by preventing lipolysis (triglyceride breakdown). ASP, on the other hand, promotes fat-storage primarily by stimulating lipogenesis (triglyceride synthesis). Think about it -- eating carbs causes insulin secretion; the insulin prevents fatty acid release from adipose tissue so that the carbs are burned for energy first. Eating fat causes ASP secretion; the ASP causes any extra fat to be stored in adipose tissue. This doesn't mean the insulin does not directly stimulate lipogenesis or that ASP doesn't directly prevent lipolysis, because they do. However, these are secondary effects. Thanks for the info. One or two questions... "Acylation stimulating protein (ASP) is a hormone produced by adipocytes and is of importance for the storage of energy as fat." Under what circumstances do the adipocytes produce ASP? What triggers the fat cells to increase or decrease production of ASP? TC Insulin causes a modest increase in ASP - about 2 times basal levels. Chylomicrons, lipoproteins produced by the intestines containing ingested fat, cause a much larger increase - about 10 times basal levels. Glucose, fatty acids, and VLDL don't stimulate ASP production directly at all. After eating a mixed meal, ASP levels in adipose tissue peak in 3 to 5 hours and decrease to baseline levels by 6 hours. ASP in plasma, however, doesn't necessarily rise after eating. ASP works locally in adipose tissue. I'm not sure how it's degraded or disposed of, but it doesn't seem to make its way into the general circulation in a predictable way AFAIK. |
#106
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Uncovering the Atkins diet secret
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#107
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Uncovering the Atkins diet secret
eat about 4 or 5 malitol based chocolate candy bars each day, (lo carb) and
watch the weight drop off ... diarrhia so bad it blows you out. Assures Outgo = Input "talkback" wrote in message ... wrote: In sci.med.nutrition tcomeau wrote: : Maybe the lesson to be learned is that calories really have little : bearing when it comes to weight gain or loss in humans. 1) Please learn to trim quotes 2) Have you somehow forgotten the laws of thermodynamics? It is quite simple: if energy in energy out, the body will gain mass. If energy out energy in, the body will lose mass. Do as I preach, not as I do. (The Late) Dr. Atkins Stroked out, fat & dead |
#108
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Uncovering the Atkins diet secret
Thermodynamics --- a law we can't live without! [grin]
wrote in message news:slbWb.19977$032.64937@attbi_s53... In sci.med.nutrition tcomeau wrote: : Maybe the lesson to be learned is that calories really have little : bearing when it comes to weight gain or loss in humans. 1) Please learn to trim quotes 2) Have you somehow forgotten the laws of thermodynamics? It is quite simple: if energy in energy out, the body will gain mass. If energy out energy in, the body will lose mass. |
#109
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Uncovering the Atkins diet secret
On Thu, 12 Feb 2004 14:06:29 GMT, J Stutzmann
wrote: Thermodynamics --- a law we can't live without! [grin] wrote in message news:slbWb.19977$032.64937@attbi_s53... In sci.med.nutrition tcomeau wrote: : Maybe the lesson to be learned is that calories really have little : bearing when it comes to weight gain or loss in humans. 1) Please learn to trim quotes 2) Have you somehow forgotten the laws of thermodynamics? It is quite simple: if energy in energy out, the body will gain mass. If energy out energy in, the body will lose mass. Let's say that eating fiber caries a certain amount of calories through your body so that you don't digest them. Then, while calories in might not change, eating more fiber would change the amount of calories out. These "laws" are based on ideal situations. For instance, "an object in motion tends to stay in motion" works great IN A VACUUM. It doesn't work nearly as well in atmosphere. People aren't closed systems. While these "laws" can help to describe what happens to people, they aren't 100% accurate. -------- Bob in CT Remove ".x" to reply |
#110
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Uncovering the Atkins diet secret
In article , Bob in CT
wrote: On Thu, 12 Feb 2004 14:06:29 GMT, J Stutzmann wrote: Thermodynamics --- a law we can't live without! [grin] wrote in message news:slbWb.19977$032.64937@attbi_s53... In sci.med.nutrition tcomeau wrote: : Maybe the lesson to be learned is that calories really have little : bearing when it comes to weight gain or loss in humans. 1) Please learn to trim quotes 2) Have you somehow forgotten the laws of thermodynamics? It is quite simple: if energy in energy out, the body will gain mass. If energy out energy in, the body will lose mass. Let's say that eating fiber caries a certain amount of calories through your body so that you don't digest them. Then, while calories in might not change, eating more fiber would change the amount of calories out. These "laws" are based on ideal situations. For instance, "an object in motion tends to stay in motion" works great IN A VACUUM. It doesn't work nearly as well in atmosphere. People aren't closed systems. While these "laws" can help to describe what happens to people, they aren't 100% accurate. And they don't matter in the long run because people can't give everlasting microscopic attention to every bite for a lifetime. They have to develop an eating "cruise control" that they can use without negative calorie theories and this fiber concept, Fiber is important for good bowel function. Eating less, exercising more and doing it ongoing is what will yield results. The one thing that stands out IMO is this has to be a lifetime committment, not annual, seasonal or now and then, not let's splurge weekends and start over Monday. -- Diva ****** There is no substitute for the right food |
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