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Stop Keto Now - The Mice Have Spoken!
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<blockquote data-quote="tim2000s" data-source="post: 1855300" data-attributes="member: 30007"><p>Or to quote their key points:</p><ul> <li data-xf-list-type="ul">A ketogenic diet is known to lead to weight loss and is considered metabolically healthy; however there are conflicting reports on its effect on hepatic insulin sensitivity.</li> <li data-xf-list-type="ul">KD fed animals appear metabolically healthy in the fasted state after 3 days of dietary challenge, whereas obesogenic high‐fat diet (HFD) fed animals show elevated insulin levels.</li> <li data-xf-list-type="ul">A glucose challenge reveals that both KD and HFD fed animals are glucose intolerant.</li> <li data-xf-list-type="ul">Glucose intolerance correlates with increased lipid oxidation and lower respiratory exchange ratio (RER); however, all animals respond to glucose injection with an increase in RER.</li> <li data-xf-list-type="ul">Hyperinsulinaemic–euglycaemic clamps with double tracer show that the effect of KD is a result of hepatic insulin resistance and increased glucose output but not impaired glucose clearance or tissue glucose uptake in other tissues.</li> </ul><p>If anything, the glucose tolerance test was made worse by fasting the mice before doing it, after 3 days of solid high fat diet, which really wouldn't help.</p><p></p><p>I think point 2 is the more important one.</p><p></p><p>Reading further through the document, the results showed:</p><p><span style="font-size: 15px"><strong>Short‐term obesogenic HFD feeding but n</strong></span><strong><span style="font-size: 15px">ot KD causes an increase in fasting insulin and homeostatic model assessment‐insulin resistance (HOMA‐IR)</span></strong></p><p><strong><span style="font-size: 15px"></span></strong></p><p><span style="font-size: 15px">also:</span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><strong>Short‐term KD or HFD feeding causes impaired glucose clearance and insulin tolerance </strong>(an already recognised phenomenon that is known about in human OGTTs)</span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px">plus:</span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><strong>Steady‐state RER inversely correlates with glucose tolerance, although all groups respond to an i.p. glucose challenge with an increase in RER</strong> which means that those on the KD diet were reliant on lipids as their energy source</span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px">In addition:</span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><strong>Hyperinsulinaemic–euglycaemic clamps reveal differences in insulin‐suppressed endogenous glucose production but not glucose disposal or tissue glucose uptake</strong> which is where they state that the glucose disposal across tissues was unchanged between diets, and it demonstrated that it was the liver that was impaired in glucose clearance after three days.</span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"></span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px">Finally:</span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><em>Interestingly, in our studies, only the HFD animals showed signs of impaired glucose homeostasis when observed in the 6 h fasted state, even though the effect on hepatic glucose output under insulin was stronger in the KD fed group. [...] It is relevant to note that a low carbohydrate KD does not cause obesity and that muscle insulin sensitivity appears to be entirely preserved in this model even after long periods of feeding, in marked contrast to obesogenic HFD [...] This is a necessary adaptation in animals on a KD. However, in animals consuming large amounts of fat together with significant amounts of carbohydrate (a hallmark of the so‐called Western diet), the increased flux of glucose from endogenous production combines with the dietary glucose, leading to a progressive deterioration of systemic insulin sensitivity caused by the elevated insulin levels released from the pancreas to cope with elevated postprandial and fasting glucose levels.</em></span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"></span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px">Or in other words, the headlines have inaccurately reported a load of old ****. The discussion in the paper itself doesn't support the headline hypothesis. </span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"></span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px">The researchers have basically said that those on the obesogenic High Fat Diet had impaired glucose homeostasis where the Ketogenic Diet fed ones didn't. In addition, the KD fed animals did not become obese. Only those on the 50% of calories HFD diet (supposed to equate to a standard western diet in a partially fasted state) and chow got fat and showed signs of progressing to T2D.</span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"></span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px">Basically, no-one in the press has read the paper properly, they've jumped to conclusions and the reports in the media are cobblers. Terrible reporting all round. </span></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"><span style="font-size: 15px"></span></span></span></p><p><span style="font-size: 15px"><span style="font-size: 15px"></span></span></p><p><span style="font-size: 15px"></span></p></blockquote><p></p>
[QUOTE="tim2000s, post: 1855300, member: 30007"] Or to quote their key points: [LIST] [*]A ketogenic diet is known to lead to weight loss and is considered metabolically healthy; however there are conflicting reports on its effect on hepatic insulin sensitivity. [*]KD fed animals appear metabolically healthy in the fasted state after 3 days of dietary challenge, whereas obesogenic high‐fat diet (HFD) fed animals show elevated insulin levels. [*]A glucose challenge reveals that both KD and HFD fed animals are glucose intolerant. [*]Glucose intolerance correlates with increased lipid oxidation and lower respiratory exchange ratio (RER); however, all animals respond to glucose injection with an increase in RER. [*]Hyperinsulinaemic–euglycaemic clamps with double tracer show that the effect of KD is a result of hepatic insulin resistance and increased glucose output but not impaired glucose clearance or tissue glucose uptake in other tissues. [/LIST] If anything, the glucose tolerance test was made worse by fasting the mice before doing it, after 3 days of solid high fat diet, which really wouldn't help. I think point 2 is the more important one. Reading further through the document, the results showed: [SIZE=4][B]Short‐term obesogenic HFD feeding but n[/B][/SIZE][B][SIZE=4]ot KD causes an increase in fasting insulin and homeostatic model assessment‐insulin resistance (HOMA‐IR) [/SIZE][/B] [SIZE=4]also: [SIZE=4][B]Short‐term KD or HFD feeding causes impaired glucose clearance and insulin tolerance [/B](an already recognised phenomenon that is known about in human OGTTs) plus: [SIZE=4][B]Steady‐state RER inversely correlates with glucose tolerance, although all groups respond to an i.p. glucose challenge with an increase in RER[/B] which means that those on the KD diet were reliant on lipids as their energy source In addition: [SIZE=4][B]Hyperinsulinaemic–euglycaemic clamps reveal differences in insulin‐suppressed endogenous glucose production but not glucose disposal or tissue glucose uptake[/B] which is where they state that the glucose disposal across tissues was unchanged between diets, and it demonstrated that it was the liver that was impaired in glucose clearance after three days. Finally: [I]Interestingly, in our studies, only the HFD animals showed signs of impaired glucose homeostasis when observed in the 6 h fasted state, even though the effect on hepatic glucose output under insulin was stronger in the KD fed group. [...] It is relevant to note that a low carbohydrate KD does not cause obesity and that muscle insulin sensitivity appears to be entirely preserved in this model even after long periods of feeding, in marked contrast to obesogenic HFD [...] This is a necessary adaptation in animals on a KD. However, in animals consuming large amounts of fat together with significant amounts of carbohydrate (a hallmark of the so‐called Western diet), the increased flux of glucose from endogenous production combines with the dietary glucose, leading to a progressive deterioration of systemic insulin sensitivity caused by the elevated insulin levels released from the pancreas to cope with elevated postprandial and fasting glucose levels.[/I] Or in other words, the headlines have inaccurately reported a load of old ****. The discussion in the paper itself doesn't support the headline hypothesis. The researchers have basically said that those on the obesogenic High Fat Diet had impaired glucose homeostasis where the Ketogenic Diet fed ones didn't. In addition, the KD fed animals did not become obese. Only those on the 50% of calories HFD diet (supposed to equate to a standard western diet in a partially fasted state) and chow got fat and showed signs of progressing to T2D. Basically, no-one in the press has read the paper properly, they've jumped to conclusions and the reports in the media are cobblers. Terrible reporting all round. [/SIZE] [/SIZE] [/SIZE] [/SIZE] [/QUOTE]
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